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1510 N CANDELLARIA W Tooele, UT 84074
Hi, Blueroof .com.
My name is
and I have a question about 1510 N CANDELLARIA W Tooele
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or call during
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Estimated Monthly Payment$5,051
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- Virtual Tour
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- Status: Pending
Listing courtesy of Wise Choice Real Estate
*** SALE FAILED FINANCING -- COME SEE IT TODAY!!!*** Curb appeal is the first thing you will notice about this adorable home. Once you enter you get an open layout that has kitchen, dining room and family room all connected with vaulted ceilings. 4 bedroom's, 2 bathroom's and a 2 car garage. Basement bathroom features a 2 person jetted tub and custom tile. Schedule a private showing today!
Interior Features Include:
Bath: Master, Closet: Walk-In, Dishwasher, Built-In, Disposal, Jetted Tub, Range/Oven: Free Stdng., Vaulted Ceilings
Basement Full
Fireplaces 0
Air Cond: Central Air; Electric
Heating: Forced Air
Floor Type: Carpet, Tile
Exterior Features Include:
Double Pane Windows, Patio: Covered, Porch: Open
Acreage: 0.1100 Acres
Lot: Corner Lot, Curb & Gutter, Fenced: Full, Road: Paved, Sidewalks, Sprinkler: Auto-Full, Terrain, Flat
Landscape Landscaping: Full
Exterior: Aluminum/Vinyl
Garage/Parking: Attached, Opener
Driveway Concrete
Garage Capacity: 2
Other Features Include:
Subdivision: OVERLAKE
Inclusions: Ceiling Fan, Microwave, Range
Amenities: Cable Tv Available, Cable Tv Wired, Park/Playground
Water: Culinary
Utilities Gas: Connected, Power: Connected, Sewer: Connected, Sewer: Public, Water: Connected
Storage Garage, Basement
Taxes 837
School District: Tooele
Information deemed reliable but not guaranteed accurate. Buyer to verify all information.The multiple listing information is provided by Wasatch Front Regional Multiple Listing Service, Inc. from a copyrighted compilation of listings. The compilation of listings and each individual listing are © 2014 Wasatch Front Regional Multiple Listing Service, Inc., All Rights Reserved. The information provided is for consumers, personal, non-commercial use and may not be used for any purpose other than to identify prospective properties consumers may be interested in purchasing.


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Home | Schedule at a Glance | House of Delegates | Keynote Speaker | Breakout Sessions | FAQsCandidates for Elected Office | Travel and Hotel | Exhibitors and Sponsors | Optional Activities | Registration
ASDA members are invited to Orlando, Florida, for the 2017 Annual Session.
Annual Session brings together more than 600 dental students from around the country who are committed to moving ASDA forward and getting more involved in organized dentistry. It is the official gathering of ASDA's House of Delegates, where policy is set and leaders are elected. (Meet the candidates standing for election.)
Annual Session 2017 will celebrate that dental school is a magical and special time of your life, where you're stretching your limits, learning to do what once seemed impossible and exploring all your potential. You will Believe in the Magic!
NEW! View the 2017 Proposed Resolutions for the House of Delegates.
Key Annual Session Deadlines
Feb. 17, 2017: Cancellation DeadlineFeb. 22, 2017: Opening Ceremonies for Annual Session 2017Feb. 23, 2017: Onsite resolutions due (1:30 p.m.)
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subset: commoncrawl


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Reviews for Pacific Loft ApartmentsAddress: 29 North Elliot Place, New York, New York, USA
Rooms from: US$ 0
Ratings Explained
(Hostelworld.com and Affiliate sites)
The following reviews were submitted by customers who booked through our sister site, Hostelworld.com, in the last 12 months.
The ratings in the rating box are based on all-time feedback for the property and are the opinions of the customers who submitted them; they do not express the opinions of Hostelworld.com or our affiliate sites.
Overall Rating (32 Ratings)
Customer Reviews for Pacific Loft Apartments
noemiiacono8244, from Italy ~ 22nd Aug 2016
traviatta21500, from USA ~ 9th Jul 2016
peterpolomka756, from Australia ~ 14th May 2016
rubabhk7146, from USA ~ 28th May 2016
achapman01649, from USA ~ 22nd May 2016
beautifulstruggle7171, from USA ~ 15th Mar 2016
zacharyjenglish4109, from USA ~ 24th Mar 2016


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Trade Assurance:
Product quality protection
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Home > Company Profile
Dongguan Shuobao Industrial Equipment Co., Ltd.
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The supplier's company premises has been checked by Alibaba.com staff to ensure onsite operations exist there. A third-party verification company has confirmed the legal status of the supplier.
|Business Type:
|Manufacturer, Trading Company
|Guangdong, China (Mainland)
|Main Products:
|Barrel Electroplating Equipment,Rack Electroplating Equipment,Automatic Electroplating Equipment,Cartridge Filter,Chemical Pump
|Total Employees:
|11 - 50 People
|Total Annual Revenue:
|US$5 Million - US$10 Million
|Year Established:
|Top 3 Markets:
|Mid East 20.00% Southeast Asia 20.00% South America 10.00%
Dongguan Shuobao Industrial Equipment Co., Ltd set up 2000, is the leading manufacturer of industria...
Dongguan Shuobao Industrial Equipment Co., Ltd set up 2000, is the leading manufacturer of industrial equipment in China. Also we are the professional exporter and service provider of plating equipments and filtering equipments. Based on our company's philosophy of " Intelligent Technology, Environmental Protection and Energy Saving", we have been devoted ourselves for more than 10years to developing, designing and researching professional Metal/ABS Automatic Control System Plating line, Waste water filtering system, Water Circulation system., chemical filter, pump and related products. Shuobao devote ours effort to make our environment protected. We have much original creation technical which can save much more operator cost for clients, and improvement the item quality, reduce chemical wasting, Raise water reuse efficiency, cleaning workshop air, reduce the energy using.
Our Industrial equipments all are with high technology strict quality control. Our products passed ISO9001 International Quality Management System Certification .All PLC control Part we all import from Taiwan, Japan. We try best to make the line as automate as we can, so that the customer Can easy management. And make sure high efficiency production. All our equipments will meet the environmental protection government requirement.
Since start our business on 2000, we have established our own brand "Shuobao" with a good reputation in domestic and international markets. Our Shenzhen Work shop with 4000 square meter and with more than 100 workers. We are the expert of Metal/ABS Automatic Control System Plating line, Waste water filtering system, Water Circulation system. For over 10 years' efforts, we have set up our sales networks around the world. Our products are used in electroplating, PCB industry, pharmaceutical dyeing industry, medical, waste water treatment, waste gas treatment, etc. We always try our best to keep our best quality, competitive price and warm service to satisfy our customers. We would like to cooperate with worldwide friends for our brighter prosperity
Thank you very much for you to give us opportunity to participate in your company production line planning and design. We will use our professional and dedicated to give you the most satisfied with the action!
Trade Capacity View More >
Trade & Market
|Main Markets
|Total Revenue(%)
|Mid East
|Southeast Asia
|South America
|Domestic Market
|South Asia
|Southern Europe
|Northern Europe
|Central America
|Western Europe
|Eastern Asia
|Eastern Europe
|North America
|Export Percentage:
|31% - 40%
|Export Mode:
|Using an agent
|No. of Employees in Trade Department:
|3-5 People
Email to this supplier
- Company Overview
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- R&D Capacity
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The living areas open straight onto a courtyard with a sleek swimming pool
Most agree commercial real estate is down since Brexit, but estimates differ over how much
Defining the two home styles is tricky because of overlapping traits. But when it comes time to sell, modern homes have higher asking prices than contemporary ones.
Designers furnished interior in 'New York' art deco style.


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Cost Efficiency of Finnish Municipalities in Basic Service Provision 1994-2002
Cost efficiency of basic welfare service provision in 353 Finnish municipalities in 1994-2002 is investigated. In a basically two tier public sector (central government and municipalities) the municipal sector has a central role in the Finnish economy as a provider of welfare services. Data Envelopment Analysis (DEA), a non-parametric linear programming method is employed, calculating a best practise total cost frontier for the decision making units, and comparing the various DMUs with this frontier. The outputs consist of up to ten volume indicators of services in health, social and educational sector. As the combined input, total real production costs of these services is used. According to the results efficiency differences were considerable between the municipalities, and a small group of a peripheral municipalities scored clearly below the others. Also annual changes in cost efficiency were estimated. As a second stage, differences in the DEA cost efficiency scores were explained with statistical models. Here the explanatory variables included structural and demographic indicators of municipalities, their location and measures of political power at local level. According to the results several of these variables had an expected effect on cost efficiency.
If you experience problems downloading a file, check if you have the proper application to view it first. In case of further problems read the IDEAS help page. Note that these files are not on the IDEAS site. Please be patient as the files may be large.
|Date of creation:
|Aug 2005
|Contact details of provider:
| Postal: Welthandelsplatz 1, 1020 Vienna, Austria
Web page: http://www.ersa.org
References listed on IDEAS
Please report citation or reference errors to , or , if you are the registered author of the cited work, log in to your RePEc Author Service profile, click on "citations" and make appropriate adjustments.:
- Loikkanen, Heikki A. & Susiluoto, Ilkka, 2002. "An evaluation of economic efficiency of finnish regions by DEA and Tobit models," ERSA conference papers ersa02p237, European Regional Science Association.
- Seiford, Lawrence M. & Thrall, Robert M., 1990. "Recent developments in DEA : The mathematical programming approach to frontier analysis," Journal of Econometrics, Elsevier, vol. 46(1-2), pages 7-38.
- DE BORGER, Bruno & KERSTENS, Kristiaan, 1994.
"Cost efficiency of Belgian local governments: A comparative analysis of FDH, DEA and econometric approaches,"
SESO Working Papers
1994002, University of Antwerp, Faculty of Applied Economics.
- De Borger, Bruno & Kerstens, Kristiaan, 1996. "Cost efficiency of Belgian local governments: A comparative analysis of FDH, DEA, and econometric approaches," Regional Science and Urban Economics, Elsevier, vol. 26(2), pages 145-170, April.
- De Borger, B & Kerstens, K. & Moesen, W. & Vanneste, J., 1994.
"Explaining Differences in Productive Efficiency: An Application to Belgian Municipalities,"
Public Choice,
Springer, vol. 80(3-4), pages 339-358, September.
- DE BORGER, Bruno & KERSTENS, K. & MOESEN, Wim & VANNESTE, Jacques, 1992. "Explaining differences in productive efficiency: An application to Belgian municipalities," SESO Working Papers 1992003, University of Antwerp, Faculty of Applied Economics.
- Baumol, William J, 1972. "Macroeconomics of Unbalanced Growth: Reply," American Economic Review, American Economic Association, vol. 62(1), pages 150-150, March.
- Maija-Liisa Järviö & Kalevi Luoma, 2000. "Productivity Changes in Finnish Health Centres: A Malmquist Index Approach," Discussion Papers 218, Government Institute for Economic Research Finland (VATT).
- Balaguer-Coll, Maria Teresa & Prior, Diego & Tortosa-Ausina, Emili, 2007.
"On the determinants of local government performance: A two-stage nonparametric approach,"
European Economic Review,
Elsevier, vol. 51(2), pages 425-451, February.
- Emili Tortosa Ausina & Diego Prior & María Teresa Balaguer-Coll, 2004. "On The Determinants Of Local Government Performance: A Two-Stage Nonparametric Approach," Working Papers. Serie EC 2004-04, Instituto Valenciano de Investigaciones Económicas, S.A. (Ivie).
- Charnes, A. & Cooper, W. W. & Rhodes, E., 1978. "Measuring the efficiency of decision making units," European Journal of Operational Research, Elsevier, vol. 2(6), pages 429-444, November.
- R. D. Banker & A. Charnes & W. W. Cooper, 1984. "Some Models for Estimating Technical and Scale Inefficiencies in Data Envelopment Analysis," Management Science, INFORMS, vol. 30(9), pages 1078-1092, September.
- Tanja Kirjavainen & Heikki A. Loikkanen, 1995. "School Resources and Student Achievement: Evidence from Finnish Senior Secondary Schools," Discussion Papers 91, Government Institute for Economic Research Finland (VATT).
- António Afonso & Sónia Fernandes, 2003. "Efficiency of Local Government Spending: Evidence for the Lisbon Region," Working Papers Department of Economics 2003/09, ISEG - School of Economics and Management, Department of Economics, University of Lisbon.
- Kirjavainen, Tanja & Loikkanen, Heikki, 1996.
"Efficiency Differences of Finnish Senior Secondary Schools: An Application of DEA and Tobit-Analysis,"
Discussion Papers
570, The Research Institute of the Finnish Economy.
- Kirjavainen, Tanja & Loikkanent, Heikki A., 1998. "Efficiency differences of finnish senior secondary schools: An application of DEA and Tobit analysis," Economics of Education Review, Elsevier, vol. 17(4), pages 377-394, October.
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For more details visit to http://contactforhelp.com/mcafee/
Ad ID: 8256


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Best of Portland
It's easy to go on and on about the wonders of Portland, as many have done. What it boils down to is this: Portland is, as the New York Times says, "hard to resist" and "one of our national capitals of cool." Nestled among towering trees and trillium-lined creeks, our campus is only six miles from the city's vibrant downtown.
Straddling the line between a big city and a small town, Portland offers attractions and opportunities for almost any interest:
- Professional sports teams in basketball and soccer with devoted following (the Trail Blazers, Timbers, and Thorns).
- Major and minor performing arts companies, ranging from the Oregon Symphony to experimental theatre performances.
- Thriving visual arts, crafts, and tech communities supported by a strong city-wide DIY culture.
- A nationally recognized food scene with options ranging from fine dining to the famous Voodoo Doughnut and budget-friendly food carts. Check out what the The Washington Post has to say.
- Easy access to the natural wonders of the Pacific Northwest, with mountains, beaches, deserts, and forests all less than a two-hour drive away.
Portland is also where our students engage in community service, industry internships, and research projects. Although most undergrads live on campus, graduate and law students find housing in neighborhoods close by. Either way, cars are optional—getting around town is easy by bike, bus, streetcar, light rail, and Lewis & Clark shuttle.
The video above was produced by TravelPortland. Visit YouTube for the full credits.
Lewis & Clark in the Community
Brian Lindstrom B.A. '84 and his wife, best-selling author Cheryl Strayed, just signed a development deal with HBO to adapt her essay collection, Tiny Beautiful Things, into a television series.
Lewis & Clark graduates leave campus prepared for life after college.
Paula Hayes B.S. '92—a Board of Trustees member and upcoming recipient of the Pioneer Alumna Leadership Award—was recently featured in Portland Business Journal for her innovative cosmetics company.


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Travelling to visit friendsSticky
I travel frequently. At least twice a month, I take a weekend and go somewhere, and it's normally to visit friends all over the country. Travelling from the West Coast can be time consuming, but it's something that I just have to deal with if I want to continue living in Cali, which I do. In the past year, I've been to 14 different states, and have had an absolute blast doing it. Fortunately, my day job gives me a great deal of time off yearly (almost a full month) so I can take long weekends routinely.
One of my close buddies works for Quicken Loans in one of their offices in Farmington Hills, Michigan. He called me up out of the blue, and wanted to know if I would come out and help him with his preparation for a Half Marathon that is taking place in Chicago in a few weeks. Most of my trips include partying with buddies, so this was a welcome change, and I immediately agreed to it. He did say that he had a few ideas about going to Detroit, or Ann Arbor as well during the weekend, and I have never been to Ann Arbor, so this sounded like a blast of a time.
Since I was flying in on a Friday in the late afternoon, and Ryan was still working, I simply needed a one way ride to his place from the Detroit Airport. I figured I would call a Limo Service and see what I could get in the form of a Lincoln Town Car, which I easily found through www.limofarmingtonhills.com. I was picked up curbside by the chauffeur, but we got stuck in traffic and didn't arrive at Ryan's house until about an hour later.
Once there, I found the hide-a-key, and made my way into the house to get settled.
After Ryan arrived home, we discussed his specific workout routine, as it included strength training along with distance running to get prepared for the Half. He said he had been taking some supplements from Advocare, which had been helping him with his cravings for sugar. I have taken some similar products in the past (from another direct sales company), and the results were awesome. If you have the money for them, the products can be absolutely amazing, but because of the direct sales aspect, and paying distributors their commission, you can spend a ton of dough.… Read More


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|Message view
|« Date » · « Thread »
|« Date » · « Thread »
|"Mamta A. Satoor (JIRA)" <j...@apache.org>
|[jira] Commented: (DERBY-5121) Data corruption when executing an UPDATE trigger
|Thu, 17 Mar 2011 21:46:30 GMT
[ https://issues.apache.org/jira/browse/DERBY-5121?page=com.atlassian.jira.plugin.system.issuetabpanels:comment-tabpanel&focusedCommentId=13008168#comment-13008168 ] Mamta A. Satoor commented on DERBY-5121: ---------------------------------------- I am working on backporting this simple fix to disbale the column read optimization from 10.7 to trunk but I am seeing OOM errors for a subset of org.apache.derbyTesting.functionTests.tests.memory.TriggerTests. The OOM should depend on how much heap the test gets run with. On both 10.7 and trunk(with 10.7 changes backported). I see no failures if I run the test with higher heap as shown below java -Dderby.tests.trace=true -Xmx256M -XX:MaxPermSize=128M junit.textui.TestRunner org.apache.derbyTesting.functionTests.tests.memory.TriggerTests But if I run the test on both 10.7 and trunk(with 10.7 changes backported) with lower heap, I see OOM errors java -Dderby.tests.trace=true -Xmx16M -Dderby.storage.pageCacheSize=100 junit.textui.TestRunner org.apache.derbyTesting.functionTests.tests.memory.TriggerTests So the behavior on the 2 codelines with restricted and generous heap is the same when the test is run directly. But when I run the junit suite as follows, I get OOM errors on trunk but not on 10.7 codeline. At this point, I am not sure why. Is there a way that we change the available heap on trunk for org.apache.derbyTesting.functionTests.tests.memory.TriggerTests when it is run through the functionTests.suites.All junit suite? That's the only reason I can think why the test would fail anywere. It appears that on 10.7, we do not change the heap for org.apache.derbyTesting.functionTests.tests.memory.TriggerTests when it is run through the functionTests.suites.All junit suite? Does anyone have any clue about this difference in behavior between 10.7 and trunk? thanks java -Dderby.tests.trace=true -Xmx256M -XX:MaxPermSize=128M junit.textui.TestRunner org.apache.derbyTesting.functionTests.suites.All > runall.out 2>&1 > Data corruption when executing an UPDATE trigger > ------------------------------------------------ > > Key: DERBY-5121 > URL: https://issues.apache.org/jira/browse/DERBY-5121 > Project: Derby > Issue Type: Bug > Components: SQL > Affects Versions: 10.7.1.1, 10.8.0.0 > Reporter: Rick Hillegas > Assignee: Mamta A. Satoor > Labels: derby_triage10_8 > Attachments: DummyProc.java, derby5121_patch1_diff.txt, triggerBug.sql, triggerBug.sql, triggeredBug2.sql, triggeredCorruption.sql > > > When executing an UPDATE trigger, the following error is raised. I will attach a test case: > ERROR XCL12: An attempt was made to put a data value of type 'org.apache.derby.impl.jdbc.EmbedClob' into a data value of type 'INTEGER'. -- This message is automatically generated by JIRA. For more information on JIRA, see: http://www.atlassian.com/software/jira
|View raw message


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Harley-Davidson for Sale
Selected Filters:Type of Ad: Vehicles for Sale Make: Harley-Davidson
2005 Harley-Davidson Deuce Softail Fxs
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Just arrived HARLEY DAVIDSON 2005 FXS SOFTAIL JUST 16,868 MILES LIKE NEW!!! LOTS OF EXTRAS SEE PIX ATTACHED!!!... More
2005 Harley-Davidson Electra Glide
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Screaming EagleTo be sold at the Indy 2017 auction, Indianapolis, IN, May 16-21, 2017. To consign a car or to register to bid, visit... More
2006 Harley-Davidson Motorcycle
Venice, FL
Harley-Davidsons deadly serious Destroyer, a competition only machine based on a V/Rod that easily cracks the 9-second barrier in quarter mile drag racing.Their is... More
Advertiser since 2011
1991 Harley-Davidson Motorcycle
Venice, FL
In 1991 Harley-Davidson built this limited edition motorcycle to commemorate the 50th anniversary of the Sturgis Rally. Â Only 1600 of these bikes were produced... More
Advertiser since 2011
1942 Harley-Davidson XA Military
Las Vegas, NV
Harley-Davidson's first 4-speed foot shift motorcycle- Shaft drive - A BMW clone machined to SAE standards- Intended for the desert war in North Africa,... More
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Restored- The WLD was the extra-high compression Sport Solo modelTo be sold at the Las Vegas Motorcycle June 2017 auction, Las Vegas, NV, June... More
1942 Harley-Davidson WLA Military
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The WLA was the US armed forces workhorse motorcycle- Known as the Liberator and the Bike That Won The War- Blackout lights- Ammo box-... More
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Purchased in Hazelton KS in 1969 - Customized by Bud Cox for his son Stan,completed in early 1971- Original period chopper- Dual upswept exhaust-... More
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To be sold at the Las Vegas Motorcycle June 2017 auction, Las Vegas, NV, June 1-3, 2017. To consign a car or to register... More
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Windshield- Royalite saddlebags with Jet ornaments- Buddy seat- Tool box- Trumpet hornTo be sold at the Las Vegas Motorcycle June 2017 auction, Las Vegas,... More
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The Knucklehead was now in it's 6th year of production and well sorted, the postwar models were essentially unchanged from the 1941 models- RestoredTo... More
1928 Harley-Davidson B Single
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Purchased in 1982 and restoredTo be sold at the Las Vegas Motorcycle June 2017 auction, Las Vegas, NV, June 1-3, 2017. To consign a... More
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2014 Orange County Coppers "New England Patriots Chopper" NFL 2017 SUPERBOWL CHAMPIONS! ONE-OF-A-KIND! BUILT BY WELL-KNOWN OCC "ORANGE COUNTY CHOPPERS"! THE ENTIRE BUILD PROCESS IS DOCUMENTED ON YOU... More
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6000 miles on new 96 cu in engine,excellent paint ,XLNT cam,xlnt seat,xlnt tires,super clean all over ,cant ride 2 bikes,call me lets talk 9365548711... More
Advertiser since 1979


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In the haunting conclusion of Hobb's Soldier Son trilogy (after 2006's Forest Mage), Gernian soldier Nevare Burvelle escapes from prison with some help from his lover, Lisana, who divided his soul so that he could become a Speck mage called Soldier's Boy. The two personalities now awkwardly time-share Nevare's body. Using Soldier's Boy's powers, Nevare tries to destroy the Gernian road that threatens to ravage the Specks' forest home, and almost dies from exhaustion. Nursed back to health by Olikea, the Speck woman whose sole duty is to feed him enough to power his magic, Nevare must find a way to keep Gernia from destroying the forest, prevent the Specks from further spreading the plague that has decimated the Gernians and reunite the severed halves of his soul. Hobb's dreamy prose is sometimes weighed down by a confusing magical system and glacial pacing, but she provides a stunning resolution to this epic fantasy about the importance of environmental and social balance. (Feb.)Copyright 2007 Reed Business Information
Renegade's Magic (Soldier Son Series #3)by Robin Hobb
The stirring conclusion to The Soldier Son Trilogy—the acclaimed epic tale of duty, destiny, and magic by New York Times bestselling master fantasist Robin Hobb
Loyal, privileged, and brave, Nevare Burvelle proudly embraced his preordained role as soldier in the service of the King of Gernia—unaware of the strange/blockquote>/p>/em>
- Overview
- Editorial Reviews
- Product Details
- Related Subjects
- Read an Excerpt
- What People Are Saying
- Meet the author
The stirring conclusion to The Soldier Son Trilogy—the acclaimed epic tale of duty, destiny, and magic by New York Times bestselling master fantasist Robin Hobb
Loyal, privileged, and brave, Nevare Burvelle proudly embraced his preordained role as soldier in the service of the King of Gernia—unaware of the strange turns his life would ultimately take. Exposed to a plague of enemy sorcery that felled many of his compatriots, he prevailed, but at a terrible cost to his soul, body, and heart. Now he stands wrongly accused of unspeakable crimes—including murder, the most heinous of them all.
Condemned by his brother soldiers and sentenced to death, Nevare has no option but to escape. Suddenly he is an outcast and a fugitive—a hostage to the Speck magic that shackles him to a savage alter ego who would destroy everything Nevare holds dear. With nowhere to turn—except, perhaps, to the Speck woman Lisana, the enemy whom he loves—he is mired in soul-rending despair. But from out of the darkness comes a bright spark of hope.
Perhaps, somehow, the hated magic that has long abused Nevare can be used by him instead. Could he not learn to wield this mighty weapon for his own purposes rather than be enslaved by it? But down what perilous road will this desperate new quest lead him? And what will be the outcome and the ultimate new incarnation of Nevare Burvelle?
Editorial Reviews
Convicted of a crime he did not commit, Nevare Burvelle has fled the town of Gettys and his former soldier comrades for an uncertain future. In desperation he gives in to the Speck magic that dwells within him as a powerful alter ego determined to prevent encroachment upon Speck-held territories. Ultimately, however, Nevare seeks to reconcile his dual nature to bring peace to both sides of his heritage. The author of the "Liveship Traders Trilogy" and the "Farseer Trilogy" brings her latest series to a fitting conclusion. Nevare's journey through war and peace is both timeless and timely and belongs in most libraries.
Jackie Cassada
Copyright © Reed Business Information, a division of Reed Elsevier Inc. All rights reserved.
Product Details
- 9780061798245
- Publisher:
- HarperCollins Publishers
- Publication date:
- 10/13/2009
- Series:
- Soldier Son Series , #3
- Sold by:
- Format:
- NOOK Book
- Pages:
- 704
- Sales rank:
- 94,068
- File size:
Read an Excerpt
Renegade's Magic
Book Three of The Soldier Son Trilogy
Chapter One
Soldier's End
Inever spoke up for myself at my court-martial.
I stood in the box where they put me, and tried not to think of the agonizing bite of the leg irons around my calves. They were too small for a man of my flesh, and the cold iron bit deep into the meat of my legs, burning and numbing at the same time. At the moment, the pain mattered to me more than the outcome of the hearing. I already knew how it would end.
That pain is chiefly what I remember of my trial. It hazes my memories in red. A number of witnesses spoke against me. I recall their righteous voices as they detailed my crimes to the assembled judges. Rape. Murder. Necrophilia. Desecration of a graveyard. My outrage and horror at being accused of such things had been eroded by the utter hopelessness of my situation. Witness after witness spoke against me. Threads of rumor, hearsay from a dead man's lips, suspicions and circumstantial evidence were twisted together into a rope of evidence, stout enough to hang me.
I think I know why Spink never addressed any questions directly to me. Lieutenant Spinrek, my friend since our Cavalla Academy days, was supposed to be defending me. I'd told him that I simply wanted to plead guilty and get it over with. That had angered him. Perhaps that was why he didn't ask me to testify on my own behalf. He didn't trust me to tell the truth and deny all the charges. He feared I'd take the easy way out.
I would have.
I didn't fear the hangman's gibbet. It would be a quick end to a life corrupted by a foreign magic. Walk up the steps,put my head into the noose, and step off into darkness. The weight of my falling body would probably have jerked my head right off. No dangle and strangle for me. Just a quick exit from an existence that was too tangled and spoiled to repair.
Whatever I might have said in my own defense would have made no difference. Wrongs had been done, ugly, evil things, and the citizens of Gettys were determined that someone had to pay for them. Gettys was a rough place to live, a settlement half military outpost and half penal colony on the easternmost boundary of the Kingdom of Gernia. Its citizens were no strangers to rape and murder. But the crimes I was accused of went beyond the spectrum of passion and violence into something darker, too dark even for Gettys to tolerate. Someone had to wear the villain's black cape and pay the toll for such transgressions, and who better than the solitary fat man who lived in the graveyard and was rumored to have doings with the Specks?
So I was convicted. The cavalla officers who sat in judgment on me sentenced me to hang, and I accepted that. I had shamed my regiment. At that moment, my execution seemed the simplest escape from a life that had become the antithesis of every dream I'd ever had. I'd die and be done with disappointment and failure. Hearing my sentence was almost a relief.
But the magic that had poisoned my life was not about to let me go so easily.
Killing me was not enough for my accusers. Evil would be punished with as cruel and vicious a vengeance as they could imagine. Darkness would be balanced with darkness. When the second half of my sentence was pronounced, horror froze me. Before I ascended the gallows to make that final drop, I'd receive one thousand lashes.
I will always recall that stunned moment. The sentence went beyond execution, beyond punishment, to total destruction. As it stripped the flesh from my bones, it would strip away all dignity as well. No man, no matter what his courage, could grit his teeth and keep silent through a thousand lashes. They would mock and jeer me as I shrieked and begged. I would go to my death hating them and myself.
I'd been born to be a soldier. As the second son of a nobleman, I had been decreed by the good god to be a soldier. Despite all that had befallen me, despite the foreign magic that had infected and poisoned me, despite my ejection from the King's Cavalla Academy, despite my father's disowning of me and the scorn of my fellows, I had done my best to serve my king as a soldier. This was what it had earned me. I would scream and weep and plead for mercy before folk who saw me only as a monster. The lash would strip my body naked of both clothing and flesh, exposing the sagging layers of fat that had been their first excuse to hate me. I would faint and be revived with a dash of vinegar on my back. I'd piss myself and dangle helplessly from my manacled wrists. I'd be a corpse long before they hanged my remains. They knew it and so did I.
Even my corrupted and maimed life seemed a better choice than that death. The magic had sought to take me from my own people and use me as a tool against them. I'd fought it. But that final night in my cell, I knew the magic of the Speck folk offered me my only opportunity to save myself. When the magic tore down the walls of my prison, I took the opportunity. I escaped.
But neither the magic nor the good folk of Gettys were done with me. I think the magic knew that I'd given only lip service to my surrender to it. But it demanded all of me, my entire life, with no ties left to bind me to this place and this people, and what I had never given willingly, it now took from me.Renegade's Magic
Book Three of The Soldier Son Trilogy. Copyright © by Robin Hobb. Reprinted by permission of HarperCollins Publishers, Inc. All rights reserved. Available now wherever books are sold.
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Meet the Author
Robin Hobb was born in California but grew up in Alaska. It was there that she learned to love the forest and the wilderness. She has lived most of her life in the Pacific Northwest and currently resides in Tacoma, Washington. She is the author of five critically acclaimed fantasy series: The Rain Wilds Chronicles (Dragon Keeper, Dragon Haven, City of Dragons, Blood of Dragons), The Soldier Son Trilogy, The Tawny Man Trilogy, The Liveship Traders Trilogy, and The Farseer Trilogy. Under the name Megan Lindholm she is the author of The Wizard of the Pigeons, Windsingers, and Cloven Hooves. The Inheritance, a collection of stories, was published under both names. Her short fiction has won the Asimov's Readers' Award and she has been a finalist for both the Nebula and Hugo awards.
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I enjoyed the other 2 books in the series. And although I was never fully engaged in the Forest Mage series, I was interested in seeing it through to the end. This book however, fell short for me. I lost interest about 1/3 of the way into the book and had to force myself to make it through the middle third. Although Ms Hobb ties everything together nicely in the end, the journey was not as enjoyable as i had hoped.
Renegade¿s Magic Robin Hobb Eos, Feb 2008, $25.95 ISBN 9780060757649 His lover, Lisana enabled Gernian soldier Nevare Burvelle to escape incarceration when she split his soul enabling him to become a Speck mage Soldier¿s Boy. However as a nasty by-product, two personalities conflict over who controls the host body. His Soldier¿s Boy¿s mage skills lead Nevare to try to destroy the Gernian road that has begun to devastate the Specks¿ woodlands. His failed efforts leave him near death, but Speck female Olikea uses her healing skills to save his life as is her duty. As he recovers he finds his two sides in conflict as each has a demand. Nevare knows that he must prevent the Gernia from demolishing the Specks¿ forest while at the same time he also must stop the Specks from distributing their deadly plague that has slaughtered the Gernians. He begins to believe that to succeed he must unite his warring split personalities. --- The final Soldier Son tale (see FOREST MAGE and SHAMAN¿S CROSSING) is an entertaining fantasy that looks deep at the issue of development vs. environment. The story line is fun to follow although the pace at times is turtle like especially when the complicated Hobbs magical structure is logically but boringly elucidated (only a fool would read this entry before the previous two books). Still this is a fine trilogy that showcases the importance of finding win-win solutions to complex social issues as the two sides seem to only employ lose-lose methods. --- Harriet Klausner
Great story
Good story but slow reading
I despised the Specks and didn't care for Hobbs partisanship.
I have become a hardcore Robin Hobb fan. She writes like Van Gogh paints or Emeril Lagasse cooks. You will be sure to experience all of the subtle nuances and rich vivid details as she weaves her stories. I love reading fantasy and I thought that I had read the best, but where as Gabaldon and Paolini are exceptional, Robin Hobb is 'the master'. You will not be disappointed with this or any of her other books. The ultimate experience of course will be to be sure to read any of her trilogy or series books in the proper order as they just continue to build in detail and intensity as they go. Check it out, you won't be sorry.
If you need a book to read to kill time then this one is ok. If you are looking for a good story that will keep your attention then this is not it.


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Peter Pavlovic's recent letter to the editor advocated for more armed civilians as the solution to mass shootings like Orlando. Let us inform that suggestion with some facts.
Two decades ago, concealed carry was illegal in 22 states. Since then it's undergone explosive growth. It's now permitted in all 50 states. Currently we have about 12.8 million permit holders, a 2.8-fold increase since 2007.


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Exeter Centre
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Riptide Editors Ginny Baily and Sally Flint will be running a day long creative writing workshop at the Royal Albert Memorial Museum and Art Gallery in Exeter.
The workshop will use RAMM's exhibitions and artefacts to inspire innovative writing. The aim is to get participants started on and to discuss writing that is memorable, sustainable and interesting by exploring both "inside and beyond the frame." In particular we will be looking at writing evoked from memories of childhood.
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Risk of breast cancer in Lynch syndrome: a systematic review
- Aung Ko Win1Email author,
- Noralane M Lindor2 and
- Mark A Jenkins1
DOI: 10.1186/bcr3405
© Win et al.; licensee BioMed Central Ltd. 2013
Received: 27 September 2012
Accepted: 18 March 2013
Published: 19 March 2013
Lynch syndrome is an autosomal dominantly inherited disorder of cancer susceptibility caused by germline mutations in the DNA mismatch repair (MMR) genes. Mutation carriers have a substantial burden of increased risks of cancers of the colon, rectum, endometrium and several other organs which generally occur at younger ages than for the general population. The issue of whether breast cancer risk is increased for MMR gene mutation carriers has been debated with evidence for and against this association.
Using the PUBMED, we identified all relevant studies of breast cancer associated with Lynch syndrome that were published by 15 December 2012. In the review, we included: (i) molecular studies that reported microsatellite instability and/or immunohistochemistry in breast cancer tumors of MMR gene mutation carriers; and (ii) risk studies that investigated risk of breast cancer for confirmed MMR gene mutation carriers or families or clinically and/or pathologically defined Lynch syndrome families.
We identified 15 molecular studies and, when combined, observed 62 of 122 (51%; 95% CI 42 to 60%) breast cancers in MMR gene mutation carriers were MMR-deficient. Of the 21 risk studies identified, 13 did not observe statistical evidence for an association of breast cancer risk with Lynch syndrome while 8 studies found an increased risk of breast cancer ranging from 2- to 18-fold compared with the general population (or non-carriers). There is only one prospective study demonstrating an elevated risk of breast cancer for MMR gene mutation carriers compared with the general population (standardized incidence ratio 3.95; 95% CI 1.59, 8.13).
Since breast cancer is a relatively common disease in the general population, more precise estimates of risk and gene-specific risks will need to utilize large prospective cohort studies with a long follow-up. While current data are inconclusive at a population level, individual tumor testing results suggest that MMR deficiency is involved with breast cancers in some individuals with Lynch syndrome.
Lynch syndrome, formerly known as hereditary nonpolyposis colorectal cancer (HNPCC) [1], is an autosomal dominantly inherited disorder of cancer susceptibility caused by germline mutations in the DNA mismatch repair (MMR) genes, MLH1, MSH2, MSH6 and PMS2. The prevalence of individuals who carry a pathogenic germline mutation in one of these genes in the population is estimated to be, depending on various assumptions, from 1 in 370 to 1 in 3,000 [2–4]. Though rare, mutation carriers have a substantial burden of increased risks of cancers of the colon, rectum, endometrium, stomach, ovary, ureter, renal pelvis, brain, small bowel, and hepatobiliary tract which generally occur at younger ages than for the general population [5].
Lynch syndrome-associated cancers typically exhibit DNA microsatellite instability (MSI) and loss of MMR protein expression. Instability of microsatellite DNA sequences characterized by the presence of random contractions or expansions in the length of simple sequence repeats, can be detected by polymerase chain reaction-based methods [6, 7]. The loss of MMR protein expressions can be detected by immunohistochemistry (IHC) [5]. These techniques have been widely used to triage colorectal cancer patients for testing for germline mutations in the MMR genes, and recently cancers at other sites [8]. As a consequence, various MMR-deficient tumors have been identified in organs that are not traditionally recognized as part of the spectrum of Lynch syndrome.
These cancers include adrenocortical adenocarcinoma [9–11], thyroid carcinoma [10], peritoneal mesothelioma [11], malignant fibrohistiocytoma [12, 13], rhabdomyosarcoma [14], dermatofibrosarcoma [15], leiomyosarcoma [16–19], liposarcoma [19], carcinoid tumour [20], non-Hodgkin lymphoma [21], malignant melanoma [22], pancreas [11, 23], prostate [24] and breast cancers [25–39]. However, for these tumors except pancreatic cancer [40], an increase in risk for MMR gene mutation carriers compared with the population (or non-carriers) has not been observed.
Initially raised by Henry Lynch and colleagues several decades ago [41], the issue of breast cancer risk in Lynch syndrome has been debated with studies providing evidence for and against breast cancer being part of Lynch syndrome [42–44]. In this article, we have reviewed the existing studies that investigated whether breast cancer is caused by a mutation in an MMR gene or whether the risk of breast cancer is increased for women who carry a mutation in an MMR gene.
Materials and methods
Identification of studies
We used PUBMED [45] to search for all relevant studies of breast cancer associated with Lynch syndrome that were published by 15 December 2012. The following combinations of key words were used: 'breast cancer/carcinoma/tumor or extracolonic cancer/tumor/neoplasia' and 'mismatch repair gene mutation or Lynch syndrome or HNPCC'. No language restrictions were imposed. References from relevant articles, letters, reviews and editorials were searched to identify any additional relevant studies. Studies were reviewed initially on the basis of title and abstracts, and then all full manuscripts for those that appeared relevant were obtained and checked for eligibility.
Eligibility criteria
For molecular studies, studies were eligible if they reported mismatch repair deficiency status (either by MSI and/or IHC) of breast cancer tumors of MMR gene mutation carriers. For risk studies, studies were eligible (i) if they were case-control or cohort studies, and (ii) if they investigated the risk of breast cancer for confirmed MMR gene mutation carriers or families or clinically and/or pathologically defined Lynch syndrome families compared with non-carriers or the general population. Studies were excluded if they were editorials or literature reviews.
Data extraction
For molecular studies, we extracted the following data: first author's name, year of publication, country in which the study was performed, number of breast cancers observed in MMR gene mutation carriers, specific mutated MMR gene, age at diagnosis of breast cancer, and the MSI and/or IHC status of the breast tumor.
For risk studies, we extracted the following data: first author's name, year of publication, country in which the study was performed, recruitment and ascertainment method of families or mutation carriers, definition of Lynch syndrome, numbers of MMR gene mutation carriers, specific mutated MMR gene, observed and expected numbers of breast cancers, estimates of breast cancer risk for mutation carriers compared with non-carriers or the general population (expressed as standardized incidence ratio, odds ratio, relative risk or hazard ratio) and absolute or cumulative risk of breast cancer for mutation carriers (expressed as lifetime risk or 10-year risk).
Statistical analysis
For molecular studies, we defined a tumor with high level of microsatellite instability (≥ 30% of markers tested) or those with loss of normal expression of any of the four DNA MMR genes by IHC to be a MMR-deficient tumor. We divided the total number of MMR-deficient breast cancers by the total number of breast cancers in MMR gene mutation carriers to estimate the proportion of breast cancers in MMR gene mutation carriers that were MMR-deficient.
For risk studies that did not provide the relative risk (or standardized incidence ratio), we calculated the estimated the standardized incidence ratio (SIR) by dividing the observed numbers of breast cancers by the reported expected numbers. When not provided by the study, we calculated the 95% CI assuming that the numbers of observed cases followed a Poisson distribution. All statistical analyses were conducted using Stata 11.2 [46].
Summary of molecular studies that investigated mismatch repair (MMR) deficiency status of breast cancer in Lynch syndrome
Single case reports
MMR gene mutated/absence of
MMR protein in IHC/MSI status
Age, years
Boyd et al. [25]
MLH1/MLH1 loss/MSI-H
71 (male)
Caluseriu et al. [26]
Westenend et al. [27]
The Netherlands
MSH2/MSH2 and MSH6/MSI-H
Akoum et al. [28]
MSH2/MSH2 and MSH6/MSS
D'Arcy et al. [29]
MSH2/MSH2 and MSH6/NR
Case series
Number of MMR-deficient breast cancers/
number of MMR gene mutation carriers
Age, years,
mean ± SD
Risinger et al. [30]
3/5 (60%)
Muller et al. [31]
0/3 (0%)
de Leeuw et al. [32]
The Netherlands
7/11 (64%)
43.6 ± 9.2
Blokhuis et al. [33]
South Africa
5/6 (83%)
51.8 ± 16.9
Shanley et al. [34]
3/4 (75%)
65.0 ± 12.3
Jensen et al. [35]
7/16 (44%)
50.4 ± 13.1
Walsh et al. [36]
Australia, USA, Canada
18/35 (51%)
57.5 ± 8.1
Buerki et al. [37]
6/7 (86%)
53.7 ± 15.2
Lotsari et al. [38]
13/20 (65%)
52.7 ± 7.0
Grandval et al. [39]
0/15 (0%)
53.1 ± 10.0
We identified 34 published studies that have reported data that can be used to address the question of whether breast cancer is a Lynch syndrome cancer. In this review, we have attempted to combine all accumulated published evidence to answer the question. There appears to be some evidence from the epidemiological risk studies favoring the concept of an increased risk of breast cancer for germline MMR gene mutation carriers, though the mechanism cannot yet be known.
Molecular studies
Overall, the 15 studies found that approximately half of the breast cancer tumors in carriers of MMR gene mutations were MMR-deficient. Further, the largest case series demonstrated that the proteins not expressed corresponded to the gene that was mutated in the carrier [36]. They also observed that the MMR-deficient breast cancers had pathology features that were consistent with the features identified in colorectal cancers caused by MMR gene mutations [66, 67], that is, MMR-deficient breast cancers were more likely to be poorly differentiated, have a higher mitotic rate, peritumoral lymphocytes, confluent necrosis, a solid growth pattern, and more likely to be estrogen receptor-negative and progesterone receptor-negative than the MMR-proficient breast cancers.
These data support the hypothesis that the MMR gene mutation carriers may have been predisposed to develop these particular breast cancers; that is, MMR gene mutations may initiate the development of breast cancer (as a driver) or accelerate carcinogenesis in breast cancers that occur in MMR gene mutation carriers (as an accelerator). However, these observations are also consistent with MMR deficiency being a phenotype arising within breast cancer that was caused by another factor (as a passenger), rather than the phenotype driving or accelerating carcinogenesis.
Risk studies
One method to overcome this problem of cause or consequence is to determine whether breast cancer is more likely to develop in carriers of MMR gene mutations compared with non-carriers (or the general population), that is, empirical evidence of risk. Eight studies [37, 47–53] estimated breast cancer risk for all female relatives of MMR gene mutation carriers not known to be a non-carrier, that is, those identified as carriers as well as those who were not tested for genetic mutations. Therefore, their study estimates are for an unknown distribution of carriers and non-carriers. If there is an increased risk of breast cancer for MMR gene mutation carriers, their estimates will therefore be attenuated, that is, they will underestimate the true risk of breast cancer for carriers [60]. This may be a reason that all of these studies [37, 48–50, 52, 53] except two [47, 51] observed no evidence of an increased risk of breast cancer or observed a reduced risk of breast cancer for Lynch syndrome families.
One retrospective study [54] compared the observed number of breast cancer in confirmed and obligate carriers with the number expected, and they observed no evidence of an increased risk of breast cancer for carriers (SIR 1.4, 95% CI 0.4, 3.7). As they ascertained carriers from a population cancer registry, the study is less likely to have ascertainment bias because of family history. The lack of evidence in the study might be due to the small sample size (360 mutation carriers).
Six studies [55–60] estimated risk of breast cancer for the female relatives of families ascertained through genetics clinics. Of these, three [55–57] observed no evidence of an increased risk of breast cancer while three [58–60] observed an approximately 2- to 13-fold increased risk of breast cancer for MMR gene mutation carriers compared with the general population. Persons attending genetics clinics are often referred because of a strong family history of cancer. Because these studies did not attempt to correct for the family history ascertainment in their statistical analyses, the estimates of breast cancer risk are likely to be upwardly biased [68] if any of the family members attended the clinics because of a family history of breast cancer.
Two studies [61, 62] from the Colon Cancer Family Registry estimated risk of breast cancer for MMR gene mutation carriers and found no evidence of an increased risk. The study samples were families ascertained through genetics clinics as well as population cancer registries. In these studies, the analyses were adjusted for how these families were ascertained. As it is very difficult to know the exact reason(s) influencing a person/family to be referred and/or attend a genetics clinic, the correction for ascertainment is usually conservative, that is, by conditioning on the cancer status of all family members to avoid overestimation of any particular cancer risk that may have, in part, contributed to referral or attendance [68]. The consequence of this method is that, if families are ascertained only because of colorectal and/or other cancers but not breast cancer, the power to identify an increased risk for breast cancer will be reduced and breast cancer risk estimates from these studies are likely to be underestimated.
Prospective studies avoid the ascertainment issue described above because the carriers used to estimate cancer risk are unaffected at the time of recruitment or first observation. To date, there is only one prospective study of MMR gene mutation carriers without prior diagnosis of cancer [63]. An increased risk of breast cancer was observed In that study for MMR gene mutation carriers (SIR 3.95, 95% CI 1.59, 8.13). An alternative explanation, for at least part of the observed increase in breast cancer risk in this prospective cohort study, is that it might be due to screen-detected cases. Mammographic screening may be more prevalent and/or frequent in women from Lynch syndrome families who are more concerned about cancer risk compared with the general population, thus resulting in breast cancer diagnoses being brought forward due to early detection. If this hypothesis was true, it might be expected to be more evident in prospective studies, given that observation time for risk used in these analyses begins from when the family was first seen in a clinic, the same time during which an increased awareness of cancer risk may arise.
The two other studies of the Colon Cancer Family Registry observed an approximately 2-fold increased risk of breast cancer for MMR gene mutation carrying women. These included those who had a previous diagnosis of colorectal cancer [64] or endometrial cancer [65]. Such studies may be more powerful to identify an increased risk if those with a previous cancer diagnosis represent a more cancer-susceptible subset of carriers.
Blokhius et al. [33] compared the number of breast cancer diagnoses observed in 87 carrier women (cases) with that for their 121 non-carrier sisters (controls) of MLH1 c.C1528T mutation. In this study design, unaffected siblings of familial cases have the same familial risk profile (that is, they could share all other multifactorial causes with their gene-carrying siblings) and therefore, share potential confounders that are correlated within siblings, in other words, it is an informative comparison within the same study base [69]. The lack of evidence in the study might be due to the small sample size given that at least 700 carriers and 700 non-carriers are needed to have 90% power to detect an odds ratio of 2 or greater at the 0.05 level of significance, assuming the 5% prevalence of breast cancer in non-carriers.
Is breast cancer a Lynch syndrome cancer?
The estimates of an increased risk of breast cancer in Lynch syndrome described in the previous studies are relatively small compared with the increased risks observed for colorectal and endometrial cancers [70]. However, even a small increase in breast cancer risk might point to interesting biological connections. Vasen et al. [55] hypothesized, '...because of the defect in the MMR system, mutations may accumulate in genes involved in the progression of breast cancer. The accumulation of mutations may lead to acceleration of tumor development...'. The later hypothesis is supported by Walsh et al. [71] who observed that microsatellite unstable breast ductal carcinoma in situ were predominantly of higher nuclear grade, suggesting that aberrations in MMR function may lead to a more aggressive phenotype in breast cancer.
The suggested small increased risk of breast cancer in Lynch syndrome is important to confirm, given that breast cancer is a common disease in women. The average lifetime risk of breast cancer in women is estimated to be 12.2% [72]. The threshold risk of breast cancer for recommended magnetic resonance imaging (MRI) screening of the breast suggested by the American Cancer Society is a lifetime risk of 20-25% or greater [73]. If the 2-fold increased risk of breast cancer in Lynch syndrome compared with the general population (estimated by previous studies [63–65]) is confirmed, then consideration of screening with breast MRI would be indicated for women carrying MMR gene mutations. Further, even if MMR deficiency does not prove that MMR mutation causes breast cancer, the 51% prevalence of the phenotype in breast cancers in carriers would strongly support the clinical feasibility of testing breast cancer tumors in families suspected of segregating an MMR gene mutation, where no colorectal tumors are available for testing. In this circumstance, a breast tumor showing loss of expression of an MMR gene by IHC would indicate a significant likelihood of an underlying germline mutation, while a normal MMR gene result would not rule out Lynch syndrome.
Most of the previous studies estimated risk of breast cancer for all MMR gene mutation carriers combined. Some studies [37, 53, 55, 58, 59, 62, 64, 65] attempted to test for differences in breast cancer risk by MMR genes; for example, Scott et al. [58] observed an increased risk of breast cancer for MLH1 mutation-carrying families but not in MSH2 families (see Additional file 1 for details). Although there is indeed some suggestion that breast cancer risk may vary by gene, there have been no formal attempts by the previous studies to examine gene- and age-specific risks for breast cancer. This may be an important consideration for future, adequately powered studies, given the heterogeneity of risk by gene that exists for other cancers in Lynch syndrome [61, 70, 74–76]. Currently there has been insufficient power to identify differences, as indicated by the overlapping confidence intervals between gene-specific cancer risks. Until these data are available and the effectiveness of screening tools for carriers is known, it is not possible to suggest the optimal screening strategies for breast cancer in Lynch syndrome.
It is premature to provide a definitive answer to whether breast cancer is a Lynch syndrome cancer because of the following limitations. There is only one prospective study demonstrating an elevated risk of breast cancer in Lynch syndrome and further independent evidence is required to confirm the findings. Given that previous epidemiological studies used different selection methods, subjects and statistical methods, a meta-analysis is not appropriate to generate a pooled estimate for breast cancer risk. Current evidence of breast cancer risk is mainly from Caucasian populations and therefore may not be applicable to other ethnicities or populations, particularly given that previous studies have demonstrated that risk of Lynch syndrome cancers vary across populations [77]. Given these limitations, and given that breast cancer is a relatively common disease in the general population, we recommend that studies to provide more precise estimates of risk will need to utilize large prospective cohort studies with a long follow-up. While current data are inconclusive at a population level, individual tumor testing results suggest that MMR deficiency is involved with breast cancers in some individuals with Lynch syndrome.
hereditary nonpolyposis colorectal cancer
mismatch repair
magnetic resonance imaging
microsatellite instability
standardized incidence ratio.
AKW is supported by the Picchi Brothers Foundation Cancer Council Victoria Cancer Research Scholarship. MAJ is a National Health and Medical Research Council Senior Research Fellow, Australia.
Authors' Affiliations
- Jass JR: Hereditary non-polyposis colorectal cancer: the rise and fall of a confusing term. World J Gastroenterol. 2006, 12: 4943-4950.View ArticlePubMedPubMed CentralGoogle Scholar
- Hampel H, de la Chapelle A: The search for unaffected individuals with Lynch syndrome: do the ends justify the means?. Cancer Prev Res. 2011, 4: 1-5. 10.1158/1940-6207.CAPR-10-0345.View ArticleGoogle Scholar
- de la Chapelle A: The incidence of Lynch syndrome. Fam Cancer. 2005, 4: 233-237. 10.1007/s10689-004-5811-3.View ArticlePubMedGoogle Scholar
- Dunlop MG, Farrington SM, Nicholl I, Aaltonen L, Petersen G, Porteous M, Carothers A: Population carrier frequency of hMSH2 and hMLH1 mutations. Br J Cancer. 2000, 83: 1643-1645. 10.1054/bjoc.2000.1520.View ArticlePubMedPubMed CentralGoogle Scholar
- Umar A, Boland CR, Terdiman JP, Syngal S, Chapelle Adl, Ruschoff J, Fishel R, Lindor NM, Burgart LJ, Hamelin R, Hamilton SR, Hiatt RA, Jass J, Lindblom A, Lynch HT, Peltomaki P, Ramsey SD, Rodriguez-Bigas MA, Vasen HFA, Hawk ET, Barrett JC, Freedman AN, Srivastava S: Revised Bethesda Guidelines for hereditary nonpolyposis colorectal cancer (Lynch Syndrome) and microsatellite instability. J Natl Cancer Inst. 2004, 96: 261-268. 10.1093/jnci/djh034.View ArticlePubMedPubMed CentralGoogle Scholar
- Liu T, Wahlberg S, Burek E, Lindblom P, Rubio C, Lindblom A: Microsatellite instability as a predictor of a mutation in a DNA mismatch repair gene in familial colorectal cancer. Genes Chromosomes Cancer. 2000, 27: 17-25. 10.1002/(SICI)1098-2264(200001)27:1<17::AID-GCC3>3.0.CO;2-Y.View ArticlePubMedGoogle Scholar
- Moslein G, Tester DJ, Lindor NM, Honchel R, Cunningham JM, French AJ, Halling KC, Schwab M, Goretzki P, Thibodeau SN: Microsatellite instability and mutation analysis of hMSH2 and hMLH1 in patients with sporadic, familial and hereditary colorectal cancer. Hum Mol Genet. 1996, 5: 1245-1252. 10.1093/hmg/5.9.1245.View ArticlePubMedGoogle Scholar
- Leenen CH, van Lier MG, van Doorn HC, van Leerdam ME, Kooi SG, de Waard J, Hoedemaeker RF, van den Ouweland AM, Hulspas SM, Dubbink HJ, Kuipers EJ, Wagner A, Dinjens WN, Steyerberg EW: Prospective evaluation of molecular screening for Lynch syndrome in patients with endometrial cancer </= 70 years. Gynecol Oncol. 2012, 125: 414-420. 10.1016/j.ygyno.2012.01.049.View ArticlePubMedGoogle Scholar
- Berends MJ, Cats A, Hollema H, Karrenbeld A, Beentjes JA, Sijmons RH, Mensink RG, Hofstra RM, Verschueren RC, Kleibeuker JH: Adrenocortical adenocarcinoma in an MSH2 carrier: coincidence or causal relation?. Hum Pathol. 2000, 31: 1522-1527. 10.1053/hupa.2000.20409.View ArticlePubMedGoogle Scholar
- Broaddus RR, Lynch PM, Lu KH, Luthra R, Michelson SJ: Unusual tumors associated with the hereditary nonpolyposis colorectal cancer syndrome. Mod Pathol. 2004, 17: 981-989. 10.1038/modpathol.3800150.View ArticlePubMedGoogle Scholar
- Karamurzin Y, Zeng Z, Stadler ZK, Zhang L, Ouansafi I, Al-Ahmadie HA, Sempoux C, Saltz LB, Soslow RA, O'Reilly EM, Paty PB, Coit DG, Shia J, Klimstra DS: Unusual DNA mismatch repair-deficient tumors in Lynch syndrome: a report of new cases and review of the literature. Hum Pathol. 2012, 43: 1677-1687. 10.1016/j.humpath.2011.12.012.View ArticlePubMedGoogle Scholar
- Sijmons R, Hofstra R, Hollema H, Mensink R, van der Hout A, Hoekstra H, Kleibeuker J, Molenaar W, Wijnen J, Fodde R, Vasen H, Buys C: Inclusion of malignant fibrous histiocytoma in the tumour spectrum associated with hereditary non-polyposis colorectal cancer. Genes Chromosomes Cancer. 2000, 29: 353-355. 10.1002/1098-2264(2000)9999:9999<::AID-GCC1042>3.0.CO;2-T.View ArticlePubMedGoogle Scholar
- Brieger A, Engels K, Schaefer D, Plotz G, Zeuzem S, Raedle J, Trojan J: Malignant fibrous histiocytoma is a rare Lynch syndrome-associated tumor in two German families. Fam Cancer. 2011, 10: 591-595. 10.1007/s10689-011-9455-9.View ArticlePubMedGoogle Scholar
- den Bakker MA, Seynaeve C, Kliffen M, Dinjens WN: Microsatellite instability in a pleomorphic rhabdomyosarcoma in a patient with hereditary non-polyposis colorectal cancer. Histopathology. 2003, 43: 297-299. 10.1046/j.1365-2559.2003.01681.x.View ArticlePubMedGoogle Scholar
- Huang RL, Chao CF, Ding DC, Yu CP, Chang CC, Lai HC, Yu MH, Liu HS, Chu TY: Multiple epithelial and nonepithelial tumors in hereditary nonpolyposis colorectal cancer: characterization of germline and somatic mutations of the MSH2 gene and heterogeneity of replication error phenotypes. Cancer Genet Cytogenet. 2004, 153: 108-114. 10.1016/j.cancergencyto.2004.01.003.View ArticlePubMedGoogle Scholar
- Medina Arana V, Barrios del Pino Y, Garcia-Castro C, Gonzalez-Aguilera JJ, Fernandez-Peralta A, Gonzalez Hermoso F: Highly aggressive leiomyosarcoma associated with Lynch II syndrome: increasing the range of extracolonic cancers related with hereditary non-polyposis colonic cancer. Ann Oncol. 2002, 13: 807-808. 10.1093/annonc/mdf162.View ArticlePubMedGoogle Scholar
- Clyne M, Offman J, Shanley S, Virgo JD, Radulovic M, Wang Y, Ardern-Jones A, Eeles R, Hoffmann E, Yu VP: The G67E mutation in hMLH1 is associated with an unusual presentation of Lynch syndrome. Br J Cancer. 2009, 100: 376-380. 10.1038/sj.bjc.6604860.View ArticlePubMedPubMed CentralGoogle Scholar
- Yu VP, Novelli M, Payne SJ, Fisher S, Barnetson RA, Frayling IM, Barrett A, Goudie D, Ardern-Jones A, Eeles R, Shanley S: Unusual presentation of Lynch Syndrome. Hered Cancer Clin Pract. 2009, 7: 12-10.1186/1897-4287-7-12.View ArticlePubMedPubMed CentralGoogle Scholar
- Nilbert M, Therkildsen C, Nissen A, Akerman M, Bernstein I: Sarcomas associated with hereditary nonpolyposis colorectal cancer: broad anatomical and morphological spectrum. Fam Cancer. 2009, 8: 209-213. 10.1007/s10689-008-9230-8.View ArticlePubMedGoogle Scholar
- Miquel C, Sabourin JC, Elias D, Grandjouan S, Viguier J, Ducreux M, Duvillard P, Praz F: An appendix carcinoid tumor in a patient with hereditary nonpolyposis colorectal cancer. Hum Pathol. 2004, 35: 1564-1567. 10.1016/j.humpath.2004.09.017.View ArticlePubMedGoogle Scholar
- Pineda M, Castellsague E, Musulen E, Llort G, Frebourg T, Baert-Desurmont S, Gonzalez S, Capella G, Blanco I: Non-Hodgkin lymphoma related to hereditary nonpolyposis colorectal cancer in a patient with a novel heterozygous complex deletion in the MSH2 gene. Genes Chromosomes Cancer. 2008, 47: 326-332. 10.1002/gcc.20536.View ArticlePubMedGoogle Scholar
- Ponti G, Losi L, Pellacani G, Wannesson L, Cesinaro AM, Venesio T, Petti C, Seidenari S: Malignant melanoma in patients with hereditary nonpolyposis colorectal cancer. Br J Dermatol. 2008, 159: 162-168. 10.1111/j.1365-2133.2008.08575.x.View ArticlePubMedGoogle Scholar
- Petersen M, Evert M, Schneider-Stock R, Pross M, Ruschoff J, Roessner A, Lippert H, Meyer F: Serous oligocystic adenoma (SOIA) of the pancreas-first reported case of a genetically fixed association in a patient with hereditary non-polyposis colorectal cancer (HNPCC). Pathol Res Pract. 2009, 205: 801-806. 10.1016/j.prp.2009.02.002.View ArticlePubMedGoogle Scholar
- Soravia C, van der Klift H, Brundler MA, Blouin JL, Wijnen J, Hutter P, Fodde R, Delozier-Blanchet C: Prostate cancer is part of the hereditary non-polyposis colorectal cancer (HNPCC) tumor spectrum. Am J Med Genet A. 2003, 121A: 159-162. 10.1002/ajmg.a.20106.View ArticlePubMedGoogle Scholar
- Boyd J, Rhei E, Federici MG, Borgen PI, Watson P, Franklin B, Karr B, Lynch J, Lemon SJ, Lynch HT: Male breast cancer in the hereditary nonpolyposis colorectal cancer syndrome. Breast Cancer Res Treat. 1999, 53: 87-91. 10.1023/A:1006030116357.View ArticlePubMedGoogle Scholar
- Caluseriu O, Cordisco EL, Viel A, Majore S, Nascimbeni R, Pucciarelli S, Genuardi M: Four novel MSH2 and MLH1 frameshift mutations and occurrence of a breast cancer phenocopy in hereditary nonpolyposis colorectal cancer. Hum Mutat. 2001, 17: 521-View ArticlePubMedGoogle Scholar
- Westenend PJ, Schutte R, Hoogmans MM, Wagner A, Dinjens WN: Breast cancer in an MSH2 gene mutation carrier. Hum Pathol. 2005, 36: 1322-1326. 10.1016/j.humpath.2005.08.025.View ArticlePubMedGoogle Scholar
- Akoum R, Ghaoui A, Brihi E, Ghabash M, Hajjar N: Early-onset breast cancer in a Lebanese family with Lynch syndrome due to MSH2 gene mutation. Hered Cancer Clin Pract. 2009, 7: 10-10.1186/1897-4287-7-10.View ArticlePubMedPubMed CentralGoogle Scholar
- D'Arcy C, Wen YH, Stadler ZK, Brogi E, Shia J: Synchronous breast cancers with different morphologic and molecular phenotypes occurring in Lynch syndrome: what does the heterogeneity imply?. Am J Surg Pathol. 2011, 35: 1743-1748. 10.1097/PAS.0b013e3182320cff.View ArticlePubMedGoogle Scholar
- Risinger JI, Barrett JC, Watson P, Lynch HT, Boyd J: Molecular genetic evidence of the occurrence of breast cancer as an integral tumor in patients with the hereditary nonpolyposis colorectal carcinoma syndrome. Cancer. 1996, 77: 1836-1843. 10.1002/(SICI)1097-0142(19960501)77:9<1836::AID-CNCR12>3.0.CO;2-0.View ArticlePubMedGoogle Scholar
- Muller A, Edmonston TB, Corao DA, Rose DG, Palazzo JP, Becker H, Fry RD, Rueschoff J, Fishel R: Exclusion of breast cancer as an integral tumor of hereditary nonpolyposis colorectal cancer. Cancer Res. 2002, 62: 1014-1019.PubMedGoogle Scholar
- de Leeuw WJ, van Puijenbroek M, Tollenaar RA, Cornelisse CJ, Vasen HF, Morreau H: Correspondence re: A. Muller et al., Exclusion of breast cancer as an integral tumor of hereditary nonpolyposis colorectal cancer. Cancer Res., 62: 1014-1019, 2002. Cancer Res. 2003, 63: 1148-1149.PubMedGoogle Scholar
- Blokhuis MM, Goldberg PA, Pietersen GE, Algar U, Vorster AA, Govender D, Ramesar RS: The extracolonic cancer spectrum in females with the common 'South African' hMLH1 c.C1528T mutation. Fam Cancer. 2008, 7: 191-198. 10.1007/s10689-007-9174-4.View ArticlePubMedGoogle Scholar
- Shanley S, Fung C, Milliken J, Leary J, Barnetson R, Schnitzler M, Kirk J: Breast cancer immunohistochemistry can be useful in triage of some HNPCC families. Fam Cancer. 2009, 8: 251-255. 10.1007/s10689-008-9226-4.View ArticlePubMedGoogle Scholar
- Jensen UB, Sunde L, Timshel S, Halvarsson B, Nissen A, Bernstein I, Nilbert M: Mismatch repair defective breast cancer in the hereditary nonpolyposis colorectal cancer syndrome. Breast Cancer Res Treat. 2010, 120: 777-782. 10.1007/s10549-009-0449-3.View ArticlePubMedGoogle Scholar
- Walsh MD, Buchanan DD, Cummings MC, Pearson SA, Arnold ST, Clendenning M, Walters R, McKeone DM, Spurdle AB, Hopper JL, Jenkins MA, Phillips KD, Suthers GK, George J, Goldblatt J, Muir A, Tucker K, Pelzer E, Gattas MR, Woodall S, Parry S, Macrae FA, Haile RW, Baron JA, Potter JD, Le Marchand L, Bapat B, Thibodeau SN, Lindor NM, McGuckin MA, et al: Lynch syndrome-associated breast cancers: clinicopathologic characteristics of a case series from the colon cancer family registry. Clin Cancer Res. 2010, 16: 2214-2224. 10.1158/1078-0432.CCR-09-3058.View ArticlePubMedPubMed CentralGoogle Scholar
- Buerki N, Gautier L, Kovac M, Marra G, Buser M, Mueller H, Heinimann K: Evidence for breast cancer as an integral part of lynch syndrome. Genes Chromosomes Cancer. 2012, 51: 83-91. 10.1002/gcc.20935.View ArticlePubMedGoogle Scholar
- Lotsari JE, Gylling A, Abdel-Rahman WM, Nieminen TT, Aittomaki K, Friman M, Pitkanen R, Aarnio M, Jarvinen HJ, Mecklin JP, Kuopio T, Peltomaki P: Breast carcinoma and Lynch syndrome: molecular analysis of tumors arising in mutation carriers, non-carriers, and sporadic cases. Breast Cancer Res. 2012, 14: R90-10.1186/bcr3205.View ArticlePubMedPubMed CentralGoogle Scholar
- Grandval P, Barouk-Simonet E, Bronner M, Buisine MP, Moretta J, Tinat J, Olschwang S: Is the controversy on breast cancer as part of the Lynch-related tumor spectrum still open?. Fam Cancer. 2012, 11: 681-683. 10.1007/s10689-012-9562-2.View ArticlePubMedGoogle Scholar
- Kastrinos F, Mukherjee B, Tayob N, Wang F, Sparr J, Raymond VM, Bandipalliam P, Stoffel EM, Gruber SB, Syngal S: Risk of pancreatic cancer in families with Lynch syndrome. JAMA. 2009, 302: 1790-1795. 10.1001/jama.2009.1529.View ArticlePubMedPubMed CentralGoogle Scholar
- Lynch H, Watson P, Kriegler M, Lynch J, Lanspa S, Marcus J, Smyrk T, Fitzgibbons R, Cristofaro G: Differential diagnosis of hereditary nonpolyposis colorectal cancer (Lynch syndrome I and Lynch syndrome II). Dis Colon Rectum. 1988, 31: 372-377. 10.1007/BF02564888.View ArticlePubMedGoogle Scholar
- Ford JM: Is breast cancer a part of Lynch syndrome?. Breast Cancer Res. 2012, 14: 110-10.1186/bcr3241.View ArticlePubMedPubMed CentralGoogle Scholar
- Bergthorsson JT, Egilsson V, Gudmundsson J, Arason A, Ingvarsson S: Identification of a breast tumor with microsatellite instability in a potential carrier of the hereditary non-polyposis colon cancer trait. Clin Genet. 1995, 47: 305-310.View ArticlePubMedGoogle Scholar
- Stone JG, Coleman G, Gusterson B, Marossy A, Lakhani SR, Ward A, Nash A, McKinna A, A'Hern R, Stratton MR, Houlston RS: Contribution of germline MLH1 and MSH2 mutations to lobular carcinoma in situ of the breast. Cancer Lett. 2001, 167: 171-174. 10.1016/S0304-3835(01)00448-7.View ArticlePubMedGoogle Scholar
- PubMed. [http://www.ncbi.nlm.nih.gov/pubmed]
- StataCorp: Stata Statistical Software: Release 11. 2009, College Station, TX: StataCorp LPGoogle Scholar
- Itoh H, Houlston RS, Harocopos C, Slack J: Risk of cancer death in first-degree relatives of patients with hereditary non-polyposis cancer syndrome (Lynch type II): a study of 130 kindreds in the United Kingdom. Br J Surg. 1990, 77: 1367-1370. 10.1002/bjs.1800771216.View ArticlePubMedGoogle Scholar
- Watson P, Lynch HT: Extracolonic cancer in hereditary nonpolyposis colorectal cancer. Cancer. 1993, 71: 677-685. 10.1002/1097-0142(19930201)71:3<677::AID-CNCR2820710305>3.0.CO;2-#.View ArticlePubMedGoogle Scholar
- Watson P, Vasen HF, Mecklin JP, Bernstein I, Aarnio M, Jarvinen HJ, Myrhoj T, Sunde L, Wijnen JT, Lynch HT: The risk of extra-colonic, extra-endometrial cancer in the Lynch syndrome. Int J Cancer. 2008, 123: 444-449. 10.1002/ijc.23508.View ArticlePubMedPubMed CentralGoogle Scholar
- Aarnio M, Mecklin JP, Aaltonen LA, Nystrom-Lahti M, Jarvinen HJ: Life-time risk of different cancers in hereditary non-polyposis colorectal cancer (HNPCC) syndrome. Int J Cancer. 1995, 64: 430-433. 10.1002/ijc.2910640613.View ArticlePubMedGoogle Scholar
- Oliveira Ferreira F, Napoli Ferreira CC, Rossi BM, Toshihiko Nakagawa W, Aguilar S, Monteiro Santos EM, Vierira Costa ML, Lopes A: Frequency of extra-colonic tumors in hereditary nonpolyposis colorectal cancer (HNPCC) and familial colorectal cancer (FCC) Brazilian families: An analysis by a Brazilian Hereditary Colorectal Cancer Institutional Registry. Fam Cancer. 2004, 3: 41-47.View ArticlePubMedGoogle Scholar
- Goecke T, Schulmann K, Engel C, Holinski-Feder E, Pagenstecher C, Schackert HK, Kloor M, Kunstmann E, Vogelsang H, Keller G, Dietmaier W, Mangold E, Friedrichs N, Propping P, Kruger S, Gebert J, Schmiegel W, Rueschoff J, Loeffler M, Moeslein G: Genotype-phenotype comparison of German MLH1 and MSH2 mutation carriers clinically affected with Lynch syndrome: a report by the German HNPCC Consortium. J Clin Oncol. 2006, 24: 4285-4292. 10.1200/JCO.2005.03.7333.View ArticlePubMedGoogle Scholar
- Geary J, Sasieni P, Houlston R, Izatt L, Eeles R, Payne SJ, Fisher S, Hodgson SV: Gene-related cancer spectrum in families with hereditary non-polyposis colorectal cancer (HNPCC). Fam Cancer. 2008, 7: 163-172. 10.1007/s10689-007-9164-6.View ArticlePubMedGoogle Scholar
- Aarnio M, Sankila R, Pukkala E, Salovaara R, Aaltonen LA, de la Chapelle A, Peltomäki P, Mecklin JP, Järvinen HJ: Cancer risk in mutation carriers of DNA-mismatch-repair genes. Int J Cancer. 1999, 81: 214-218. 10.1002/(SICI)1097-0215(19990412)81:2<214::AID-IJC8>3.0.CO;2-L.View ArticlePubMedGoogle Scholar
- Vasen HF, Morreau H, Nortier JW: Is breast cancer part of the tumor spectrum of hereditary nonpolyposis colorectal cancer?. Am J Hum Genet. 2001, 68: 1533-1535. 10.1086/320610.View ArticlePubMedPubMed CentralGoogle Scholar
- Parc Y, Boisson C, Thomas G, Olschwang S: Cancer risk in 348 French MSH2 or MLH1 gene carriers. J Med Genet. 2003, 40: 208-213. 10.1136/jmg.40.3.208.View ArticlePubMedPubMed CentralGoogle Scholar
- Pande M, Wei C, Chen J, Amos CI, Lynch PM, Lu KH, Lucio LA, Boyd-Rogers SG, Bannon SA, Mork ME, Frazier ML: Cancer spectrum in DNA mismatch repair gene mutation carriers: results from a hospital based Lynch syndrome registry. Fam Cancer. 2012, 11: 441-447. 10.1007/s10689-012-9534-6.View ArticlePubMedPubMed CentralGoogle Scholar
- Scott RJ, McPhillips M, Meldrum CJ, Fitzgerald PE, Adams K, Spigelman AD, du Sart D, Tucker K, Kirk J: Hereditary nonpolyposis colorectal cancer in 95 families: differences and similarities between mutation-positive and mutation-negative kindreds. Am J Hum Genet. 2001, 68: 118-127. 10.1086/316942.View ArticlePubMedGoogle Scholar
- Barrow E, Robinson L, Alduaij W, Shenton A, Clancy T, Lalloo F, Hill J, Evans DG: Cumulative lifetime incidence of extracolonic cancers in Lynch syndrome: a report of 121 families with proven mutations. Clin Genet. 2009, 75: 141-149. 10.1111/j.1399-0004.2008.01125.x.View ArticlePubMedGoogle Scholar
- Engel C, Loeffler M, Steinke V, Rahner N, Holinski-Feder E, Dietmaier W, Schackert HK, Goergens H, von Knebel Doeberitz M, Goecke TO, Schmiegel W, Buettner R, Moeslein G, Letteboer TG, Garcia EG, Hes FJ, Hoogerbrugge N, Menko FH, van Os TA, Sijmons RH, Wagner A, Kluijt I, Propping P, Vasen HF: Risks of less common cancers in proven mutation carriers with lynch syndrome. J Clin Oncol. 2012, 30: 4409-4415. 10.1200/JCO.2012.43.2278.View ArticlePubMedGoogle Scholar
- Baglietto L, Lindor NM, Dowty JG, White DM, Wagner A, Gomez Garcia EB, Vriends AHJT, Dutch Lynch Syndrome Study G, Cartwright NR, Barnetson RA, Farrington SM, Tenesa A, Hampel H, Buchanan D, Arnold S, Young J, Walsh MD, Jass J, Macrae F, Antill Y, Winship IM, Giles GG, Goldblatt J, Parry S, Suthers G, Leggett B, Butz M, Aronson M, Poynter JN, Baron JA, et al: Risks of Lynch Syndrome Cancers for MSH6 Mutation Carriers. J Natl Cancer Inst. 2010, 102: 193-201. 10.1093/jnci/djp473.View ArticlePubMedPubMed CentralGoogle Scholar
- Dowty JG, Win AK, Buchanan DD, Lindor NM, Macrae FA, Clendenning M, Antill YC, Thibodeau SN, Casey G, Gallinger S, Marchand LL, Newcomb PA, Haile RW, Young GP, James PA, Giles GG, Gunawardena SR, Leggett BA, Gattas M, Boussioutas A, Ahnen DJ, Baron JA, Parry S, Goldblatt J, Young JP, Hopper JL, Jenkins MA: Cancer risks for MLH1 and MSH2 mutation carriers. Hum Mutat. 2013, 34: 490-497. 10.1002/humu.22262.View ArticlePubMedGoogle Scholar
- Win AK, Young JP, Lindor NM, Tucker K, Ahnen D, Young GP, Buchanan D, Clendenning M, Giles G, Winship I, Macrae F, Goldblatt J, Southey M, Arnold J, Thibodeau SN, Gunawardena SR, Bapat B, Baron JA, Casey G, Le Marchand L, Newcomb P, Haile R, Hopper JL, Jenkins MA: Colorectal and other cancer risks for carriers and noncarriers from families with a DNA mismatch repair gene mutation: a prospective cohort study. J Clin Oncol. 2012, 30: 958-964. 10.1200/JCO.2011.39.5590.View ArticlePubMedPubMed CentralGoogle Scholar
- Win AK, Lindor NM, Young JP, Macrae FA, Young GP, Williamson E, Parry S, Goldblatt J, Lipton L, Winship I, Leggett B, Tucker K, Giles G, Buchanan D, Clendenning M, Rosty C, Arnold J, Levine AJ, Haile RW, Gallinger S, Le Marchand L, Newcomb PA, Hopper JL, Jenkins MA: Risks of primary extracolonic cancers following colorectal cancer in Lynch syndrome. J Natl Cancer Inst. 2012, 104: 1363-1372. 10.1093/jnci/djs351.View ArticlePubMedPubMed CentralGoogle Scholar
- Win AK, Lindor NM, Winship I, Tucker KM, Buchanan DD, Young JP, Rosty C, Leggett B, Giles GG, Goldblatt J, Macrae FA, Parry S, Kalady MF, Baron JA, Ahnen DJ, Marchand LL, Gallinger S, Haile RW, Newcomb PA, Hopper JL, Jenkins MA: Risks of Colorectal and Other Cancers After Endometrial Cancer for Women With Lynch Syndrome. J Natl Cancer Inst. 2013, 105: 274-279. 10.1093/jnci/djs525.View ArticlePubMedPubMed CentralGoogle Scholar
- Shia J, Ellis NA, Paty PB, Nash GM, Qin J, Offit K, Zhang XM, Markowitz AJ, Nafa K, Guillem JG, Wong WD, Gerald WL, Klimstra DS: Value of histopathology in predicting microsatellite instability in hereditary nonpolyposis colorectal cancer and sporadic colorectal cancer. Am J Surg Pathol. 2003, 27: 1407-1417. 10.1097/00000478-200311000-00002.View ArticlePubMedGoogle Scholar
- Jenkins MA, Hayashi S, O'Shea AM, Burgart LJ, Smyrk TC, Shimizu D, Waring PM, Ruszkiewicz AR, Pollett AF, Redston M, Barker MA, Baron JA, Casey GR, Dowty JG, Giles GG, Limburg P, Newcomb P, Young JP, Walsh MD, Thibodeau SN, Lindor NM, Lemarchand L, Gallinger S, Haile RW, Potter JD, Hopper JL, Jass JR: Pathology features in Bethesda guidelines predict colorectal cancer microsatellite instability: a population-based study. Gastroenterology. 2007, 133: 48-56. 10.1053/j.gastro.2007.04.044.View ArticlePubMedPubMed CentralGoogle Scholar
- Carayol J, Khlat M, Maccario J, Bonaiti-Pellie C: Hereditary non-polyposis colorectal cancer: current risks of colorectal cancer largely overestimated. J Med Genet. 2002, 39: 335-339. 10.1136/jmg.39.5.335.View ArticlePubMedPubMed CentralGoogle Scholar
- Miettinen OS: Theoretical epidemiology. Principles of occurrence research in medicine. 1985, New York: John Wiley and SonsGoogle Scholar
- Bonadona V, Bonaiti B, Olschwang S, Grandjouan S, Huiart L, Longy M, Guimbaud R, Buecher B, Bignon YJ, Caron O, Colas C, Nogues C, Lejeune-Dumoulin S, Olivier-Faivre L, Polycarpe-Osaer F, Nguyen TD, Desseigne F, Saurin JC, Berthet P, Leroux D, Duffour J, Manouvrier S, Frebourg T, Sobol H, Lasset C, Bonaiti-Pellie C: Cancer risks associated with germline mutations in MLH1, MSH2, and MSH6 genes in Lynch syndrome. JAMA. 2011, 305: 2304-2310. 10.1001/jama.2011.743.View ArticlePubMedGoogle Scholar
- Walsh T, Chappell SA, Shaw JA, Walker RA: Microsatellite instability in ductal carcinoma in situ of the breast. J Pathol. 1998, 185: 18-24. 10.1002/(SICI)1096-9896(199805)185:1<18::AID-PATH41>3.0.CO;2-G.View ArticlePubMedGoogle Scholar
- SEER Cancer Statistics Review, 1975-2007. Edited by: Altekruse S, Kosary C, Krapcho M, Neyman N, Aminou R, Waldron W, Ruhl J, Howlader N, Tatalovich Z, Cho H, Mariotto A, Eisner M, Lewis D, Cronin K, Chen H, Feuer E, Stinchcomb D, Edwards B. 2009, Bethesda, MD: National Cancer Institute
- Saslow D, Boetes C, Burke W, Harms S, Leach MO, Lehman CD, Morris E, Pisano E, Schnall M, Sener S, Smith RA, Warner E, Yaffe M, Andrews KS, Russell CA: American Cancer Society guidelines for breast screening with MRI as an adjunct to mammography. CA Cancer J Clin. 2007, 57: 75-89. 10.3322/canjclin.57.2.75.View ArticlePubMedGoogle Scholar
- Vasen HF, Stormorken A, Menko FH, Nagengast FM, Kleibeuker JH, Griffioen G, Taal BG, Moller P, Wijnen JT: MSH2 mutation carriers are at higher risk of cancer than MLH1 mutation carriers: a study of hereditary nonpolyposis colorectal cancer families. J Clin Oncol. 2001, 19: 4074-4080.PubMedGoogle Scholar
- Jenkins MA, Baglietto L, Dite GS, Jolley DJ, Southey MC, Whitty J, Mead LJ, St John DJ, Macrae FA, Bishop DT, Venter DJ, Giles GG, Hopper JL: After hMSH2 and hMLH1-what next? Analysis of three-generational, population-based, early-onset colorectal cancer families. Int J Cancer. 2002, 102: 166-171. 10.1002/ijc.10670.View ArticlePubMedGoogle Scholar
- Senter L, Clendenning M, Sotamaa K, Hampel H, Green J, Potter JD, Lindblom A, Lagerstedt K, Thibodeau SN, Lindor NM, Young J, Winship I, Dowty JG, White DM, Hopper JL, Baglietto L, Jenkins MA, de la Chapelle A: The clinical phenotype of Lynch syndrome due to germ-Line PMS2 mutations. Gastroenterology. 2008, 135: 419-428. 10.1053/j.gastro.2008.04.026.View ArticlePubMedPubMed CentralGoogle Scholar
- Park J-G, Park YJ, Wijnen JT, Vasen HFA: Gene-environment interaction in hereditary nonpolyposis colorectal cancer with implications for diagnosis and genetic testing. Int J Cancer. 1999, 82: 516-519. 10.1002/(SICI)1097-0215(19990812)82:4<516::AID-IJC8>3.0.CO;2-U.View ArticlePubMedGoogle Scholar
- Vasen HF, Mecklin JP, Khan PM, Lynch HT: The International Collaborative Group on Hereditary Non-Polyposis Colorectal Cancer (ICG-HNPCC). Dis Colon Rectum. 1991, 34: 424-425. 10.1007/BF02053699.View ArticlePubMedGoogle Scholar
- Vasen HFA, Watson P, Mecklin JP, Lynch HT: New clinical criteria for hereditary nonpolyposis colorectal cancer (HNPCC, Lynch syndrome) proposed by the International Collaborative Group on HNPCC. Gastroenterology. 1999, 116: 1453-1456. 10.1016/S0016-5085(99)70510-X.View ArticlePubMedGoogle Scholar
- Rodriguez-Bigas M, Boland C, Hamilton S, Henson D, Srivastava S, Jass J, Khan P, Lynch H, Smyrk T, Perucho M: A National Cancer Institute workshop on hereditary nonpolyposis colorectal cancer syndrome: meeting highlights and Bethesda guidelines. J Natl Cancer Inst. 1997, 89: 1758-1762. 10.1093/jnci/89.23.1758.View ArticlePubMedGoogle Scholar
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Paraguay Vs England - World Cup
June 2006
Paraguay vs England
10th June
Match #3
Date : 10-Jun-2006
Venue: FIFA World Cup Stadium, Frankfurt
Kick Off Time: 15:00
Referee: RODRIGUEZ Marco
Temperature: 11
Daniel M STAFF
June 2006
COME ON ENGLAND!!!! Peter Crouch and Michael Owen up-front - England expects!! I reckon we should get a nice win to start us off, 2-0 would be OK with me! I can't bl**dy wait!
June 2006
that was a dreadful game of football everybody pretending to get hacked, jumping about everywhere
June 2006
Half Time Update
England lead 1-0 after the first half of their World Cup opener against Paraguay. A solid start by Sven-Goran Eriksson's team - but perhaps they should have had more.
Jim B STAFF
June 2006
Well here we go again, life as an England fan is never easy and this was another typical roller coaster of emotions. I was half waiting for one of them to fall over in the box in the last five minutes as it was the only way they were going to score.
If this were a premiership game you would take heart that we got 3 points without playing well. and the old saying of "you can't win a tournament in the first game, but you can lose it" holds well here.
Great for the first 20 minutes and I am sure the very hot temperatures played their part in the second half.
Gerrard played well, with the exception of when he tried to shoot - did he have Crouch's boots on ?
Nice touches from Beckham and Lampard had a great game as usual.
Defence looked solid (Cole was a little shaky at times), but to be honest Paraguay could have played all day without scoring, unless they got a penalty.
All in all, its only going to get better from here in my opinion and with the points on the board, no red cards and no injuries... result !
Magnus A STAFF
June 2006
A pretty boring game.
England started off nice and offensive. Poor poor Paraguay scores an own goal and their keeper get injured in what? 15 minutes.
Englands tactics are pretty straight forward and effective. Crouch dominates the air but also showed some skill in dribbling. The Paraguayian defence were about 25 cm shorter than him so I guess he didn't have to put that much effort into his it. Owen ran up and down the field as he is supposed to but due to a somewhat poor effort from Beckham he didn't get that many good passes.
Cole showed that he hasn't been playing that many games this season, he had to think in alot of situations rather than act automatically. Paraguay didn't do jack in the first half. I wonder if they have even trained together as a team prior to this match.
In the second half England fell back. Owen were substituted for Downing which made and COle came up as some sort of semi forward. Englands game turned very passsive. Thanks to the defence line (Terry in particular) England didn't have that much of a problem with keeping Paraguay from scoring even though there were a couple of breakthroughs.
All in all, Paraguay will hopefully keep the form and loose big time against Sweden in the next game.
The game we are looking forward towards in this group is Sweden-England :clap:
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Daniel M STAFF
June 2006
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June 2006
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June 2006
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Guns, Germs And SteelBy: Jared Diamond (author)eBook
This book answers the most obvious, the most important, yet the most difficult question about human history: why history unfolded so differently on different continents. Geography and biogeography, not race, moulded the contrasting fates of Europeans, Asians, Native Americans, sub-Saharan Africans, and aboriginal Australians.
An ambitious synthesis of history, biology, ecology and linguistics, Guns, Germs and Steel is one of the most important and humane works of popular science.
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- publication date: 04/07/2013
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Which would you reccomend more for metal music?
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6/9/13 at 5:15pm
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Which would you reccomend more for metal music?
For metal, amperiors.
What do you mean adjustable? Like DT1350? Yes, they are.
Of course they are adjustable. Unless you have a really tiny head, I won't worry about it.
IMO, yes. It fits your needs perfectly.
No problem. Hope you like them.


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It has been a lonely year
My brother, my friend
There's something broken in my heart.
Without you here.
You were an exceptional being
In this world, in my life
Your smile was contagious
Your voice, my comfort.
You were a very special man
One that I hoped
Would be in my life
Much longer than you were.
Never again will I hear
Your voice
Your laugh
Except in my memories.
I think of you every day
And love you more than ever
You are my best friend
My brother!
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Happy 4th Of July
No one is to use this photo for any purpose other than a blog, download is set to small. Posting it on your facebook is not blogging if you are a business, especially a Walmart!
Not to be used on commercial sites, web sites, facebook pages for any business's
The Annual 4th of July Fireworks show at North lake, michigan... fun times had by everyone!!
We are not sure this firework was planned, must have gone off early to blow so close to the water... but sure glad the camera was ready
My son and his friends... thanks neighbors for the fun night...
its to bad the boys couldn't keep still for the 1 second shot.. :)
there is also two kakayer's in the shot.. 2 more of my sons friends---
I had 15 minutes of internet this past weekend to quickly find out about the flickr blog.. so excited and then no internet for 36 hours... :( so it is great to come back and find all these wonderful comments and faves... thanks so much.
BTW--- it is an owl on the corner of the dock.. to keep the birds from making a nest in our boat shore station.. and it worked... (1st time we tried it)
and thanks flickr for the blog post... pretty cool


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