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- Adelo Vant
- Beverly Hills, CA
- United States
human, Unknown
This conversation is closed.
Is the cultural anthropological impact of technology and information changing?
Future: Information creates social change and technology application?
Legacy: Technology creates social change and information application!
Do government, academic, economic, and industry leaders understand an Information Society Environment (ISE) will impact technology spending, require information compliance by hardware, software and standards?
Will government, academic, economic, and industry leaders be changed or impacted by an ISE dynamics, social/cultural boundary and borders flexibility?
Will the ISE be as disruptive (more or less) to society/culture, governments, academics, economics, and industry as 1900...2000 digital and telecommunications information technology ... hardware and software?
Closing Statement from Adelo Vant
Presently valuable information is lumped together in an information pile by most, but not all folks. IOW: Human gnome information for most folks is like all outer information not very useful. In the future as metadata/structure is added to information far more people will discover and use available information for presently unknown and unique purposes.
Legal mandates by governments or societies will be a waste of time, like the present war on drugs, the past prohibitions on booze and sex, and the concerns on printable guns. I like a few others (are not nihilist) expect the future will be far better, because information discovery and use will be uncontrollable by any means, and information application controllable by all folks. Maybe government will eventually be pure DEMOCRACY, which should scare the heck out of the powers that be presently.
May 12 2013: Yes. But unfortunately by default rather than visionary design or cultural imperatives. Human intellectual capacity is now known to be "neuroplastic" in nature. This is so profound that it provides an answer to crush something like racism forever. It says that regardless of our appearance there is a dynamic at work in each individual in which he or she grows intellect in the form of "wiring" in the brain in response to challenges placed upon the brain in which people grow access to unused grey matter. No one is sentenced by race to be more or less than anyone else. Education demand reform on this criterion alone. It is never that people should be written off as incapable--it is only that they are unready at a given time. Motivation must become the horse in front of the cart of learning whereas until now learning has been in from of the horse of motivation. Why should education be viewed as an expense and children viewed as liabilities when that could be flipped around entirely to make education an economic profit center where motivation, autonomy and conduits for cooperation invite our progeny to shape the world they will inherit. It is only because we have drawn wrong assumptions and institutionalized dysfunction and set ourselves up as the standard by which young folk are to be judged. Well, we haven't done very good jobs in a lot of areas need to question if we are holding back an extraordinarily rich source of economic stimulus.
May 13 2013: First Thanks, I have been keeping up a little on neuroplastic brain development. Together with the on-coming Information Society Environment (ISE) for didactic learning and global culture change "a fall from hubris" is very likely for the "Powers That Be" today, unless the "Powers That Be" want to move on with the rest of US, EU, RU, CN … folks. With "Powers That Be" attempts at disruption and oppression, it still looks like early next century culture. I will hope for much sooner, I am +60yo/BBG.
May 13 2013: The powers that be will be a powerless that those who dismissed the automobile as a fad when someone delivers a product that illuminates and circumvents institutionalized dysfunction. Kids already text each other under their desks. Why not build a model that embraces cooperation through technology? The powers that be are all products of systems the were devoid of social development imperatives and formal models. So like the automobile they will be skeptical. But if done in such a way as to energize student motivation it would become one of those things like surrendering to the inevitability that your barn must be converted into a garage. I think we're so wrong about ourselves that some of what we call attention deficit syndrome could actually be solved with facilitation of motivation and autonomy rather than medication and a slap with a yard stick. It may take a long time to achieve the kind a of surrender to progress "d like to live to see but a lot will happen in the 21 st Century that will be good. I'm 57 and may not witness it. But I believe in people overcoming wrong eventually.May 11 2013: Yes.
As more people have devices avaliable to allienate them from other people, there will be less use for governments other than as a regulating function. If I could use a robot or could purchase items on line and have them delivered to my home at an affordable price, (or build them with a printer device), I'd probably never leave home. This means less fuel used for transportation by individuals and growing fuel inventories. If I could print my own food and water from simple amino acids to my liking, it means less farming and other agricultural facilities.
In short, we may have to regulate how fast technology progresses, in order to prevent the wholesale collapse of a system of trade and social regulation to keep from dissolving into social chaos.
May 13 2013: Yes, I agree, regulating technology progresses/innovation would sustain the "status quo" of hubris in business-government.
So, why prevent the wholesale collapse of a system of trade and social regulation?
An Information Society Environment (ISE) is the most culturally disruptive advancement possible, and only dangerous to the present "status quo" of hubris in US, EU, RU, CN ….
May 14 2013: Why kill the dog because it has fleas? Couldn't we just remove the fleas from the dog?May 13 2013: Oh, Thanks
May 14 2013: Your welcome.
May 3 2013: In my opinion, we haven't even begun to scratch the surface of the cultural/socio impact of tech. We don't even have the language to discuss the impact that our tech ability will reveal. The 'farming' of genetically reproduced replacement bodies, 'downloading' personalities to whomever, customized children, who 'owns' what, what are 'rights'. Disruptive? 'Unrecognizable' is probably closer.Apr 23 2013: One thing that is inevitable as far as cultures are concerned is dynamism. The interaction between cultures (diffussion of ideas being an example) brings about changes, whether it is thought to be perceptible or whether it is thought to be subtle.
- +1
Governments and other social institutions are helpless against these changes, like a boulder rolling down a steep slope.
Sometimes our ignorance of history makes us think that there is this massive, outlandish (or better still, out of space) change going on in the world.
Information has always created social change, and so has technology.
Apr 23 2013: Access to technology creates cultural disparity.
Access to information creates cultural disparity.
Will a 2000s information culture / economy create more disruption or less disruption to the status quo of the 1900s technology society / economy?
Can / Will information be distributed and controlled by the laws and economic models of the 1900s? Will the (IMO) Information Society Environment brake the global / social / family / government / dogma ... cast-mold of the 1700s...1900s?May 16 2013: There is a sort of daunting over-choice that is present with all the technology. People have all this readily information available from the internet at their fingertips. A result of this is a subconscious anxiety. People being anxious and intimidated from this over-choice choose to stick to a habitual action and have a safe ground of familiarity. This explains why people route to social media kinds of things. Technology also parallels to people brains. Because technology makes tasks shorter, people can accomplish a reward with less effort. With sort of positive reinforcement operant conditioning, mixed with generalization learning people will believe short cuts make rewards quicker. People develop this idea into every day tasks and everyone slowly becomes lazy because they know the minimum effort to make themselves feel rewarded. This may not be all true but this is just my take on how our culture slowly became as an effect of technology.
May 22 2013: Readily discoverable and available information at the fingertips on the internet is not possible today.
Social media as presently modeled is an everything-bin for whatever. Social media websites of the future will be far more focused communities with common and specific information interest.
Technology is a tool. Information is the sustenance for communities, activities, collaboration, synergy ... the brain. IOW: A national science information archive has a paper on warp-bubbles, but can you or most folks interested find the subject paper for reference, discussion, or reading? Answer: No
In the near future, about +10 years, the whole (or parts) community with interest in any subject will have immediate availability of associated information for collaboration and resultant derivatives / synergy.
In an Information Society Environment (ISE) cultures will change, because information is instantly discoverable and available, not the ubiquitous background technology.May 13 2013: 9 days, 1 hours and 46 minutes remain, I know now I am not alone ... others do see where we will be and what the ISE can save or cost in the future.May 8 2013: Technology has very little meaning as compared to information. They are complementary.
Fact is, the two go together. For most of my lifetime, the internet was impossible. The net did not exist. Cell phones were adult toys for the super rich. The rest of us had to sit by our land-line telephones and worry because our kids were still not home at 1 hour past curfew. Only the super-rich could get a cell phone for their kids! If I could, I'd tattoo a cell phone to my kid's arm and NOT provide for an off-button. There would be an auto-answer feature like an answering machine (no voice mail). My dis-embodied voice would proclaim: "Hey kid! I want your posterior HERE, at home, on the couch in front of me! You've got 20 minutes to get here or I call the cops and tell them you and/or your buddies stole my car!" And I'd want the volume loud enough to make sure that ALL his friends heard that message too! Now THAT would be some useful technology!
But seriously: Information DOES create social change. But technology contributes significantly to our ability to receive and achieve information. And that process, in turn, is a major driver of the fundamental information exchange that makes technological innovation possible. The two go together.May 8 2013: Information, changes culture, is the future actuality. Technology is the legacy distraction.
Syntax, Semantics ... Ontology INFORMATION changes culture!May 7 2013: I see technology as a potentially significant tool in the enrichment of society. It seems that too many people see technology as a new theology. I find this troubling. Is there a need for another world religion? Consider. Do most people look at technology rationally? Lines forming at midnight to buy the newest phone does not really attest to rational behavior. Neither does the hours spent by people worshiping at the altar of Facebook, posting on walls not unlike people at the wall of the temple in Jerusalem and with the same fervor. Technology has become a religion. Of course, there is freedom to form religions in this country.
But, does society need a tool or a religion?
Yes, technology has the promise to give us better and longer more fulfilling lives, but I see it as millions of worshipers
telling the world that they are going to the market in 140 characters or less.May 1 2013: I guess that's a world I'm not interested in living in.
May 2 2013: More or less depends on when privacy issues are addressed. Before BigDogmaBro dejure exploits and enslave privacy to products and services or after BigBizBro dejure consumes more privacy (theft of property) for profits.
Science and technology are good, but S&T applications by BigDogmaBro government, private, and religious institutions are damnation for US, EU ....
May 2 2013: Privacy Issues aside. Anybody that has ever had a mistake in their credit report can tell you why this is a bad idea.
May 12 2013: Ok. But aren't u using current social constructs (Bigbiz/Dogma) to describe a future structure we cannot, as yet, envision? These potential technologies are outside the realm of current ethical/legal precedent/consideration. What is 'privacy' when we're not sure a genetically farmed body double has rights, or a convicted criminal eligible for 'download' can refuse? The trinkets of info access for medical and entertainment value will be the 'tells' for the powers that be of what's possible. But we cant know what that looks like. My point is that our moral and ethical abilities must evolve - as quickly or quicker - than the incentivised BigBroDogma currently has unreservedly under the guise of competitive progress. This, to me, has incalcuable socio/cultural ramifications, regardless of how 'good' tech is. I am not a 'restrictionist' for science and tech, but we're not just making 'tools' anymore as a humans, we're transforming as a species.Apr 30 2013: Information Society Environment? What is that? About the only thing technology has accomplished is to allow people to forward ridiculous ideas as though they were credible. Ideas now form out of thin air with no basis in fact, and never any pretense of academic rigor.
- +1
May 1 2013: Information Society Environment (ISE [iz-ee]): Global information presence and access. Information presence and access in a society requires the information have meta-tags placed in a registry for information discovery and recovery by all members and systems of the community / society.
ISE analogy: The year is 1985 we shop at books and record stores, theaters and news stands for prepackaged information collections [Dang, I got stuff I don't want]. The year is 2010 we shop at online businesses for stories and music, movies and news collections of personal information [Dang, How do I get what I want]. The year is 2035 we shop for specific things we know exist or we hope exist [Fycken Magic, I have the information I want, when and where I need].
I suspect 2020 is more likely for Fycken Magic, but to get to the ISE period information and computer science, society and laws need to innovate and change far faster. In the Fycken Magic ISE age a person with ailments will have sensors in cloths/skin that can initiate a call for an ambulance when they are in an accident. Ambulance medical diagnostics (xMRI, BP/P, Blood) will auto update personal medical records, the PCP, and doctor on duty at the ER will be consulting on your injuries and treatments prior to your arrival at the hospital. Early intervention … early out and home.
Information is not technology. Information application makes technology possible. Information availability, usability and application will innovate education, medicine, quality of life ….Apr 30 2013: Part of what we are starting to see—and will see more of—is that there is a universal maximum on the curve of information-technology's impact. People are moving from idea to idea and paradigm to paradigm faster and faster to feed the addiction for novelty, and the result is that the potential applicability of claims in a given paradigm is not being tested out in meat-space. The impact is that hope of change and optimism about potential disruption will accelerate, but actual progress on the ground will slow toward 0, and without competition among paradigms in anything more than a virtual arena, the evolution of infrastructure and superstructure will be stunted. The biggest change will be the decline of change - except within the system to support the novelty-stream of the armchair rationalists.
May 1 2013: A dystopian society in an entropic universe actually progressing will slow toward zero. Sounds like only gods and heroic leaders (like Marvel/DC super heroes) will be able to save or enslave US, EU, all others. (IMO) Zero is a concept number expressing the unknown or absent as well as the unmeasured and/or unwanted, but never will zero express nothing. Zero indicates we are forced or decide to ignore something important.
Sometimes the number "0" and/or negative numbers are used to express the problems or unimportance by foolish people. The value or vector relative to other values or vectors can always be set as equal to zero. So, in some weird way for me "0" is always the starting point for everything in time and space.
Information or technology is the topic. Information Technology (IT) impact and advancements are always proportional to available information. More information means more technology, science, engineering, learning, application, innovation, synergy …. Technology, opinion, humor … are not the problem, but a distraction (some more fun than others). Information is not the problem. (IMO) Information availability and application could be part of the solution or problem.
Humans without reliable (best factual available) information will use fantasy, dogma, mythology information to explain anything and everything. Maybe eventually schools will teach students to seek reliable information to form ideas and opinions about themselves, family, friends …and the universe.
Armchair-rationalists or Dogma-drunks are not the same. The rationalist is sane (rational), the dogmatist may be insane (irrational). A qualified (PhD) scientist has methods/facts for reasons. A certified (PhD) scientist has an agenda/dogma for opinions.
Objective: Information creates change and application.
Legacy: Technology creates change and application.Apr 29 2013: I think technology is already changing our culture. Society is maturing very rapidly.
ISE is already being much more disruptive. Some would even say exponentially(Decade-wise)
Apr 29 2013: Information Technology provides infrastructure and applications to people. Information (data/content) is the material that traverses the infrastructure and manipulated by the applications. The information as a material is a raw usable commodity when available.
I agree technology is and has changed our culture, but information as the commodity (not the technology) needs many more tools (XML ...) to make the information discoverable and available to everyone, everyplace at any time for an ISE.
IOW: Presently technology creates social change and information application and/or available, much public information is not discoverable or obtainable. Information creates social change and technology application becomes focused on discovery and availability of information. What you cannot (discover/obtain) know cannot help social change.Apr 27 2013: ya bro information is a diguise for knowledge and knowlege is a disguise for wisdom. we have a bunch of wisdom out there right now but its being desguised by lots of information. wich is good because it protects us from knowing too much too fast. yay!!!!!!!
Adelo Vant
Apr 29 2013: IMO: Information (data/content …) is a material commodity that may or may not be available to acquire for personal knowledge. Explicit information is documented (oral traditions included) and applied (the textbook example). Implicit information is experiential (hands-on) application of explicit information with curiosity about results or intent to produce a specific result, and knowledge confirmation and acquisition are collateral results. Implicit knowledge has limited use, because it is not distributed or readily available by explicit documentation.
- +1
Knowledge is frequently trivia for people to regurgitate at appropriate social occasions. Personal knowledge acquisition by a person is highly certifiable. Knowledge when used to exploit a social, economic, or personal weakness may be a crime, and will always indicate a pitiable human condition. So, for me IMO, there is no wisdom in knowledge. Applied knowledge for personal reasons may or may not show wisdom, and may expose personal character. Information availability for knowledge acquisition is essential to all endeavors (knowledge application), there is never too much. Also, information used as dogma is knowledge for exploiting social, economic, and personal weaknesses by politicians, clergy, plutocrats and other hubris filled fools. Dogma has no acceptable application.
Apr 29 2013: i agree knowledge in itself is useless. same with information. only when its combined with love and is built upon a foundation that cant crumble will it then be of any use to anyone. it can be harder to find the light in things that have a ton of information. when i say light, its also like the good, or whats going to make us better from that. love guides to what that person needs if, theres too much then it can be difficult to sift through all that to get to what is needed. so love and a strong foundation and we got somewhere to stand and go.Apr 25 2013: My dad always says that 'information will be the next form of currency'. I don't truly get the statement yet, but I'm sure I will -- one day.
I think the main eyebrow-raiser here is the open availability of information and how readily compact it can be. Portable to the extent that if a disk is stolen, thousands of people are at risk of being taken to the cleaners.
Ahem: http://news.bbc.co.uk/1/hi/7103566.stm
Apr 29 2013: Henry,
I think your dad is right.
Information availability, you mentioned, is a critical part of my question.
You may be interested in something US, UK and others are doing with learning material online. USA education petition http://wh.gov/eEaI may be appropriate for US, EU ...?
Now, back to Information availability and currency, Information as a material is always a commodity in every culture (IMO). Presently the information is put in publications (hard-copy and virtual) and audio-visual presentations (like music and movies) we buy. In the USA education (URLink above) learning materials are becoming a big part of that Information Society Environment (ISE).
How can we make all information available to everyone globally? How can someone that speaks/reads only Spanish learn from a book that maybe is only in Russian, while they are on vacation in Japan, all while listening to some great fusion-jazz using bagpipes, sax, base and Taiko drums? Presently, there just ain't no dang way to affordable find/discover all those things and bring them together for one person, in one place, for one time.
Science, technology, and folks still need to get more creative/innovative. Open and available ISO (like *.odt), W3C (like XML), OASIS (like QUOMOS) standards will help some. Also, http://www.gutenberg.org, www.edx.org, www.coursera, and many others people and things will make the information material affordable and available to everyone. Heck, even kids attending school in a small farm community in Vietnam and at the moon colony will have access to the same great teachers and information material ... plus the games, music and movies after completing homework. But, how do we make it easy and affordable for everyone is the currency and economy of the future (maybe).Apr 23 2013: IMO
1500s...1900s, The printing press "applied technology" made society / culture change.
2000s...Until, The Information Society Environment (ISE) "applied information" makes society / culture change. Today information about the printing press is essential to rendering to paper / screen information on request. The virtual (information), I think, does not diminish the importance of printing, but does (potentially) add exceptional value to the quality of life on earth and where we settle next. We now have technology (G4 Tablets) in our hand that allows access to learning and information on a scale not considered a decade ago.
What will be more disruptive to culture in this century; The access to information needed or the ubiquitous technology?Apr 23 2013: Information creates social change and technology application?
Technology creates social change and information application!
Information Technology application IMO was the disruptor of the last century.
Information Data / Content application IMO is the disruptor for this century.
The century behind us technology was the more culturally / socially disruptive. I suspect, the century we are now in will be culturally / socially disrupted far more significantly by information discovery, availability, sharing, collecting / mining, aggregating, analysis, collaboration, innovation, synergy ... and application. Hence, the concept of Information Society Environment (ISE) where technology complies with the ISE requirements (family, friends, needs, workplace and home automation, robotics, learning, entertainment ...).
IMO, the last century was dominated by "Technology" application (industrial...telecommunications). This century will be dominated by "Information" application (learning, entertainment ...). If correct, then the next hackers/geeks will more likely be librarians, information scientist .... Nothing to say about global economics, products, markets, sales, laws ...?
The disruption will be significant but not bad, I think, if we can keep information "Open and Available" for innovation and sharing. The software and genetic patents IMO would be legacy methods restricting innovation and economic growth.Apr 23 2013: Your question is related to the video put up on the TED Blog this morning, the debate that opened TED 2013. Two scholars argue about whether the century behind us was the more disruptive or the century we are now in.
Apr 23 2013: Information application in this century, I suspect, will be more disruptive than the technology application of the past century.
So what makes the proportional difference in social / cultural disruption when (1900 & 2000) compared in 2100+? I guess, they will say information application in the2000s day-to-day (physics, medicine, engineering, farming, Sol-system exploration / pioneering ...) made proportionally far more human advancement possible than technology application of the 1900s.
IOW: 2000s Information is the cause of culture, science, technology ... advancement, and the 1900s Technology is the cause of culture, science, and information advancement.Apr 23 2013: I count 5 question marks in your post. Can that be reduced to one?
Apr 23 2013: Will information science or technology products produce the greatest impact on culture, economics, innovations ... in this century?
Apr 23 2013: Thank you. I am sorry to have bothered you. Even with the dumb-downed version of your question I still do not know what you are asking. It is probably best to proceed without me. I'll just go look for a coversation about what constitutes happiness.


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Percentage of Chlamydia Cases Grows in Yakima County
The percentage of people with Chlamydia in Yakima County continues to grow. And our news partner KIMA Action News reports if you haven't been screened for STDs you probably should.
Two years ago, Yakima County's Chlamydia rate was not only higher than the state average, but it was the second highest throughout Washington with about 464 cases for every 100,000 people

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You are hereHome › Programs & Events › Readings & Conversations ›
Other Worlds: Afzal Ahmed Syed with Mahwash Shoaib
Date and Time:
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$10, $7 for students and seniors, free to Poets House Members
Born in India and a longtime resident of Pakistan, Afzal Ahmed Syed is an acclaimed master of classical and modern Urdu poetic forms. Syed reads from Rococo and Other Worlds: Selected Poems, his first English-language publication, and discusses Urdu poetry, Middle Eastern and South Asian history, and the politics of translation with poet and translator Mahwash Shoaib.
Event Sponsored By:
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Upcoming Readings and Conversations
Current Exhibition
June 12, 2015 to September 19, 2015


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Moderators: Can't Hit Open Putts, ADGO BOD
billnchristy wrote:
I was thinking take the top, or in this case top 2 since Christy & Vicki are within a couple percent and make them 0, make Kari -2 or something and so forth...average to the average score not par.
Vicki wrote:I'll also have to miss the June 3rd round, as my daughter and I are going to the James Taylor/Carole King concert that night.
Redan Randy wrote:
Steve Adams wrote:Is Randy indicating he is signing up for the 2nd session of Lenora Bag Tag, the summer season?
Can't Hit Open Putts wrote:
Sign ups for Summer league can be done any time at any Gwinnett Co. rec center. It starts June 10th and runs through July.
Can't Hit Open Putts wrote:Can't Hit Open Putts wrote:
Sign ups for Summer league can be done any time at any Gwinnett Co. rec center. It starts June 10th and runs through July.
I guess I should have put picture with it!?!
billnchristy wrote:Just give her the last place tag and let her try to get a better one...she doesn't care, no need to make concessions.
If you normally golf on Thursdays or can get off work early enough.... You need to get over there and sign up!!
djester wrote:I'm number "last"... maybe Cha Ching? O think I see that he shot a 7 down
Cha Ching wrote:Steve Adams was about 15 feet behind the basket, but that was our first hole. Not sure if anyone beat it or not.
Dusty wrote:No. Steve never marked it. Mikey had it marked & I parked it to take it. I personally gave the pink piece of paper used to mark it to Mikey at the parking lot while they were adding up the scores & never heard them announce paying out the CTPs. I definitely had 15. Who got hole 3?
gvan wrote:The GCPR sign-up only has the "Men over 18" categories available. Is there a place for my 12 year old daughter?
...now don't make her cry.
Dusty wrote:I will not be there this Thursday the 23rd. I will be heading to Central Park for the GSSS #6 weekend.
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text: Lorelei Martins returns, determined to find out if Red John had a role in her sister's death, and Jane is forced to confess to Lisbon his part in Lorelei's prison escape, on THE MENTALIST, Sunday, March 10 (10:00-11:00 PM, ET/PT) on the CBS Television Network. Pictured: Emmanuelle Chriqui as Lorelei Martins. Photo: Robert Voets/Warner Bros. ©2013 Warner Bros. Television. All Rights Reserved.


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Other IngredientsHypromellose (derived from cellulose) capsule, Leucine, Silicon Dioxide.
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Why are Hanna babies so happy? This super-cozy little sleeper is surely part of it...our legendary babysuit cuddles them in extra-huggable comfort that's zippity-quick at changing time, and makes life just as easy for newborns as it does for new walkers. Truly Hanna-me-down quality. 100% organic cotton ribbknit Super-smooth flatlock seams Handy neck-to-knee zipper has protective top tab Ready-to-grow cuffs keep the fit Certified by Oeko-Tex® Standard 100 Prewashed Imported Wear snug fitting; not flame resistant. Please use the snug fit cotton sleepwear size chart.
Item # VA33081


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Society Diaries
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Santa's Elves party raises money for pediatric cancer
Seven Christmas trees, festive garland, white lights, pine cones and candles added holiday glamour to the River Oaks home of Paige and Tilman Fertitta, who entertained 250 at the eighth annual Santa Elves Party. The event benefitted the M.D. Anderson Children's Cancer Hospital. A special attraction was the Houston Children's Chorus — directed by […] [Read More]


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Hang tight!
Recipe by Dee
"This batter can be stored in your refrigerator, unbaked for 6 weeks. Use only the amount you want each day. Mine never seems to last that long!"
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6 cups
boiling water
6 cups
whole bran cereal
3 cups
9 cups
white sugar
12 cups
15 cups
all-purpose flour
5 tablespoons
baking soda
1 tablespoon
12 cups
whole bran cereal
First off, do NOT try to cream the fat & sugar with the buttermilk. What a mess! Cream the fat & sugar. Then mix in the egg(s) and THEN stir in the buttermilk. Also, this never says what size of muffin tin is a 'serving' which completely changes your baking time. That being said....I really love the taste of these muffins! I think for anyone who said they were bland, I think it's because of the type of cereal they used. I substituted the shortening with 1/2 applesauce & 1/2 butter. I used raisin bran cereal and threw in a tablespoon of vanilla extract with the buttermilk (which really was 1 Tablespoon lemon juice to 1 cup of skim milk because I didn't have buttermilk). Half wheat flour, half all purpose. I changed this to 36 servings (which really turned out to be 24 on a regular sized muffin tin). I baked them for 18 minutes. They turned out perfect. Thankfully the next time I won't follow the directions blindly.
I made this last year and was SHOCKED at how much it made. It was WAY too much batter, even for a family of 6. I didn't have a bowl large enough to store the batter. It took a large disposable 9x13 deep dish pan just to store 1/2 the batter (not including the bran cereal!!!). I did get 1/2 the batter cooked up (it was all I could fit into a gigantic canning pot at the time) and it was pretty good. Just be warned- this recipe needs to be MAJORLY scaled back unless you have a large supply of canning pots to cook it in!
146 Ratings
Wonderful!!! I did add Molasses the first time I made them. The second time I added honey and vanilla ( ran out of molasses). Even those at work who say they do not like bran muffins, LOVE this recipe. Extremely easy to make, and versatile. You can add just about any dried fruit to it and they come out even better!!!! We have tried raisins, cranberries, and even dried mango and apricots... Yumm mm Yummmmm!!
I've been trying literally dozens of bran muffin recipes lately trying to find a favorite and so far this is it. I skipped the whole step involving breaking up the bran cereal into two parts and just crushed up all of it at once into the boiling water. I also scaled this down to 12 servings and made giant "texas muffins". YUM!
My mom made these for us as kids. I now make them for my kids. My absolute favorite thing to do with this is something we did as kids. My mom always had a big bowl of it in the fridge. we took a big glump of it and put it in the microwave. cook it until it's not shiney. Pour a little milk over the top of it and you have a quick super yummy hot healthy breakfast.
These are very versatile muffins. I like to get creative with different kinds of grain cereal. The first 6 cup should be something like All bran the other 12 can be anything from shredded wheat to granola. Granola is really yummy. I've added all kinds of dried fruits. I like to have a batch in my fridge around the holidays. It's super easy to make up a dozen to give to friends and family as gifts. It's the perfect quick fix
Recipe is very tasty! I got a lot of compliments. You don't need to use those paper liners the muffins tip right out of the muffins tins. I baked all the muffins at one time since I've got a chest freezer to store them. Next time I make this recipe I'm going to cut it in half as I do not have a bowl large enough to hold the entire recipe.
We really like these for using up stale bran cereal. I've tried different kinds and they all seem to work! I down size to 1/6th and it makes 24 muffins perfectly. I also don't use the liners as they are really unnecessary. I like to add different things to the tops of them before they bake, they bake up very well this way... sometimes I add chopped walnuts, sometimes dried cranberries or raisins, always add a little bit of raw sugar to give it a finished crunch/bakery style top.
This recipe brings back some fond memories of my daughter when she was little. I always had this batter in the fridge and I popped six of these in the oven moments before she and her friends were due home from school. She arrived home everyday to the smell of these baking, and as soon as she changed her clothes she and her buddies each munched on a hot muffin with a tall glass of cold milk. To this day whenever we run into any of her friends from the old neighborhood, they remind me of the great smells and flavors from our house after school.
Now I take this batter to work once a week and bake them in the kitchen mid day to share - there is never a crumb left.
* Percent Daily Values are based on a 2,000 calorie diet.
Six Week Bran Muffins
Serving Size: 1/216 of a recipe
Servings Per Recipe: 216
Amount Per Serving
** Calories: 106
** Calories from Fat: 30
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Academic research could be strengthened by thinking more and doing less.
Spotlight on the Cytoskeleton
May 27, 2014|
Technique allows researchers to see the inner workings of cellular scaffolding molecules actin and tubulin.
May 27, 2014|
Technique allows researchers to see the inner workings of cellular scaffolding molecules actin and tubulin.
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Assistant Professor, Department of Cell & Tissue Biology, University of California, San Francisco. Age: 38
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Clathrin-mediated endocytosis shuts down during mitosis in eukaryotic cells because all of the required actin is hoarded by the cytoskeleton.
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In the midst of news that engineered organs are being implanted into animals and people, researchers announce the creation of artificial blood for transplant.


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This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
Incidence and Mortality
Estimated new cases and deaths from melanoma in the United States in 2014:[1]
Risk Factors
The incidence of melanoma has been increasing over the past four decades. Risk factors for melanoma include the following:
(Refer to the PDQ summary on Genetics of Skin Cancer for more information about risk factors.)
Melanoma is a malignant tumor of melanocytes, which are the cells that make the pigment melanin and are derived from the neural crest. Although most melanomas arise in the skin, they may also arise from mucosal surfaces or at other sites to which neural crest cells migrate. Melanoma occurs predominantly in adults, and more than 50% of the cases arise in apparently normal areas of the skin. Early signs in a nevus that would suggest malignant change include darker or variable discoloration, itching, an increase in size, or the development of satellites. Ulceration or bleeding are later signs. Melanoma in women occurs more commonly on the extremities and in men, it occurs most commonly on the trunk or head and neck, but it can arise from any site on the skin surface. A biopsy, preferably by local excision, should be performed for any suspicious lesions, and the specimens should be examined by an experienced pathologist to allow for microstaging. Suspicious lesions should never be shaved off or cauterized. Studies show that distinguishing between benign pigmented lesions and early melanomas can be difficult, and even experienced dermatopathologists can have differing opinions. To reduce the possibility of misdiagnosis for an individual patient, a second review by an independent qualified pathologist should be considered.[2]
Prognostic Factors
Prognosis is affected by clinical and histological factors and by anatomic location of the lesion. Thickness and/or level of invasion of the melanoma, mitotic index, presence of tumor infiltrating lymphocytes, number of regional lymph nodes involved, and ulceration or bleeding at the primary site affect the prognosis.[3,4,5,6] Microscopic satellites in stage I melanoma may be a poor prognostic histologic factor, but this is controversial.[7] Patients who are younger, female, and who have melanomas on the extremities generally have a better prognosis.[3,4,5,6]
Follow-up and Survival
Clinical staging is based on whether the tumor has spread to regional lymph nodes or distant sites. For disease clinically confined to the primary site, the greater the thickness and depth of local invasion of the melanoma are, the higher the chance of lymph node or systemic metastases, and the worse the prognosis is. Melanoma can spread by local extension (through lymphatics) and/or by hematogenous routes to distant sites. Any organ may be involved by metastases, but lungs and liver are common sites. The risk of relapse decreases substantially over time, though late relapses are not uncommon.[8,9]
Related Summaries
Other PDQ summaries containing information related to melanoma include the following:
Following is a list of clinicopathologic cellular subtypes of malignant melanoma. These should be considered descriptive terms of historic interest only as they do not have independent prognostic or therapeutic significance.
Identification of activating mutations in the mitogen-activated protein kinase pathway has led to the definition of molecular subtypes of melanoma and provided potential drug targets.
BRAF (V-raf murine sarcoma viral oncogene homolog B1) gene, first reported in 2002, are the most frequent mutation in cutaneous melanoma. Approximately 40% to 60% of malignant melanomas harbor a single nucleotide transversion. The majority have a mutation that results in a substitution from valine to glutamic acid at position 600 BRAF (V600E); less frequent mutations include valine 600 to lysine or arginine residues (V600K/R).[1] Drugs that target this mutation by inhibiting BRAF are under evaluation in clinical trials. One such drug, vemurafenib, was approved by the U.S. Food and Drug Administration (FDA) in 2011 for the treatment of unresectable or metastatic melanoma in patients who test positive for the BRAF mutation as detected by an FDA-approved test (e.g., cobas® 4800 BRAF V600 Mutation Test).
In smaller subsets of cutaneous melanoma, other activating mutations have been described, including NRAS [neuroblastoma RAS viral (v-ras) oncogene homolog], c-KIT, and CDK4 (cyclin-dependent kinase 4).
Drugs developed to target these mutations are currently in clinical trials. Additional oncogenes and tumor-suppressor gene candidates currently under evaluation include P13K, AKT, P53, PTEN, mTOR, Bcl-2, MITF.
Uveal melanomas differ significantly from cutaneous melanomas; in one series, 83% of 186 uveal melanomas were found to have a constitutively active somatic mutation in GNAQ or GNA11.[9,10]
Agreement between pathologists in the histologic diagnosis of melanomas and benign pigmented lesions has been studied and found to be considerably variable. One such study found that there was discordance on the diagnosis of melanoma versus benign lesions in 37 of 140 cases examined by a panel of experienced dermatopathologists.[1] For the histologic classification of cutaneous melanoma, the highest concordance was attained for Breslow thickness and presence of ulceration, while the agreement was poor for other histologic features such as Clark level of invasion, presence of regression, and lymphocytic infiltration. In another study, 38% of cases examined by a panel of expert pathologists had two or more discordant interpretations. These studies convincingly show that distinguishing between benign pigmented lesions and early melanoma can be difficult, and even experienced dermatopathologists can have differing opinions. To reduce the possibility of misdiagnosis for an individual patient, a second review by an independent qualified pathologist should be considered.[2]
The microstage of malignant melanoma is determined on histologic examination by the vertical thickness of the lesion in millimeters (Breslow classification) and/or the anatomic level of local invasion (Clark classification). The Breslow thickness is more reproducible and more accurately predicts subsequent behavior of malignant melanoma in lesions larger than 1.5 mm in thickness and should always be reported. Accurate microstaging of the primary tumor requires careful histologic evaluation of the entire specimen by an experienced pathologist. Estimates of prognosis should be modified by sex and anatomic site as well as by clinical and histologic evaluation.
Clark Classification (Level of Invasion)
Definitions of TNM
The American Joint Committee on Cancer (AJCC) has designated staging by TNM classification to define melanoma.[3]
Melanomas that have not spread beyond the site at which they developed are highly curable. Most of these are thin lesions that have not invaded beyond the papillary dermis (Clark level I–II; Breslow thickness ?1 mm). The treatment of localized melanoma is surgical excision with margins proportional to the microstage of the primary lesion; for most lesions 2 mm or less in thickness, this means 1 cm radial re-excision margins.[1,2]
Melanomas with a Breslow thickness of 2 mm or more are still curable in a significant proportion of patients, but the risk of lymph node and/or systemic metastasis increases with increasing thickness of the primary lesion. The local treatment for these melanomas is surgical excision with margins based on Breslow thickness and anatomic location. For most melanomas more than 2 mm to 4 mm in thickness, this means 2 cm to 3 cm radial excision margins. These patients should also be considered for sentinel lymph node biopsy followed by complete lymph node dissection if the sentinel node(s) are microscopically or macroscopically positive. Sentinel node biopsy should be performed prior to wide excision of the primary melanoma to ensure accurate lymphatic mapping. Patients with melanomas that have a Breslow thickness more than 4 mm should be considered for adjuvant therapy.
Some melanomas that have spread to regional lymph nodes may be curable with wide local excision of the primary tumor and removal of the involved regional lymph nodes.[3,4,5,6] A completed, multicenter, phase III randomized trial (SWOG-8593) of patients with high-risk primary limb melanoma did not show a benefit from isolated limb perfusion with melphalan in regard to disease-free survival (DFS) or overall survival (OS) when compared to surgery alone.[7] Systemic treatment with high dose and pegylated interferon alpha-2b are approved for the adjuvant treatment of patients who have undergone a complete surgical resection but are considered to be at high risk for relapse. Prospective, randomized, controlled trials with both agents have not shown an increase in OS when compared with observation.[8,9,10] Clinicians should be aware that high-dose and pegylated interferon regimens have substantial side effects, and patients should be monitored closely. Adjuvant therapy with lower doses of interferon have not been consistently shown to have an impact on either relapse-free survival or OS.[11] Therapies that have impacted OS in patients with recurrent or metastatic disease are now being tested as adjuvant therapy in clinical trials, including NCT01274338, NCT01667419, and NCT01682083.
Although melanoma that has spread to distant sites is rarely curable, both ipilimumab and vemurafenib have demonstrated an improvement in progression-free survival (PFS) and OS in international, multicenter, randomized trials in patients with unresectable or advanced disease, resulting in U.S. Food and Drug Administration (FDA) approval in 2011. These single agents are rarely curative; however, clinical trials that incorporate these agents are testing combinations in an attempt to prevent development of drug resistance. Vemurafenib is a selective BRAF V600E kinase inhibitor, and its indication is limited to patients with a demonstrated BRAF V600E mutation by an FDA-approved test. Clinical trials are testing targeted therapies in the smaller patient subsets (e.g., those with mutations in NRAS, c-KIT, CDK4, GNAQ or GNA11). Information about ongoing clinical trials is available from the NCI Web site.
Interleukin-2 (IL-2) was approved by the FDA in 1998 on the basis of durable complete response (CR) rates in a minority of patients (0% –8%) with previously treated metastatic melanoma in eight phase I and II studies. No improvement in OS has been demonstrated in randomized trials.
Dacarbazine (DTIC) was approved in 1970 based on overall response rates. Phase III trials indicate an overall response rate of 10% to 20%, with rare CRs observed. An impact on OS has not been demonstrated in randomized trials.[12,13,14,15,16] Temozolomide, an oral alkylating agent, appeared to be similar to DTIC (intravenous administration) in a randomized phase III trial with a primary endpoint of OS; however, the trial was designed for superiority, and the sample size was inadequate to prove equivalency.[13]
Patients with all stages of melanoma may be considered candidates for ongoing clinical trials. Information about ongoing clinical trials is available from the NCI Web site.
Stage 0 melanoma is defined by the American Joint Committee on Cancer's TNM classification system:[1]
Patients with stage 0 disease may be treated by excision with minimal, but microscopically free, margins.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with stage 0 melanoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
Stage I melanoma is defined by the American Joint Committee on Cancer's TNM classification system:[1]
Standard Treatment Options for Patients With Stage I Melanoma
Elective regional lymph node dissection is of no proven benefit for patients with stage I melanoma. Lymphatic mapping and sentinel lymph node (SNL) biopsy for patients who have tumors of intermediate thickness and/or ulcerated tumors, however, may allow the identification of individuals with occult nodal disease who might benefit from regional lymphadenectomy and adjuvant therapy.[7,8,9,10]
The International Multicenter Selective Lymphadenectomy Trial (MSLT-1 [JWCI-MORD-MSLT-1193]) included 1,269 patients with intermediate-thickness (defined as 1.2 mm–3.5 mm in this study) primary melanomas.[11] There was no melanoma-specific survival advantage (the primary endpoint) for those patients randomly assigned to wide excision plus SLN biopsy followed by immediate complete lymphadenectomy for node positivity versus patients randomly assigned to nodal observation and delayed lymphadenectomy for subsequent nodal recurrence at a median of 59.8 months.[11][Level of evidence: 1iiB]
This trial was not designed to detect a difference in the impact of lymphadenectomy in patients with microscopic lymph node involvement.[11]
Treatment Options Under Clinical Evaluation for Patients With Stage I Melanoma
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with stage I melanoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
Stage II melanoma is defined by the American Joint Committee on Cancer's TNM classification system:[1]
Standard Treatment Options for Patients With Stage II Melanoma
The Intergroup Melanoma Surgical Trial compared 2-cm margins versus 4-cm margins for patients with 1-mm thick melanomas to 4-mm thick melanomas. With a median follow-up of more than 10 years, no significant difference was observed between the two groups in terms of local recurrence or survival. The reduction in margins from 4 cm to 2 cm was associated with a statistically significant reduction in the need for skin grafting (46% to11%; P < .001) and a reduction in the length of the hospital stay.[2] Depending on the location of the melanoma, most patients can now have this surgery performed on an outpatient basis.
A study conducted in the United Kingdom randomly assigned patients with melanomas more than 2 mm in thickness to excision with either 1 cm margins or 3 cm margins.[3] Patients treated with 1 cm margins of excision had a higher rate of local regional recurrence (hazard ratio [HR], 1.26; 95% confidence interval [CI], 1.00–1.59; P = .05), but no difference in survival was seen (HR, 1.24; 95% CI, 0.96–1.61; P = .1).
This suggests that 1 cm margins may not be adequate for patients with melanomas that are more than 2 mm in thickness. Few data are available to guide treatment in patients with melanomas more than 4 mm thick; however, most guidelines recommend margins of 3 cm whenever anatomically possible. Although prophylactic regional lymph node dissections (LNDs) have been used in patients with stage II melanomas, four prospective randomized trials have failed to show a benefit for this procedure in terms of survival.[4,5,6,7]
Lymphatic mapping and sentinel lymph node (SLN) biopsy have been used to assess the presence of occult metastasis in the regional lymph nodes of patients with stage II disease, which potentially identifies individuals who may be spared the morbidity of regional LND and individuals who may benefit from adjuvant therapy.[8,9,10,11,12] The diagnostic accuracy of SLN biopsy has been demonstrated in several studies with a false-negative rate of 0% to 2%.[8,13,14,15,16,17] Using a vital blue dye and a radiopharmaceutical agent, which are injected at the site of the primary tumor, the first lymph node in the lymphatic basin that drains the lesion can be identified, removed, and examined microscopically. If metastatic melanoma is detected, a complete regional lymphadenectomy can be performed in a second procedure. To ensure accurate identification of the SLN, lymphatic mapping and removal of the SLN should be performed prior to wide excision of the primary melanoma.
To date, no published data from prospective trials are available on the clinical significance of micrometastatic melanoma in regional lymph nodes, but some evidence suggests that for patients with tumors of intermediate thickness and occult metastasis, survival is better among those patients who undergo immediate regional lymphadenectomy than it is among those who delay lymphadenectomy until the clinical appearance of nodal metastasis.[7] Because this finding arose from a post-hoc subset analysis of data from a randomized trial, it should be viewed with caution.
The International Multicenter Selective Lymphadenectomy Trial (MSLT-1 [JWCI-MORD-MSLT-1193]) included 1,269 patients with intermediate-thickness (defined as 1.2 mm–3.5 mm in this study) primary melanomas.[18] There was no melanoma-specific survival advantage (the primary endpoint) for those patients randomly assigned to wide excision plus SLN biopsy followed by immediate complete lymphadenectomy for node positivity versus patients randomly assigned to nodal observation and delayed lymphadenectomy for subsequent nodal recurrence at a median of 59.8 months.[18][Level of evidence: 1iiB]
This trial was not designed to detect a difference in the impact of lymphadenectomy in patients with microscopic lymph node involvement.[18]
Adjuvant Treatment Options for Patients With Stage II Melanoma
Treatment Options Under Clinical Evaluation for Patients With Stage II Melanoma
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with stage II melanoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
Stage III melanoma is defined by the American Joint Committee on Cancer's TNM classification system:[1]
Standard Treatment Options for Patients With Stage III Melanoma
Adjuvant Treatment Options for Patients With Resected Stage III Disease
Prospective, randomized, multicenter treatment trials have demonstrated that high-dose interferon alpha-2b and pegylated interferon do not improve overall survival (OS). Agents that have demonstrated improved OS in patients with recurrent or metastatic disease are now being tested in clinical trials of adjuvant therapy in patients at high risk for relapse after surgical resection of tumor. These trials include: NCT01274338, NCT01667419, and NCT01682083.
The median OS for patients who received the high-dose regimen of interferon alpha-2b was 3.8 years compared with 2.8 years for those in the observation group.[9][Level of evidence: 1iiA] A subset analysis of the stage II patients, however, failed to show any benefit from high-dose interferon in terms of RFS or OS. Because the number of stage II patients was small in this subset analysis, it is difficult to draw meaningful conclusions from this study for this specific group.
Clinicians should be aware that the high-dose regimens have significant toxic effects.
Treatment Options for Patients With Unresectable Stage III Disease
Treatment Options Under Clinical Evaluation for Patients With Stage III Melanoma
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with stage III melanoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
Stage IV melanoma is defined by the American Joint Committee on Cancer's TNM classification system:[1]
Treatment Options for Patients With Stage IV and Recurrent Melanoma
Treatment option overview for patients with stage IV and recurrent melanoma
Although melanoma that has spread to distant sites is rarely curable, two approaches have demonstrated clinical benefit by prolonging overall survival (OS) in randomized trials: immunotherapy (e.g., ipilimumab) and inhibition of the mitogen-activated protein (MAP) kinase pathway (e.g., with vemurafenib in patients whose tumors have a V600 mutation in the BRAF gene). Both ipilimumab and vemurafenib were approved by the U.S. Food and Drug Administration (FDA) in 2011. Although neither appears to be curative when used as a single agent, clinical trials are currently testing combinations of these and similar agents to prevent the development of resistance. Ipilimumab and vemurafenib are available to newly diagnosed and previously treated patients.
IL-2 was approved by the FDA in 1998 on the basis of durable complete response (CR) rates in a minority of patients (0%–8%) with previously treated metastatic melanoma in eight phase I and II studies. No improvement in OS has been demonstrated in randomized trials.
Dacarbazine (DTIC) was approved in 1970 based on overall response rates. Phase III trials indicate an overall response rate of 10% to 20% with rare CRs observed. An impact on OS has not been demonstrated in randomized trials.[2,3,4,5,6] Temozolomide, an oral alkylating agent, appeared to be similar to DTIC (intravenous administration) in a randomized phase with a primary endpoint of OS; however, the trial was designed for superiority, and the sample size was inadequate to prove equivalency.[3]
Attempts to develop combination regimens that incorporate chemotherapy, for example, multiagent chemotherapy;[7,8] combinations of chemotherapy and tamoxifen;[9,10,11] and combinations of chemotherapy and immunotherapy [7,12,13,14,15,16,17] have not demonstrated an improvement of the combination on OS.
In smaller subsets of melanoma, activating mutations may occur in NRAS [neuroblastoma RAS viral (v-ras) oncogene homolog] (15%–20%), c-KIT (28%–39% of melanomas arising in chronically sun-damaged skin, or acral and mucosal melanomas), and CDK4 (cyclin-dependent kinase 4) (<5%), whereas GNAQ is frequently mutated in uveal melanomas. Drugs developed to target the pathways activated by these mutations are currently in clinical trials.
Malignant melanoma has been reported to spontaneously regress; however, the incidence of spontaneous complete regressions is less than 1%.[18]
Checkpoint inhibitors
Anti-CTLA-4: ipilimumab
Ipilimumab is a human monoclonal antibody that blocks the activity of CTLA-4, blocking the function of CTLA-4 as a down regulator of T-cell activation. It is approved for the treatment of unresectable or metastatic melanoma and supported by two prospective, randomized, international trials, one each in previously untreated and treated patients.[6,19]
Previously treated patients. A total of 676 patients with previously treated, unresectable stage III or stage IV disease, who were HLA-A*0201-positive patients, were entered into a three-arm, multinational, randomized, double-blind trial comparing ipilimumab with or without glycoprotein 100 (gp100) peptide vaccine to the gp100 vaccine plus placebo.[19] Patients were stratified by baseline metastases and prior receipt or nonreceipt of IL-2 therapy. Of the patients, 82 had metastases to the brain at baseline. The median OS was 10 months and 10.1 months among patients receiving ipilimumab alone or with the gp100 vaccine, respectively, versus 6.4 months for patients receiving the vaccine alone (hazard ratio [HR], 0.68; P < .001; HR, 0.66; P < .003).
An analysis at 1 year showed that among those patients treated with ipilimumab, 44% and 45% of them were alive compared with 25% of the patients who received vaccine only. Grade 3 to grade 4 immune-related adverse events (AEs) occurred in 10% to 15% of patients treated with ipilimumab. These immune-related AEs most often included diarrhea or colitis, and endocrine-related events (i.e., inflammation of the pituitary) that required cessation of therapy and institution of anti-inflammatory agents, such as corticosteroids or in four cases, infliximab (i.e., an anti-tumor necrosis factor-alpha antibody). There were 14 deaths related to study drugs (2.1%), and seven were associated with immune-related AEs.[19][Level of evidence: 1iA]
Previously untreated patients. A multicenter, international trial randomly assigned 502 patients untreated for metastatic disease (adjuvant treatment was allowed) in a 1:1 ratio to ipilimumab (10 mg/kg) plus dacarbazine (850 mg/m2) or placebo plus dacarbazine (850 mg/m2) at weeks 1, 4, 7, and 10 followed by dacarbazine alone every 3 weeks through week 22.[6] Patients with stable disease or an objective response and no dose-limiting toxic effects received ipilimumab or placebo every 12 weeks thereafter as maintenance therapy. The primary endpoint was survival.
Patients were stratified according to Eastern Cooperative Oncology Group (ECOG) performance status (PS) and metastatic stage. Approximately 70% of the patients had an ECOG PS of 0, and the remainder of the patients had an ECOG PS of 1. Approximately 55% of the patients had stage M1c disease. The median OS was 11.2 months (95% confidence interval [CI], 9.4–13.6) versus 9.1 months (95% CI, 7.8–10.5). Estimated survival rates in the two groups respectively were 47.3% and 36.3% at 1 year; 28.5% and 17.9% at 2 years; and 20.9% and 12.2% at 3 years (HR for death with ipilimumab-dacarbazine, 0.72; P < .001). The most common study-drug–related AEs were those classified as immune related. Grade 3 to 4, immune-related AEs were seen in 38.1% of patients treated with ipilimumab plus dacarbazine versus 4.4% in patients treated with placebo plus dacarbazine, the most common being hepatitis and enterocolitis. No drug-related deaths occurred.[6][Level of evidence: 1iA]
Clinicians and patients should be aware that immune-mediated adverse reactions may be severe and fatal. Early identification and treatment, including potential administration of systemic glucocorticoids or other immunosuppressants according to the immune-mediated–adverse reaction management guide provided by the manufacturer, is necessary.[20]
Anti-PD-1 and PD-L1
Anti-PD-1 and PD-L1 are immune checkpoint inhibitors; however, they inhibit different targets than ipilimumab. Promising early data have supported testing anti-PD-1 against DTIC in a phase III trial (NCT01721772).[21]
Response to high-dose IL-2 regimens generally ranges from 10% to 20%.[12,13,22] Approximately 4% to 6% of patients may obtain a durable complete remission and be long-term survivors; these results were the basis for approval by the FDA in 1998. Phase III confirmatory trials have not been conducted, and there are currently no predictive biomarkers to select who is likely to respond to treatment.
Attempts to improve on this therapy have included the addition of lymphokine-activated killer cells (i.e., autologous lymphocytes activated by IL-2 ex vivo) and tumor-infiltrating lymphocytes (TIL) (i.e., lymphocytes derived from tumor isolates cultured in the presence of IL-2). A single-institution trial reports that adoptive cell therapy (ACT) with lymphodepletion (using cyclophosphamide plus fludarabine with or without total-body irradiation) followed by autologous TIL transfer and high-dose IL-2 may improve durable response.[23][Level of evidence: 3iiiDiv] A multicenter, randomized trial of high-dose IL-2 with and without a peptide vaccine [gp100:209–217(210M)] in patients with locally advanced stage III or stage IV melanoma who were HLA*A0201-positive reported an increase in response rate with the combination.[24][Level of evidence:1iiDiv] Multicenter, phase III trials powered for an assessment on OS are needed for validation, because response rates are not known to be a surrogate for OS in melanoma.
Signal transduction inhibitors
Studies to date indicate that both BRAF and MEK (mitogen-activated ERK-[extracellular signal-regulated kinase] activating kinase) inhibitors can significantly impact the natural history of melanoma, although as single agents, they do not appear to provide a cure.
BRAF inhibitors
Vemurafenib is an orally available, small molecule, selective BRAF inhibitor that is approved by the FDA for patients with unresectable or metastatic melanoma that tests positive for the BRAF V600E mutation. Treatment with vemurafenib is discouraged in wild-type BRAF melanoma because data from preclinical models has demonstrated that BRAF inhibitors can enhance rather than downregulate the MAPK (mitogen-activated protein kinase) pathway in tumor cells with wild-type BRAF and upstream RAS mutations.[25,26,27,28]
Previously untreated patients. The approval of vemurafenib was supported by an international, multicenter trial (BRIM-3 [NCT01006980]) that screened 2,107 patients with previously untreated, stage IIIC or IV melanoma for the BRAF V600 mutation and identified 675 patients by the cobas® 4800 BRAF V600 Mutation Test.[5] Patients were randomly assigned to receive either vemurafenib (960 mg orally twice daily) or dacarbazine (1000 mg/m2 intravenously [ IV] every 3 weeks). Coprimary endpoints were rates of OS and PFS.[5][Levels of evidence: 1iiA and 1iiDiii]
At the planned interim analysis, the Data and Safety Monitoring Board determined that both the OS and PFS endpoints had met the prespecified criteria for statistical significance in favor of vemurafenib and recommended that patients in the dacarbazine group be allowed to cross over to receive vemurafenib. A total of 675 patients were evaluated for OS; although the median survival had not yet been reached for vemurafenib and the data were immature for reliable Kaplan-Meier estimates of survival curves, the OS in the vemurafenib arm was clearly superior to that in the dacarbazine arm. The HR for death in the vemurafenib group was 0.37 (95% CI, 0.26–0.55; P < .001). The survival benefit in the vemurafenib group was observed in each prespecified subgroup; for example, age, sex, ECOG PS, tumor-stage lactic dehydrogenase, and geographic region. The HR for tumor progression in the vemurafenib arm was 0.26 (95% CI, 0.20–0.33; P < .001). The estimated median PFS was 5.3 months versus 1.6 months in the vemurafenib and dacarbazine arms, respectively.
Twenty patients had non-V600E mutations: 19 with V600K and 1 with V600D. Four patients with a BRAF V600K mutation had a response to vemurafenib.
AEs required dose modification or interruption in 38% of patients receiving vemurafenib and 16% of those receiving dacarbazine. The most common AEs with vemurafenib were cutaneous events, arthralgia, and fatigue. Cutaneous squamous cell carcinoma (SCC), keratoacanthoma, or both, developed in 18% of patients and were treated by simple excision. The most common AEs with dacarbazine were fatigue, nausea, vomiting, and neutropenia.
Previously treated patients. A total of 132 patients with a BRAF V600E or BRAF V600K mutation were enrolled in a multicenter phase II trial of vemurafenib, which was administered as 960 mg orally twice daily.[29] Of the enrolled patients, 61% percent had stage M1c disease, and 49% had an elevated lactate dehydrogenase level. All patients had received one or more prior therapies for advanced disease. Median follow-up was 12.9 months. An Independent Review Committee (IRC) reported a 53% response rate (95% CI, 44–62) with eight patients (6%) achieving CR. Median duration of response per IRC assessment was 6.7 months (95% CI, 5.6–8.6). Most responses were evident at the first radiologic assessment at 6 weeks; however, some patients did not respond until they received therapy for more than 6 months.[29][Level of evidence: 3iiiDiv]
Dabrafenib is an orally available, small molecule, selective BRAF inhibitor that has been compared with DTIC in an international, multicenter trial (BREAK-3 [NCT01227889]). A total of 250 patients with unresectable stage III or IV melanoma and BRAF V600E mutations were randomly assigned in a 3:1 ratio (dabrafenib 150 mg orally twice a day or DTIC 1000 mg/m2 IV every 3 weeks). IL-2 was allowed as prior treatment for advanced disease. The primary endpoint was PFS; patients could cross over at the time of progressive disease after confirmation by a blinded IRC.[30]
With 126 events, the HR for PFS was 0.30 (95% CI, 0.18–0.51; P < .0001). The estimated median PFS was 5.1 months versus 2.7 months for dabrafenib and DTIC, respectively. OS data are limited by the median duration of follow up and crossover. Partial response was 47% versus 5%, and CR was 3% versus 2% in patients receiving dabrafenib versus DTIC, respectively.[30][Level of Evidence: 1iiDiii]
The most frequent AEs in patients treated with dabrafenib were cutaneous (i.e., hyperkeratosis, papillomas, palmar-plantar erythrodysesthesia), pyrexia, fatigue, headache, and arthralgia. Cutaneous SCC or keratoacanthoma occurred in twelve patients, basal cell carcinoma occurred in four patients, mycosis fungoides occurred in one patient, and new melanoma occurred in two patients.[30]
MEK inhibitors
Trametinib is an orally available, small molecule, selective inhibitor of MEK1 and MEK2. Preclinical data suggest that MEK inhibitors can restrain growth and induce cell death of some BRAF-mutated human melanoma tumors. BRAF activates MEK1 and MEK2 proteins, which, in turn, activate MAP kinases.
A total of 1,022 patients were screened for BRAF mutations, resulting in 322 eligible patients (281 with V600E, 40 with V600K and 1 with both mutations).[31] Patients were randomly assigned in a 2:1 ratio to receive trametinib (2 mg once daily) or IV chemotherapy (either DTIC 1000 mg/m2 every 3 weeks or paclitaxel 175 mg/m2 every 3 weeks). Crossover was allowed, and the primary endpoint was PFS. The investigator-assessed PFS was 4.8 months in patients receiving trametinib versus 1.5 months in the chemotherapy group (HR for PFS or death, 0.45; 95% CI, 0.33–0.63; P < .001). Median OS has not yet been reached.
AEs leading to dose interruptions occurred in 35% of patients in the trametinib group and 22% of those in the chemotherapy group. AEs leading to dose reductions occurred in 27% of patients receiving trametinib and 10% of those receiving chemotherapy. The most common AEs included rash, diarrhea, nausea, vomiting, fatigue, peripheral edema, alopecia, hypertension, and constipation. Central serous retinopathy and retinal-vein occlusion are uncommon, but serious, AEs associated with trametinib. On-study cutaneous SCCs were not observed.
Combinatorial therapy with signal transduction inhibitors
Resistance to BRAF inhibitors, in patients with BRAF V600 mutations, may be associated with reactivation of the MAP kinase pathway. Early phase II data with combinations of BRAF and MEK inhibitors have supported testing this combination in phase III trials, such as NCT01584648, NCT01597908, and NCT01689519.[32] Combination therapy to address other mechanisms of resistance (e.g., via activation of the PI3K/Akt pathway) are in early-phase trials.
Multikinase inhibitors
The multikinase inhibitor sorafenib has activity against both the vascular endothelial growth-factor signaling and the Raf/MEK/ERK pathway at the level of RAF kinase. This agent had minimal activity as a single agent in melanoma and two large, multicenter, placebo-controlled, randomized trials of carboplatin and taxol plus or minus sorafenib showed no improvement over chemotherapy alone as either first-line treatment or second-line treatment.[33,34]
KIT inhibitors
Early data suggest that mucosal or acral melanomas with activating mutations or amplifications in c-KIT may be sensitive to a variety of c-KIT inhibitors.[35,36,37] Phase II and phase III trials are available for patients with unresectable stage III or stage IV melanoma harboring the c-KIT mutation.
The objective response rate to DTIC and the nitrosoureas, carmustine and lomustine, is approximately 10% to 20%.[2,38,39,40] Responses are usually short-lived, ranging from 3 to 6 months, though long-term remissions can occur in a limited number of patients who attain a CR.[38,40] A randomized trial compared IV DTIC with temozolomide (TMZ), an oral agent that hydrolyzes to the same active moiety as DTIC; OS was 6.4 months versus 7.7 months, respectively (HR, 1.18; 95% CI, 0.92–1.52). While these data suggested similarity between DTIC and TMZ, no benefit in survival has been demonstrated for either DTIC or TMZ and therefore, demonstration of similarity did not result in approval from the FDA.[3][Level of evidence: 1iiA] An extended schedule and escalated dose of TMZ was compared with DTIC in a multicenter trial (NCT00091572) that randomly assigned 859 patients. No improvement was seen in OS or PFS for the TMZ group, and this dose and schedule resulted in more toxicity than standard dose, single-agent DTIC.[41][Level of evidence: 1iiA]
The design of two recent randomized, phase III trials in previously untreated patients with metastatic melanoma included DTIC as the standard therapy arm. Vemurafenib (in BRAF V600 mutant melanoma) and ipilimumab showed superior OS compared with DTIC in the two separate trials.
Other agents with modest, single-agent activity include vinca alkaloids, platinum compounds, and taxanes.[38,39]
Palliative local therapy
Melanoma metastatic to distant, lymph node-bearing areas may be palliated by regional lymphadenectomy. Isolated metastases to the lung, gastrointestinal tract, bone, or sometimes the brain, may be palliated by resection with occasional long-term survival.[15,16,17]
Although melanoma is a relatively radiation-resistant tumor, palliative radiation therapy may alleviate symptoms. Retrospective studies have shown that patients with multiple brain metastases, bone metastases, and spinal cord compression may achieve symptom relief and some shrinkage of the tumor with radiation therapy.[42,43] (Refer to the PDQ summary on Pain for more information.) The most effective dose-fractionation schedule for palliation of melanoma metastatic to the bone or spinal cord is unclear, but high-dose-per-fraction schedules are sometimes used to overcome tumor resistance. A phase I and II clinical trial (MCC-11543 [NCT00005615]) evaluated adjuvant radiation therapy plus interferon in patients with recurrent melanoma and results are pending.
A published data meta-analysis of 18 randomized trials (15 of which had survival information) that compared chemotherapy with biochemotherapy (i.e., the same chemotherapy plus interferon alone or with IL-2) demonstrated no impact on OS.[44][Level of evidence:1iiA]
Other Treatment Options Under Clinical Evaluation for Patients With Stage IV and Recurrent Melanoma
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with stage IV melanoma and recurrent melanoma. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
General Information About Melanoma
Updated statistics with estimated new cases and deaths for 2014 (cited American Cancer Society as reference 1).
This summary is written and maintained by the PDQ Adult Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of melanoma. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Adult Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
The lead reviewers for Melanoma Treatment are:
Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
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Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Adult Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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The preferred citation for this PDQ summary is:
National Cancer Institute: PDQ® Melanoma Treatment. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/treatment/melanoma/HealthProfessional. Accessed <MM/DD/YYYY>.
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Last Revised: 2014-03-19
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text:
31 January 2011
Posted in NatureWorks
Happy news occurred on January 14 - a baby black rhinoceros was born at the St. Louis Zoo! The baby is a boy and weighs 120.5 pounds. This is an important birth because the black rhino is critically endangered. There are only about 4,240 black rhinos in the world. The reason why the black rhino is so endangered is because they are heavily poached for their horns. Many Asian countries believe that their horns have medicinal powers.
However, with the joyous birth of this baby boy, and hopefully more births to come at zoos throughout the world, this new generation will be able to go back out into Africa and continue the survival of the species. If you would like to learn more about the black rhinoceros and their fight for survival, please visit: http://www.rhinos-irf.org/black.


text: First details and screenshots for Madden NFL 11. What do you guys think? The screenshots don't look too different from last year and I could have sworn they already had something about WR AI knowing where the sidelines were, etc. I hope that they actually make improvements and just don't forcefeed "small adjustments" down our throats with these blogs and actually make the changes to make the game better.