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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.
Fortunately, cancer in children and adolescents is rare, although the overall incidence of childhood cancer has been slowly increasing since 1975.[1] Children and adolescents with cancer should be referred to medical centers that have a multidisciplinary team of cancer specialists with experience treating the cancers that occur during childhood and adolescence. This multidisciplinary team approach incorporates the skills of the primary care physician, pediatric surgical subspecialists, radiation therapists, pediatric oncologists/hematologists, rehabilitation specialists, pediatric nurse specialists, social workers, and others to ensure that children receive treatment, supportive care, and rehabilitation that will achieve optimal survival and quality of life. (Refer to the PDQ Supportive and Palliative Care summaries for specific information about supportive care for children and adolescents with cancer.)
Guidelines for pediatric cancer centers and their role in the treatment of pediatric patients with cancer have been outlined by the American Academy of Pediatrics.[2] At these pediatric cancer centers, clinical trials are available for most types of cancer that occur in children and adolescents, and the opportunity to participate in these trials is offered to most patients/families. Clinical trials for children and adolescents with cancer are generally designed to compare potentially better therapy with therapy that is currently accepted as standard. Most of the progress made in identifying curative therapies for childhood cancers has been achieved through clinical trials. Information about ongoing clinical trials is available from the NCI Web site.
Dramatic improvements in survival have been achieved for children and adolescents with cancer. Between 1975 and 2002, childhood cancer mortality has decreased by more than 50%.[1] Childhood and adolescent cancer survivors require close follow-up since cancer therapy side effects may persist or develop months or years after treatment. (Refer to Late Effects of Treatment for Childhood Cancer for specific information about the incidence, type, and monitoring of late effects in childhood and adolescent cancer survivors.)
Hepatoblastoma and Hepatocellular Carcinoma
Liver cancer is a rare malignancy in children and adolescents and is divided into two major histologic subgroups: hepatoblastoma and hepatocellular carcinoma.
The incidence of hepatoblastoma in the United States appears to have doubled from 0.8 (1975–1983) to 1.6 (2002–2009) per year per 1 million children aged 19 years and younger.[3,4] The cause for the increase in incidence of hepatoblastoma is unknown, but the increasing survival of very low-birth-weight premature infants, which is known to be associated with hepatoblastoma, may contribute.[5] In Japan, the risk of hepatoblastoma in children who weighed less than 1,000 g at birth is 15 times the risk in normal birth-weight children.[6] Other data has confirmed the high incidence of hepatoblastoma in very low-birth-weight premature infants.[7]
The age of onset of liver cancer in children is related to tumor histology. Hepatoblastomas usually occur before the age of 3 years, and approximately 90% of malignant liver tumors in children aged 4 years and younger are hepatoblastomas.[8]
The incidence of hepatocellular carcinoma in the United States is 0.8 in children between the ages of 0 and 14 years and 1.5 in adolescents aged 15 to 19 years per year per 1 million.[3] In several Asian countries, the incidence of hepatocellular carcinoma in children is 10 times more than that in North America. The high incidence appears to be related to the incidence of perinatally acquired hepatitis B, which can be prevented in most cases by vaccination and administration of hepatitis B immune globulin to the newborn.[9]
The overall 5-year survival rate for children with hepatoblastoma is 70%,[10,11,12] but is only 42% for those with hepatocellular carcinoma.[3] The 5-year survival for hepatocellular carcinoma may be dependent on stage; in an Intergroup chemotherapy study conducted in the 1990s, seven of eight stage I patients survived and less than 10% of stage III and IV patients survived.[3,13]
Risk factors
Risk factors associated with hepatoblastoma and hepatocellular carcinoma are described in Table 1.
Beckwith-Wiedemann syndrome and hemihyperplasia
The incidence of hepatoblastoma is increased 1,000-fold to 10,000-fold in infants and children with Beckwith-Wiedemann syndrome.[15,16] Hepatoblastoma is also increased in hemihypertrophy, now termed hemihyperplasia, a condition that results in asymmetry between the right and left side of the body when a body part grows faster than normal.[28,29]
Beckwith-Wiedemann syndrome can be caused by genetic mutations and be familial, or much more commonly, by epigenetic changes and be sporadic. Either mechanism can be associated with an increased incidence of embryonal tumors, including Wilms tumor and hepatoblastoma.[16] The gene dosage and ensuing increased expression of insulin-like growth factor 2 (IGF-2) has been implicated in the macrosomia and embryonal tumors in Beckwith-Wiedemann syndrome.[16,30] When sporadic, the types of embryonal tumors associated with Beckwith-Wiedemann syndrome have frequently also undergone somatic changes in the Beckwith-Wiedemann syndrome locus and IGF-2.[31,32] The genetics of tumors in children with hemihyperplasia have not been clearly defined.
All children with Beckwith-Wiedemann syndrome or isolated hemihyperplasia should be screened regularly by ultrasound to detect abdominal malignancies at an early stage.[29] Screening using alpha-fetoprotein (AFP) levels, in addition to abdominal ultrasound, has helped in the early detection of hepatoblastoma in children with Beckwith-Wiedemann syndrome or hemihyperplasia.[33] Other somatic overgrowth syndromes, such as Simpson-Golabi-Behmel syndrome, may also be associated with hepatoblastoma.[34]
Familial adenomatous polyposis
There is an association between hepatoblastoma and familial adenomatous polyposis (FAP); children in families that carry the APC gene are at an 800-fold increased risk for hepatoblastoma. However, hepatoblastoma has been reported to occur in less than 1% of FAP family members, so ultrasound and AFP screening for hepatoblastoma in members of families with FAP has been controversial.[17,18,19,35]
A study of 50 sequential children with apparent sporadic hepatoblastoma reported five children (10%) had APC mutations.[35] Data to date cannot rule out the possibility that predisposition to hepatoblastoma may be limited to a specific subset of APC mutations. Another study of children with hepatoblastoma found a predominance of the mutation in the 5' region of the gene, but some patients had mutations closer to the 3' region.[36] Perhaps, screening children with hepatoblastoma for APC mutations may be appropriate, as they should be followed for potential colon cancer. This preliminary study provides some evidence that screening children with hepatoblastoma for APC mutations may be appropriate.
In the absence of APC germline mutations, childhood hepatoblastomas do not have somatic mutations in the APC gene; however, they frequently have mutations in the beta-catenin gene, the function of which is closely related to APC.[37]
Hepatitis B and hepatitis C infection
Hepatocellular carcinoma is associated with hepatitis B and hepatitis C infection in adults,[21,22,23] while in children there is an association with perinatally acquired hepatitis B virus. Widespread hepatitis B immunization has decreased the incidence of hepatocellular carcinoma in Asia.[9] Compared with adults, the incubation period from hepatitis virus infection to the genesis of hepatocellular carcinoma is extremely short in a small subset of children with perinatally acquired virus. Mutations in the met/hepatocyte growth factor receptor gene occur in childhood hepatocellular carcinoma, and this could be one mechanism that results in a shortened incubation period. Hepatitis C infection is associated with development of cirrhosis and hepatocellular carcinoma that takes decades to develop and is generally not seen in children.[38]
Several specific types of nonviral liver injury and cirrhosis are associated with hepatocellular carcinoma in children, including tyrosinemia and biliary cirrhosis. Tyrosinemia patients should be screened for hepatoblastoma on a regular basis, whether or not they are treated with 2-(2 nitro-4-3 trifluoro-methylbenzoyl)-1, 3-cyclohexanedione.[27] Hepatocellular carcinoma may also arise in very young children with mutations in the bile salt export pump ABCB11, which causes progressive familial hepatic cholestasis.[24] Despite these findings, cirrhosis in children, compared with cirrhosis in adults, is much less commonly involved in the development of hepatocellular carcinoma, and is found in only 20% to 35% of livers bearing childhood hepatocellular carcinoma tumors.
A biopsy of the tumor is always indicated to secure the diagnosis of a liver tumor except:
The AFP and beta-hCG tumor markers are very helpful in diagnosis and management of liver tumors. Although AFP is elevated in most children with hepatic malignancy, it is not pathognomonic for a malignant liver tumor.[40] The AFP level can be elevated due to a benign tumor, as well as a malignant solid tumor. AFP is very high in neonates and steadily falls after birth. The half-life of AFP is 5 to 7 days, and by age 1 year, it should be less than 10 ng/ml.[41]
Treatment-related factors
Cure of hepatoblastoma or hepatocellular carcinoma requires gross tumor resection. If a hepatoblastoma is completely removed, the majority of patients survive, but less than one-third of patients have lesions amenable to complete resection at diagnosis. Thus, it is critically important that a child with probable hepatoblastoma be evaluated by a pediatric surgeon who is experienced in the resection of hepatoblastoma in children and has access to a liver transplant program.
Chemotherapy can often decrease the size and extent of hepatoblastoma, allowing complete resection.[10,11,12,42,43] Orthotopic liver transplantation provides an additional treatment option for patients whose tumor remains unresectable after preoperative chemotherapy;[43,44,45] however, the presence of microscopic residual tumor at the surgical margin does not preclude a favorable outcome.[46,47] This may be due to the additional courses of chemotherapy that are administered before or after resection for patients with stage I and pure fetal histology and after resection for all other patients.[10,11,47]
Hepatoblastoma is most often unifocal, and resection is often possible. Hepatocellular carcinoma is often extensively invasive or multicentric, and less than 30% are resectable. Orthotopic liver transplantation has been successful in selected children with hepatocellular carcinoma.[45]
Tumor marker–related factors
Ninety percent of patients with hepatoblastoma and two-thirds of patients with hepatocellular carcinoma have a serum tumor marker, AFP, which parallels disease activity. The level of AFP at diagnosis and rate of decrease in AFP during treatment should be compared with the age-adjusted normal range. Lack of a significant decrease of AFP levels with treatment may predict a poor response to therapy.[48] Absence of elevated AFP levels at diagnosis occurs in a small percentage of children with hepatoblastoma and appears to be associated with very poor prognosis, as well as with the small cell undifferentiated variant of hepatoblastoma. Some of these variants do not express INI1 due to INI1 mutation and may be considered rhabdoid tumors of the liver; all small cell undifferentiated hepatoblastomas should be tested for loss of INI1 expression by immunohistochemistry.[46,49,50,51,52,53]
Beta-hCG levels may also be elevated in children with hepatoblastoma or hepatocellular carcinoma, which may result in isosexual precocity in boys.[54,55] Extremely high levels of beta-hCG are associated with infantile choriocarcinoma of the liver.
Undifferentiated Embryonal Sarcoma of the Liver
Undifferentiated embryonal sarcoma of the liver (UESL) is the third most common liver malignancy in children and adolescents, comprising 9% to 13% of liver tumors. It presents as an abdominal mass, often with pain or malaise, usually between the ages of 5 and 10 years. Widespread infiltration throughout the liver and pulmonary metastasis are common. It may appear solid or cystic on imaging, frequently with central necrosis. Distinctive features are characteristic intracellular hyaline globules and marked anaplasia on a mesenchymal background.[56] Many UESL contain diverse elements of mesenchymal cell maturation, such as smooth muscle and fat. Undifferentiated sarcomas and small cell undifferentiated hepatoblastomas should be examined for loss of INI1 expression by immunohistochemistry to help rule out rhabdoid tumor of the liver.
It is important to make the diagnostic distinction between UESL and biliary tract rhabdomyosarcoma because they share some common clinical and pathologic features but treatment differs between the two, as shown in Table 2.[57] (Refer to the PDQ summary on Childhood Rhabdomyosarcoma Treatment for more information.)
It has been suggested that some UESLs arise from mesenchymal hamartomas of the liver, which are large benign multicystic masses that present in the first 2 years of life.[57] Strong clinical and histological evidence suggest that UESL can arise within preexisting mesenchymal hamartomas of the liver. In a report of 11 cases of UESL, five arose in association with mesenchymal hamartomas of the liver, and transition zones between the histologies were noted.[58] Many mesenchymal hamartomas of the liver have a characteristic translocation with a breakpoint at 19q13.4 and several UESLs have the same translocation.[59,60] Some UESLs arising from mesenchymal hamartomas of the liver may have complex karyotypes not involving 19q13.4.
Infantile Choriocarcinoma of the Liver
Choriocarcinoma of the liver is a very rare tumor that appears to originate in the placenta and presents with a liver mass in the first few months of life. Infants are often unstable due to hemorrhage of the tumor. Clinical diagnosis may be made without biopsy based on tumor imaging of the liver associated with extremely high serum beta-hCG levels and normal AFP levels for age.[39]
Epithelioid Hemangioendothelioma
Epithelioid hemangioendothelioma is a rare vascular cancer that occurs in the liver and other organs. (Refer to the Hemangioendothelioma section in the PDQ summary on Childhood Soft Tissue Sarcoma Treatment for more information.)
Hepatoblastoma arises from precursors of hepatocytes and can have several morphologies, including the following:
Most often the tumor consists of a mixture of epithelial hepatocyte precursors. About 20% of tumors have stromal derivatives such as osteoid, chondroid, and rhabdoid elements. Occasionally neuronal, melanocytic, squamous, and enteroendocrine elements are found. Two histologic subtypes have clinical relevance: pure fetal histology throughout the tumor and foci of small cell undifferentiated cells.
Pure fetal histology hepatoblastoma
Analysis of patients with initially resected hepatoblastoma tumors (prior to receiving chemotherapy) has suggested that those patients with pure fetal histology tumors have a better prognosis than those having an admixture of more primitive and rapidly dividing embryonal components or other undifferentiated tissues. In a study of patients with hepatoblastoma and pure fetal histology tumors, there was a 100% survival rate for patients who received four doses of single-agent doxorubicin.[1] This suggested that patients with pure fetal histology tumors might not need chemotherapy after complete resection of a stage I tumor.[2,3] In the Children's Oncology Group (COG) study COG-P9645, 16 patients with stage I pure fetal histology hepatoblastoma with two or fewer mitoses per 10 high power fields were not treated with chemotherapy. Their retrospective PRETEXT stages were stage I (n = 4), stage II (n = 6), and stage III (n = 2). Survival was 100% with no chemotherapy given.[4] All 16 patients entered on this study were alive with no evidence of disease at a median follow-up of 4.9 years (range, 9 months to 9.2 years).[4] Thus, complete resection of a pure fetal hepatoblastoma may preclude the need for chemotherapy.
Small cell undifferentiated hepatoblastoma
Small cell undifferentiated hepatoblastoma is an uncommon hepatoblastoma variant that represents a few percent of all hepatoblastomas. It tends to occur at a younger age (6–10 months) compared with other cases of hepatoblastoma [5,6] and is associated with AFP normal for age at presentation.[5,7]
Histologically, small cell undifferentiated hepatoblastoma is typified by a diffuse population of small cells with scant cytoplasm resembling neuroblasts.[8] The chromosomal abnormalities reported for small cell undifferentiated hepatoblastoma are distinct from those occurring in other hepatoblastoma subtypes and are more similar to those observed in malignant rhabdoid tumors. These abnormalities include translocations involving a breakpoint on chromosome 22q11 and homozygous deletion at the chromosome 22q12 region that harbors the SMARCB1/INI1 gene.[5,9] Lack of detection of INI1 by immunohistochemistry is another characteristic shared by some small cell undifferentiated hepatoblastomas and malignant rhabdoid tumors.[5] A third characteristic shared between small cell undifferentiated hepatoblastomas and malignant rhabdoid tumors is the poor prognosis associated with each.[5,6,10] Patients with small cell undifferentiated hepatoblastoma whose tumors are unresectable have an especially poor prognosis.[5] Patients with stage I tumors appear to have increased risk of treatment failure when small cell elements are present.[11] For this reason, completely resected tumors composed of pure fetal histology or of mixed fetal and embryonal cells must have a thorough histologic examination as small foci of undifferentiated small cell histology indicates a need for aggressive chemotherapy.[11] Aggressive treatment for this histology is under investigation in the current COG study, COG-AHEP0731. Hepatoblastoma that would otherwise be considered very low or low risk is upgraded to intermediate risk if any small cell undifferentiated elements are found (refer to the Stage Information section of this summary for more information).
Hepatocellular Carcinoma
The cells of hepatocellular carcinoma are epithelial while hepatoblastoma has a less differentiated embryonal appearance. Hepatocellular carcinoma also differs from hepatoblastoma in that it often arises in a previously abnormal, cirrhotic liver. Both histologic types more commonly arise in the right lobe of the liver. Chronic hepatitis B is the leading cause of hepatocellular carcinoma in children in Asian and African countries; however, underlying liver disease can be identified in less than one-third of the children and adolescents with hepatocellular carcinoma in western countries.[12]
Fibrolamellar carcinoma
A distinctive histologic variant of hepatocellular carcinoma, termed fibrolamellar carcinoma, has been described in the livers of older children and young adults. Fibrolamellar carcinoma is thought to be associated with an improved prognosis and is not associated with cirrhosis.[13,14,15] The improved outcome in older studies may be related to a higher proportion of tumors being less invasive and more resectable in the absence of cirrhosis, because the outcome in recent prospective studies, when compared stage for stage, is not different from other hepatocellular carcinomas.[12,16] Fibrolamellar hepatocellular carcinoma has also been reported in infants.[17]
Transitional liver cell tumor
Transitional liver cell tumor is a rare neoplasm that is found in older children and adolescents, and has a putative intermediate position between hepatoblasts and more mature hepatocyte-like tumor cells. The tumor cells may vary in regions of the tumor between classical hepatoblastoma and obvious hepatocellular carcinoma. The tumors are usually unifocal and may have central necrosis at presentation. Response to chemotherapy is poor, much like hepatocellular carcinoma.[18]
Undifferentiated embryonal sarcoma of the liver is a distinct clinical and pathologic entity and accounts for 2% to 15% of pediatric hepatic malignancies.[19] Distinctive features are intracellular hyaline globules and marked anaplasia on a mesenchymal background.[20]
These tumors are usually very friable and hemorrhagic and may present with bleeding into the tumor. The diagnosis can be made by imaging and findings of extremely high beta-human chorionic gonadotropin levels.
Cytotrophoblasts and syncytiotrophoblasts are both present. The former are closely packed nests of medium-sized cells with clear cytoplasm, distinct cell margins, and vesicular nuclei. The latter are very large multinucleated syncytia formed from the cytotrophoblasts.[21]
There are two standard surgical staging systems for pediatric liver tumors. The International Society of Pediatric Oncology Epithelial Liver Tumor Group (SIOPEL) uses a presurgical-based (PRETEXT) staging system, while the Children's Oncology Group (COG) uses a postsurgical-based staging system. The SIOPEL presurgical staging system is used with neoadjuvant chemotherapy followed by definitive surgery, while the COG staging system is based on the findings at time of operation, whenever possible.
Both staging systems are used in the United States, although initial resection of PRETEXT 1 and 2 hepatoblastomas are routinely undertaken in the United States. In a retrospective comparison of the two staging systems at diagnosis using data from patients entered on a North American randomized trial, both staging systems predicted outcome. The presurgical PRETEXT staging system may add prognostic information compared with postsurgical staging alone. The European PRETEXT staging system can also be used to restage patients after surgery, which has been termed POSTTEXT staging.[1] The COG is investigating the use of PRETEXT/POSTTEXT stage before and after chemotherapy to determine the optimal surgical approach (COG-AHEP0731).
Presurgical Staging for Hepatoblastoma and Hepatocellular Carcinoma
The European PRETEXT staging system for hepatoblastoma categorizes the primary tumor based on extent of liver involvement at diagnosis. In Europe, all children with hepatoblastoma are treated with chemotherapy prior to attempted resection of the primary tumor. The liver tumors are staged by interpretation of computerized tomography or ultrasound with or without additional imaging by magnetic resonance. The presence or absence of metastases is noted, but it does not alter the PRETEXT stage. Tumor involvement of the vena cava, hepatic veins, and portal vein, and extrahepatic extension are also noted.
The imaged liver is divided into four sectors and involvement of each sector with tumor is determined. Stage increases and prognosis decreases as the number of liver sectors radiologically involved with tumor increases from one to four.[2,3] Experienced radiologist review is important because it may be difficult to discriminate between real invasion beyond the anatomic border of a given sector and displacement of the anatomic border.[3,4]
PRETEXT stage 1
PRETEXT stage 2
PRETEXT stage 3
PRETEXT stage 4
PRETEXT designations
Any group may have involvement of:
Hepatoblastoma and hepatocellular carcinoma prognosis by PRETEXT stage
The PRETEXT staging system has a moderate degree of interobserver variability, and the preoperative PRETEXT stage agrees with postoperative pathologic findings only 51% of the time, with overstaging in 37% of patients and understaging in 12% of patients.[3]
The 5-year overall survival (OS) in the first international study of hepatoblastoma, in which the study protocol called for treatment of children with preoperative doxorubicin and cisplatin chemotherapy and included children with metastasis, was as follows:
The second international study compared 3-year OS among hepatoblastoma patients by PRETEXT stage absent of extrahepatic disease. The 3-year OS was as follows:
The study also prospectively analyzed OS in patients by the presence of intraabdominal extrahepatic disease without distant metastasis (OS, 58%) and distant metastases (OS, 44%).[7] Patients who underwent orthotopic liver transplant are included in all of the international study results.[8] The COG is investigating prospective staging of hepatoblastoma patients using the PRETEXT system to determine the timing of surgery and the timing of early notification of liver transplant centers (COG-AHEP0731).
The 5-year OS for PRETEXT staged hepatocellular carcinoma was as follows:
Postsurgical Staging for Childhood Liver Cancer
A staging system based on operative findings and surgical resectability has been used in the United States to group children with liver cancer. This staging system is used to determine treatment.[10,11,12]
Hepatoblastoma prognosis by postsurgical stage
Stages I and II
In stage I hepatoblastoma, the tumor is completely resected.
In stage II hepatoblastoma, microscopic residual tumor remains after resection.
Approximately 20% to 30% of children with hepatoblastoma are stage I or II. Prognosis varies depending on the subtype of hepatoblastoma:
Stage III
In stage III hepatoblastoma, there is no distant metastases and one of the following is true:
Approximately 50% to 70% of children with hepatoblastoma are stage III. The 3- to 5-year OS rate for children with stage III hepatoblastoma is less than 70%.[1,5,7,12,16]
Stage IV (distant metastases)
In stage IV hepatoblastoma, there is distant metastases regardless of the extent of liver involvement.
Approximately 10% to 20% of children with hepatoblastoma are stage IV. The 3- to 5-year OS rate for children with stage IV hepatoblastoma vary widely based on published reports, from 20% to approximately 60%.[1,5,6,7,12,16]
Hepatocellular carcinoma prognosis by postsurgical stage of disease at diagnosis
Treatment Options Under Clinical Evaluation: COG Hepatoblastoma Risk Groups
The COG study COG-AHEP0731 (Combination Chemotherapy in Treating Children With Newly Diagnosed Hepatoblastoma) incorporates the following risk groups:
Many of the improvements in survival in childhood cancer have been made using new therapies that have attempted to improve on the best available, accepted therapy. Clinical trials in pediatrics are designed to compare potentially better therapy with therapy that is currently accepted as standard. This comparison may be done in a randomized study of two treatment arms or by evaluating a single new treatment, comparing the results with those previously obtained with standard therapy.
Because of the relative rarity of cancer in children, all children with liver cancer should be considered for entry into a clinical trial. Treatment planning by a multidisciplinary team of cancer specialists with experience treating tumors of childhood is required to determine and implement optimum treatment.[1]
Historically, complete surgical resection of the primary tumor has been required to cure malignant liver tumors in children.[2,3,4,5]; [6][Level of evidence: 3iiA] Complete surgical resection of the primary tumor continues to be the goal of definitive surgical procedures, but surgical resection is often combined with other treatment modalities (e.g., chemotherapy) to achieve this goal.
Surgical Approaches
There are three ways in which surgery is used to treat primary pediatric liver cancer:
The timing of the surgical approach is critical. For this reason, surgeons with experience in pediatric liver resection and transplantation should be involved early in the decision-making process for determining optimal timing and extent of resection. In children and adolescents with primary liver tumors, the surgeon has to be prepared to perform a highly sophisticated liver resection after confirmation of the diagnosis by pathological investigation of intraoperative frozen sections. While complete surgical resection is important for all liver tumors, this is especially true for hepatocellular carcinoma because no effective chemotherapy is available.
If the tumor can be completely excised by an experienced surgical team, less postoperative chemotherapy may be needed. If the tumor is determined to be unresectable and preoperative chemotherapy is to be administered, it is very important to frequently consult with the surgical team concerning the timing of resection, as prolonged chemotherapy can lead to unnecessary delays and, in rare cases, tumor progression.
Early involvement with an experienced pediatric liver surgeon is especially important in patients with PRETEXT stage 3 or 4 disease, involvement of major liver vessels, and low alpha-fetoprotein (AFP) levels.[7] While vascular involvement was initially thought to be a contraindication to resection, experienced liver surgeons are able to perform aggressive approaches avoiding transplantation.[7,8]; [9][Level of evidence: 3iiA] Accomplishing a complete resection is imperative because rescue transplant of incompletely resected patients has an inferior outcome compared with patients who are transplanted as the primary surgical therapy.[10]
The decision as to which surgical approach to use depends on many factors including the following:
In North American clinical trials, the Children's Oncology Group (COG) has recommended that surgery be performed initially if a complete resection can be accomplished (refer to the Postsurgical Staging for Childhood Liver Cancer section of this summary for more information). COG is investigating the use of PRETEXT stage at diagnosis and after chemotherapy to determine the optimal surgical approach and its timing (COG-AHEP0731).
Orthotopic liver transplantation
Liver transplantation has recently been associated with significant success in the treatment of children with unresectable hepatic tumors.[11,12,13,14][Level of evidence: 3iiA] A review of the world experience has documented a posttransplant survival rate of 70% to 80% for children with hepatoblastomas.[10,15,16] Intravenous invasion, positive lymph nodes, and contiguous spread did not have a significant adverse effect on outcome. It has been suggested that adjuvant chemotherapy following transplant may decrease the risk of tumor recurrence.[17]
There are discrepant results on the outcomes for patients with lung metastases at diagnosis who undergo orthotopic liver transplantation following complete resolution of lung disease in response to pretransplant chemotherapy. Some studies have reported favorable outcomes for this group of patients,[10] while others have noted high rates of hepatoblastoma recurrence.[16,18] All of these studies are limited by small patient numbers; further study is needed to better define outcomes for this subset of patients.
The United Network for Organ Sharing (UNOS) Standard Transplant and Research Files registry reported all children younger than 18 years listed for a liver transplant in the United States from October 1987 through July 2004. Of these children, 135 had hepatoblastoma and 41 had hepatocellular carcinoma and both groups received liver transplant with 5-year survival rates of 69% for hepatoblastoma and 63% for hepatocellular carcinoma. The 10-year survival rates were similar to the 5-year rates.[19,20] In a separate three-institution study for children with hepatocellular carcinoma, the overall 5-year disease-free survival rate was approximately 60%.[21] Application of the Milan criteria for UNOS selection of recipients of deceased donor livers is controversial.[22] However, living donor liver transplants are more common with children and the outcome is similar.[18,23] In hepatocellular carcinoma, vascular invasion, distant metastases, lymph node involvement, tumor size, and male gender were significant risk factors for recurrence. Because of the poor prognosis in patients with hepatocellular carcinoma, liver transplant should be considered for disorders such as tyrosinemia and familial intrahepatic cholestasis early in the course, prior to the development of liver failure and malignancy.
It should be noted that the Milan criteria for liver transplantation is directed toward adults with cirrhosis and hepatocellular carcinoma. It should not be applied to children and adolescents with hepatocellular carcinoma, especially those without cirrhosis.
Special considerations for surgical resection
Tumor rupture at presentation, resulting in major hemorrhage that can be controlled by transcatheter arterial embolization or partial resection to stabilize the patient, does not preclude a favorable outcome when followed by chemotherapy and definitive surgery.[24]
Microscopic residual disease after resection
Second resection of positive margins and/or radiation therapy may not be necessary in patients with incompletely resected hepatoblastoma whose residual tumor is microscopic and who receive subsequent chemotherapy.[16,25] In a European study conducted between 1990 and 1994, 11 patients had tumor found at the surgical margins following hepatic resection and only two patients died, neither of whom had a local recurrence. None of the 11 patients underwent a second resection and only one patient received radiation therapy postoperatively. All of the patients were treated with four courses of cisplatin and doxorubicin prior to surgery and received two courses of postoperative chemotherapy. In another European study of high-risk hepatoblastoma, 11 patients had microscopic residual tumor remaining after initial surgery and received two to four postoperative cycles of chemotherapy with no additional surgery. Of these 11 patients, 9 survived.[16]
Surgical resection for metastatic disease
Surgical resection of distant disease has also contributed to the cure of children with hepatoblastoma. Resection of pulmonary metastases is recommended when the number of metastases is limited [26,27] and is often performed at the same time as resection of the primary tumor. When possible, resection of areas of locally invasive disease, such as in the diaphragm, and of isolated brain metastasis is recommended.[28]
In recent years, virtually all children with hepatoblastoma have been treated with chemotherapy, and in some centers, even children with resectable hepatoblastoma are treated with preoperative chemotherapy, which may reduce the incidence of surgical complications at the time of resection.[25,29,30]
Presurgical chemotherapy
In an international study, pre-resection neoadjuvant chemotherapy (doxorubicin and cisplatin) was given to all children with hepatoblastoma with or without metastases. The chemotherapy was well tolerated. Following chemotherapy, and excluding those who received liver transplant (less than 5% of patients), complete resection was obtained in 87% of children. This strategy resulted in an overall survival (OS) of 75% at 5 years after diagnosis for all children entered in the study.[29] Identical overall results were seen in a follow-up international study.[30] The International Society of Pediatric Oncology Epithelial Liver Tumor Group (SIOPEL) compared cisplatin alone with cisplatin and doxorubicin in patients with preoperative standard-risk hepatoblastoma. Standard-risk was defined as tumor confined to the liver and not involving more than three sectors. The rates of resection were similar for the cisplatin (95%) and cisplatin/doxorubicin (93%) groups, as were OS (95% and 93%), respectively.[31][Level of evidence:1iiA] Another SIOPEL study of high-risk hepatoblastoma patients treated with cisplatin alternating with carboplatin/doxorubicin in a dose intensive fashion. In 74 patients with PRETEXT stage 4 tumors, 22 of whom also had metastases, 31 became resectable and 26 underwent transplant. The 3-year OS of this group was 69% ± 11%. The 3-year OS of all patients with metastases was 62% ± 12%.[16]
Postsurgical chemotherapy
In contrast, an American Intergroup protocol for treatment of children with hepatoblastoma encouraged resection at the time of diagnosis for all tumors amenable to resection without undue risk. The protocol (COG-P9645) did not treat children with stage I tumors of purely fetal histology with preoperative or postoperative chemotherapy unless they developed progressive disease. Further study will be needed to determine whether presurgical chemotherapy is preferable to resection followed by chemotherapy for children with PRETEXT stage 2, 3, and 4 hepatoblastoma.
Chemotherapy and metastatic disease
In rare cases, chemotherapy has eradicated pulmonary metastases and eliminated multinodular tumor foci in the liver. Intensive platinum- and doxorubicin-based multidrug chemotherapy can induce complete regressions in approximately 50% of patients, with subsequent 3-year event-free survival of 56%.[16] Chemotherapy has been much more successful in the treatment of hepatoblastoma than in hepatocellular carcinoma.[4,5,29,30,32,33,34]
Limited Role for Radiation Therapy
The utility of radiation therapy is questioned because the liver cannot tolerate high doses of radiation.[33,35]
Radiation therapy, even in combination with chemotherapy, has not cured children with unresectable tumors. There may be a role for radiation therapy in the management of incompletely resected hepatoblastoma,[33,35] although a study of 154 patients with hepatoblastoma did not confirm this finding.[25] This study showed that second resection of positive margins and/or radiation therapy may not be necessary in patients with incompletely resected hepatoblastoma whose residual tumor is microscopic.[25]
For patients with stage IV disease in which extrahepatic disease is controlled, but the primary tumor remains unresectable following standard chemotherapy, radiation therapy has been used as an interim treatment measure prior to surgical re-exploration.
Other Treatment Approaches
Other treatment approaches such as transarterial chemoembolization, have been used for patients with inoperable stage III hepatoblastoma.[36,37]
Cryosurgery, intratumoral injection of alcohol, and radiofrequency ablation can successfully treat small (<5 cm) tumors in adults with cirrhotic livers.[38,39,40,41] Some local approaches such as cryosurgery, radiofrequency ablation, and transarterial chemoembolization that suppress hepatocellular carcinoma tumor progression are used as bridging therapy in adults to delay tumor growth while on a waiting list for cadaveric liver transplant.[42] Transarterial chemoembolization has been used in a few children to successfully shrink tumor size to permit resection.[37] (Refer to the PDQ summary on Adult Primary Liver Cancer Treatment for more information.)
Treatment Options for Stages I and II
In the Children's Oncology Group (COG) study COG-P9645, stage I pure fetal histology hepatoblastomas with two or fewer mitoses per 10 high power fields were not treated with chemotherapy. Completely excised tumor of purely fetal and favorable histology may be carefully followed without further therapy.[1] A small focus of undifferentiated small cell histology within an otherwise pure fetal histology tumor must be treated with aggressive chemotherapy.[2]
Combination chemotherapy has been demonstrated to have significant benefit in children with hepatoblastoma. Cisplatin-based chemotherapy has resulted in a survival rate of greater than 90% for children with postsurgical stage I and stage II disease.[3,4,5,7]
A randomized clinical trial demonstrated comparable efficacy with cisplatin/vincristine/fluorouracil and cisplatin/doxorubicin in the treatment of hepatoblastoma. Although outcome was nominally higher for children receiving cisplatin/doxorubicin, this difference was not statistically significant, and the combination of cisplatin/vincristine/fluorouracil was significantly less toxic than the doses of cisplatin/doxorubicin, to which it was compared.[6]
Treatment Options for Stage III
In approximately 75% of children and adolescents with initially unresectable hepatoblastoma, tumors can be rendered resectable with cisplatin-based preoperative chemotherapy, and 60% to 65% will survive disease-free.[8]
A North American randomized clinical trial demonstrated comparable efficacy with cisplatin/vincristine/fluorouracil and cisplatin/doxorubicin in the treatment of hepatoblastoma. Although outcome was nominally higher for children receiving cisplatin/doxorubicin, this difference was not statistically significant, and the combination of cisplatin/vincristine/fluorouracil was significantly less toxic than the doses of cisplatin/doxorubicin used.[6]
A combination of ifosfamide, cisplatin, and doxorubicin has also been successfully used in the treatment of advanced-stage disease.[9] A regimen of intensified platinum therapy with alternating cisplatin and carboplatin was associated with a decrease in event-free survival (EFS).[10]
Patients whose tumors remain unresectable should be considered for liver transplantation.[5,11,12,13,14,15] In the presence of features predicting unresectability, early coordination with a pediatric liver transplant service is desirable.[16]
Treatment Options for Stage IV
The outcome for metastatic hepatoblastoma at diagnosis is poor, but long-term survival and cure is possible.[3,6,7] Survival rates at 3 to 5 years range from 20% to 60%.[19,20,21]
The standard regimen is four courses of cisplatin/vincristine/fluorouracil [6] or doxorubicin/cisplatin combination chemotherapy [5,19] followed by attempted complete tumor resection. If the tumor is completely removed, two postoperative courses of the same chemotherapy should be given.
In a study employing a well-tolerated regimen of doxorubicin/cisplatin chemotherapy, about 50% of patients with metastases at presentation survived 5 years from diagnosis. Half of these survivors had developed progressive disease that was successfully treated with surgery and other interventions.[5] In another study, platinum- and doxorubicin-based multidrug chemotherapy induced complete regression in approximately 50% of patients, with subsequent 3-year EFS of 56%.[20]
Several studies have tested different chemotherapy regimens. A randomized clinical trial compared cisplatin/vincristine/fluorouracil with cisplatin/doxorubicin. Although outcome was nominally higher for children receiving cisplatin/doxorubicin, this difference was not statistically significant, and the combination of cisplatin/vincristine/fluorouracil was less toxic than the regimen of cisplatin/doxorubicin.[6] The cisplatin/doxorubicin used in the international studies appears to be less toxic than that in the North American study.[5] Addition of carboplatin to intensify the cisplatin/doxorubicin may have reduced its efficacy.[4] A regimen of intensified platinum therapy with alternating cisplatin and carboplatin was associated with a decrease in EFS.[10] A combination of ifosfamide, cisplatin, and doxorubicin has also been successfully used in the treatment of advanced-stage disease.[9]
If possible, stage IV patients with resected primary tumor should have remaining pulmonary metastases surgically removed.[19] A review of patients treated on a U.S. Intergroup trial suggested that resection may be done at the time of resection of the primary tumor.[21][Level of evidence: 3iiA]
Patients whose extrahepatic tumors remain unresectable or who are not transplant candidates should be considered for alternative chemotherapy such as irinotecan,[22,23,24] high-dose cisplatin/etoposide, continuous-infusion doxorubicin, radiation therapy,[3,25] or chemoembolization by hepatic arterial infusion.[18,26]
Treatment Options Under Clinical Evaluation
The following are examples of national and/or institutional clinical trials that are currently being conducted. Information about ongoing clinical trials is available from the NCI Web site.
The following treatment option is under investigation in a COG clinical trial. Information about ongoing clinical trials is available from the NCI Web site.
Stage IV
In a randomized trial, seven of eight patients with stage I hepatocellular carcinoma survived disease free after adjuvant cisplatin-based chemotherapy.[1] In a survey of childhood liver tumors treated prior to the consistent use of chemotherapy, only 12 of 33 patients with hepatocellular carcinoma who had complete excision of the tumor survived.[2] This suggests that adjuvant chemotherapy may benefit children with completely resected hepatocellular carcinoma. Treatment with cisplatin and doxorubicin may be recommended as adjuvant therapy since these are active agents in the treatment of hepatocellular carcinoma.[3] Despite improvements in surgical techniques, chemotherapy delivery, and patient supportive care in the past 20 years, clinical trials of cancer chemotherapy for hepatocellular carcinoma have not shown improved outcome.[3]
Studies in adults in China suggest that repeated hepatic transarterial chemoembolization before surgery may improve the outcome of subsequent hepatectomy.[4] (Refer to the PDQ summary on Adult Primary Liver Cancer Treatment for more information.)
The use of neoadjuvant chemotherapy followed by complete gross surgical resection of the primary tumor is necessary for cure.
Liver transplantation has been a successful therapy for children with unresectable hepatocellular carcinoma; survival is about 60% with most deaths resulting from tumor recurrence.[5,6,7,8]
No specific treatment has proven effective for unresectable hepatocellular carcinoma in the pediatric age group. A prospective study of 41 patients who were to receive preoperative cisplatin/doxorubicin chemotherapy resulted in some degree of decrease in tumor size with a decrease in alpha-fetoprotein (AFP) levels in about 50% of patients. The responders had a superior tumor resectability and survival, although the overall survival (OS) was 28% and only those undergoing complete resection survived.[3] Cryosurgery, intratumoral injection of alcohol, and radiofrequency ablation can successfully treat small (<5 cm) tumors in adults with cirrhotic livers.[4,9,10] Some local approaches such as cryosurgery, radiofrequency ablation, and transarterial chemoembolization that suppress hepatocellular carcinoma tumor progression are used as bridging therapy in adults to delay tumor growth while on a waiting list for cadaveric liver transplant.[11] Transarterial chemoembolization has been used in a few children to successfully shrink tumor size to permit resection.[4,12] (Refer to the PDQ summary on Adult Primary Liver Cancer Treatment for more information.)
Treatment Options for Presurgically Staged (PRETEXT) Stage 4
Liver transplantation has been successful therapy for children with unresectable hepatocellular carcinoma; survival is about 60% with most deaths resulting from tumor recurrence.[5,6,7]
No specific treatment has proven effective for unresectable hepatocellular carcinoma in the pediatric age group. A prospective study of 41 patients who were to receive preoperative cisplatin/doxorubicin chemotherapy resulted in some degree of decrease in tumor size with a decrease in AFP level in about 50% of patients. The responders had a superior tumor resectability and survival, although the OS was 28% and only those undergoing complete resection survived.[3] The 5-year OS for PRETEXT stage 4 patients, including those with metastasis and/or extrahepatic disease, was 1 in 13.[3] Cryosurgery, intratumoral injection of alcohol, and radiofrequency ablation can successfully treat small (<5 cm) tumors in adults with cirrhotic livers.[4,9,10] Some local approaches such as cryosurgery, radiofrequency ablation, and transarterial chemoembolization that suppress hepatocellular carcinoma tumor progression are used as bridging therapy in adults to delay tumor growth while on a waiting list for cadaveric liver transplant.[6,11,13] Transarterial chemoembolization has been used in a few children to successfully shrink tumor size to permit resection.[4,12] (Refer to the PDQ summary on Adult Primary Liver Cancer Treatment for more information.)
Treatment Options for Postsurgically Staged Stage IV
No particular treatment has proven effective for metastatic hepatocellular carcinoma in the pediatric age group. In two prospective trials, cisplatin plus either vincristine/fluorouracil or continuous infusion doxorubicin was ineffective in adequately treating 25 patients with metastatic hepatocellular carcinoma.[1,3] Occasional patients may benefit from treatment with cisplatin/doxorubicin therapy, especially if localized hepatic tumor shrinks adequately to allow resection of disease. (Refer to the PDQ summary on Adult Primary Liver Cancer Treatment for more information.)
Treatment Options
Undifferentiated embryonal sarcoma of the liver is so rare that only small series have been published regarding treatment. However, use of aggressive chemotherapy regimens seems to have improved the overall survival (OS). The generally accepted approach is to resect the primary tumor mass in the liver when possible. Neoadjuvant chemotherapy can be effective in decreasing an unresectable primary tumor mass, resulting in resectability.[1,2,3,4] The OS of these children appears to be substantially better than 50% when combining reports, although all series are small and most may be selected to report successful treatment.[1,2,3,4,5,6,7,8] The majority of patients were treated with chemotherapy regimens often used for pediatric rhabdomyosarcoma or Ewing sarcoma without cisplatin.
Liver transplantation has on occasion been used successfully to treat an otherwise unresectable primary tumor.[7,9] In the only prospective series from the Italian and German Soft Tissue Sarcoma Cooperative Groups, patients were treated with conservative surgery or biopsy followed by neoadjuvant chemotherapy consisting of varying combinations of vincristine, cyclophosphamide, dactinomycin, doxorubicin, and ifosfamide. Disease evaluation, usually after four cycles of chemotherapy, was followed by second-look surgery when appropriate to try to remove residual primary tumor followed by additional and/or adjuvant chemotherapy. Ten of 17 patients survived in their first complete remission, and one patient survived in his or her third complete remission.[5]
Choriocarcinoma of the liver is a very rare tumor that appears to originate in the placenta during gestation and presents with a liver mass in the first few months of life. Metastasis from placenta to maternal tissues occurs in many cases, necessitating beta-human chorionic gonadotropin (beta-hCG) testing of the mother. Infants are often anemic and can be unstable at presentation due to hemorrhage from the tumor. Clinical diagnosis may be made without biopsy based on extremely high serum beta-hCG levels and normal alpha-fetoprotein levels for age.[1] Initial surgical removal of the tumor mass may be difficult because of its friability and hemorrhagic tendency. Often surgical removal of the residual primary tumor is performed after neoadjuvant chemotherapy.[1]
Maternal gestational trophoblastic tumors are exquisitely sensitive to methotrexate, and many women, including those with distant metastases, are cured with single-agent chemotherapy. Maternal and infantile choriocarcinoma both come from the same placental malignancy. The combination of cisplatin, etoposide, and bleomycin, as used in other pediatric germ cell tumors, has been effective in some patients and is followed by resection of residual mass. Use of neoadjuvant methotrexate in infantile choriocarcinoma, although often resulting in a response, has not been uniformly successful.[1]
Recurrent Hepatoblastoma
The prognosis for a patient with recurrent or progressive hepatoblastoma depends on many factors, including the site of recurrence, prior treatment, and individual patient considerations. For example, in patients with stage I hepatoblastoma at initial diagnosis, aggressive surgical treatment of isolated pulmonary metastases that develop in the course of the disease may make extended disease-free survival possible.[1,2] Analysis of survival after recurrence demonstrated that some patients treated with cisplatin/vincristine/fluorouracil could be salvaged with doxorubicin-containing regimens, but patients treated with doxorubicin/cisplatin could not be salvaged with vincristine/fluorouracil.[3] Addition of doxorubicin to vincristine/fluorouracil/cisplatin is under clinical evaluation in the Children's Oncology Group (COG) study COG-AHEP0731. Combined vincristine/irinotecan has been used with some success.[4][Level of evidence: 3iiiA] If possible, isolated metastases should be resected completely in patients whose primary tumor is controlled.[5] Liver transplant should be considered for patients with isolated recurrence in the liver.[6,7,8] Treatment in a clinical trial should be considered if all of the recurrent disease cannot be surgically removed. Phase I and phase II clinical trials may be appropriate and should be considered.
Recurrent Hepatocellular Carcinoma
The prognosis for a patient with recurrent or progressive hepatocellular carcinoma is poor.[9] Chemoembolization or liver transplant should be considered for those with isolated recurrence in the liver.[6,7,8] Phase I and phase II clinical trials may be appropriate and should be considered. (Refer to the PDQ summary on Adult Primary Liver Cancer Treatment for more information.)
Sorafenib has resulted in improved progression-free survival in adults with advanced hepatocellular carcinoma. For adult patients who received sorafenib, the median survival and time to radiologic progression were about 3 months longer than those who received a placebo.[10] A phase I trial has been completed in children, and a single-agent, phase II COG trial is underway.
Limited data from a European pilot study suggest that sorafenib may have been beneficial to 12 newly diagnosed patients with advanced hepatocellular carcinoma when given in combination with standard chemotherapy with cisplatin and doxorubicin.[11]
Treatment options under clinical evaluation for recurrent hepatocellular carcinoma
The following treatment option is under investigation in a COG clinical trial. Information about ongoing clinical trials is available from the NCI Web site.
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood liver cancer. 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.
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.
This summary was comprehensively reviewed and extensively revised.
This summary is written and maintained by the PDQ Pediatric 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 childhood liver cancer. 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 Pediatric 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 Childhood Liver Cancer 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.
Levels of Evidence
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 Pediatric Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
Permission to Use This Summary
PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as "NCI's PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary]."
The preferred citation for this PDQ summary is:
National Cancer Institute: PDQ® Childhood Liver Cancer Treatment. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/treatment/childliver/HealthProfessional. Accessed <MM/DD/YYYY>.
Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.
Based on the strength of the available evidence, treatment options may be described as either "standard" or "under clinical evaluation." These classifications should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Coping with Cancer: Financial, Insurance, and Legal Information page.
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More information about contacting us or receiving help with the Cancer.gov Web site can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the Web site's Contact Form.
Call 1-800-4-CANCER
For more information, U.S. residents may call the National Cancer Institute's (NCI's) Cancer Information Service toll-free at 1-800-4-CANCER (1-800-422-6237) Monday through Friday from 8:00 a.m. to 8:00 p.m., Eastern Time. A trained Cancer Information Specialist is available to answer your questions.
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The NCI's LiveHelp® online chat service provides Internet users with the ability to chat online with an Information Specialist. The service is available from 8:00 a.m. to 11:00 p.m. Eastern time, Monday through Friday. Information Specialists can help Internet users find information on NCI Web sites and answer questions about cancer.
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The NCI Web site provides online access to information on cancer, clinical trials, and other Web sites and organizations that offer support and resources for cancer patients and their families. For a quick search, use the search box in the upper right corner of each Web page. The results for a wide range of search terms will include a list of "Best Bets," editorially chosen Web pages that are most closely related to the search term entered.
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The NCI has booklets and other materials for patients, health professionals, and the public. These publications discuss types of cancer, methods of cancer treatment, coping with cancer, and clinical trials. Some publications provide information on tests for cancer, cancer causes and prevention, cancer statistics, and NCI research activities. NCI materials on these and other topics may be ordered online or printed directly from the NCI Publications Locator. These materials can also be ordered by telephone from the Cancer Information Service toll-free at 1-800-4-CANCER (1-800-422-6237).
Last Revised: 2012-12-03
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The Lucca Planter comes with an attached basin that can be filled for the plant to feed from once the root system is established. To start the plant, use convention top watering techniques and then switch to bottom watering by filling the basin as needed for the roots to wick the water up. The fill spot is more subtle than traditional self-watering planters, giving the flower pot a more acceptable appearance.
- Self watering
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- 100% UV stable and weather resistant
- Safe to leave out all winter long and will hold up for many years in the strongest sun
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Pictures relating to Inverleigh, VIC
Not the 'Inverleigh' you were after? Try: Inverleigh (the homestead) near Karumba in Queensland; Inverleigh (the locality) near Warwick in Queensland; or Inverleigh (the regional area) in Victoria.
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The love of acoustic fingerstyle guitar brought Don Ablett and Brent Cooper together some years ago. With common influences such as Bruce Cockburn, John Fahey, and Stefan Grossman, they have developed a style that has thrilled fans young and old around Southern Ontario. Both have a strong history of performance, Brent through his former years touring with the rock band, Mankind, and Don through many years of coffee houses and festivals.
Two of the most outstanding features noted by audiences are Brent and Don's vocal harmonies and the complex and spectacular fingerstyle interplay between the two guitars. They provide audiences of all ages with memorable instrumentals and songs with thought provoking lyrics. Some recent quotes clearly attest to their success:
"Your superb fingerstyle guitar and vocal harmonies are indeed a listening delight. The audience clearly enjoyed every piece you played and sang".
Becky Ryder, Museums of Mississauga
"Don and Brent have a wonderful sound and the songs stay with you. I find myself singing them around the house and in the car.
Red Rover is destined to become a Canadian classic. The instrumental pieces are moving and evocative".
Jeannine Farrar
Don and Brent are not satisfied to keep their music local. They love playing for audiences large and small. With encouragement from virtually every quarter, their plans include more radio play, magazine coverage and travel around the province.


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Heat exhaustion: A warning that the body is getting too hot. The person may be thirsty, giddy, weak, uncoordinated, nauseous, and sweating profusely. The body temperature is usually normal and the pulse is normal or raised. The skin is cold and clammy. Although heat exhaustion often is caused by the body's loss of water and salt, salt supplements should only be taken with advice from a doctor.
Heat exhaustion is the body's response to an excessive loss of water and salt contained in sweat. Those most prone to heat exhaustion are elderly people, people with high blood preset and people working or exercising in a hot environment.The warning signs of heat exhaustion include:
The skin may be cool and moist. The victim's pulse rate will be fast and weak, and breathing will be fast and shallow. If heat exhaustion is untreated, it may progress to heat stroke. Seek medical attention immediately if:
Otherwise, help the victim to cool off, and seek medical attention if symptoms worsen or last longer than 1 hour. Cooling measures that may be effective include:


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(formerly called toxemia of pregnancy) is a pregnancy-related condition that
causes high blood pressure and affects the mother's kidneys, liver, brain, and
placenta. Its cause is unknown.
Although preeclampsia
usually develops after the 20th week of pregnancy, it can very rarely begin
earlier. Preeclampsia can develop gradually or suddenly, and it may remain mild or
become severe. If untreated, preeclampsia may damage the mother's liver or
kidneys, deprive the fetus of oxygen, and cause
eclampsia (seizures).
Signs of
preeclampsia include:
A woman with any signs of preeclampsia is closely monitored
by her doctor or midwife. Moderate preeclampsia is treated in the hospital with
bed rest, magnesium sulfate, and sometimes medicine for high blood pressure.
Delivery is the only true "cure" for preeclampsia.
When a woman
has severe preeclampsia or is near term with mild to moderate preeclampsia,
delivery is the best treatment. Labor may be started with medicine, unless a
cesarean section is deemed necessary.
Within the first few days
following delivery, the mother's blood pressure usually returns to normal; with
severe preeclampsia, it may take several weeks for blood pressure to return to
Last Revised:
November 5, 2012
Healthwise Staff
Medical Review:
Sarah Marshall, MD - Family Medicine & William Gilbert, MD - Maternal and Fetal Medicine
This information does not replace the advice of a doctor. Healthwise, Incorporated disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use. How this information was developed to help you make better health decisions.
To learn more visit Healthwise.org
© 1995-2012 Healthwise, Incorporated. Healthwise, Healthwise for every health decision, and the Healthwise logo are trademarks of Healthwise, Incorporated.


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Laptop display pixel counts to quadruple in 2012
2880 x 1800 panel on your MacBook, anyone?
Buy one of Apple's next MacBook Pro notebooks and you'll get yourself a - glossy, no doubt - 2880 x 1800 resolution display.
So say the inevitably anonymous Asia moles, who add that next year's fresh crop of Ultrabooks - likely to be demo'd at the Consumer Electronics Show (CES) in January but not go on sale until Q2 when Intel's Ivy Bridge platform arrives - will sport 1920 x 1080 displays, DigiTimes notes.
Current MacBook screen resolutions max out at 1680 x 1050 on the 15in model - though 1440 x 900 is the standard size - and 1920 x 1200 on the 17-incher. Both have non-glossy alternatives, BTW.
Given the claimed resolution jump is double - in each dimension - that of the current 15-incher, it seems likely the sources are referring to that model rather than the larger machine.
Incidentally, there's been talk of late of a 15in MacBook Air, and it's possible that Apple will use the 2880 x 1800 to stamp this model as a premium offering.
Ultrabooks currently offer 1280 x 800 or 1366 x 768 screens. ®
Sponsored: Beyond the Data Frontier


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via Budget Bytes
If you've been reading here for awhile, you already know I'm going to suggest skipping the chicken entirely and either substitute extra black beans or add another kind of bean,too. This shaves even more money from the recipe but also, many readers have mentioned that they wish they could buy more ethical or organic meat but just can't afford it. Me,too. My way around this is just to not buy it at all and eat a mostly vegetarian diet (which has turned out to save a lot of money. Bonus!)
If you have time, I always recommend using dry beans. A bag of dried beans goes further than a can.
Budget Bytes says this recipe works out to be $1.33 per serving. It makes 9 servings, so if you're not using that all for one meal, freeze the rest for another quick freezer meal.
Here's the recipe:
- 1½ lbs. chicken breasts $2.90
- 1 (16 oz.) jar salsa $1.99
- 1 (15 oz.) can black beans, drained $1.19
- ½ lb. (8 oz.) frozen corn $0.57
- 1 Tbsp chili powder $0.15
- ½ Tbsp cumin $0.07
- ½ Tbsp minced garlic $0.10
- ½ tsp dried oregano $0.03
- ¼ tsp cayenne pepper $0.02
- ¼ tsp salt $0.02
- to taste cracked pepper $0.02
- 2 cups dry rice $0.66
- 8 oz. shredded cheddar $2.49
- ½ bunch cilantro (optional) $0.45
- Add everything except the rice, cheese, and cilantro to the slow cooker along with ¼ cup of water (for good measure). Give everything a good stir and make sure the chicken is covered in the mixture.
- Secure the lid on your slow cooker and cook on low for 8 hrs.
- Near the end of the cooking time, cook the two cups of rice according to the package directions (Bring the rice and 3 cups of water to a boil in a medium pot with a lid in place, as soon as it reaches a boil, reduced the heat to low and let simmer for 20 minutes. Fluff with a fork before serving).
- After 8 hours of cooking, carefully remove the lid of the slow cooker. Stir with a fork to shred the chicken (it should be super tender and will shred easily). Build the taco bowls by placing rice on the bottom, then the taco chicken mix, shredded cheese and fresh cilantro.


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With new video conferencing solutions available for small and medium businesses, it is possible to have a higher standard of video conferencing without the quality issues presented by consumer products. Are these higher quality business grade solutions worth the higher cost, or do savings from consumer grade versions justify their lower quality?
"I am the Inspector Morse of IT journalism. I haven't a clue. D'oh" - Mike Magee


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iMac Pro puts the power of a workstation behind a stunning Retina 5K display, in a sleek enclosure just 5 mm wide at its edge. With your whole system powered by a single cable, your workspace stays free of clutter. It's a beautifully efficient design that lets you focus all your attention on what you're creating — not what you're creating with.
All-new speakers. Make some noise.
The enhanced stereo speakers in iMac Pro deliver broad frequency response, rich bass, and more volume. So you'll be able to hear that crashing cymbal, multilayered effect, or sample-based sound, all with remarkable fidelity. And with four beamforming mics, your voice is heard loud and clear over any background noise.
2.5GHz 14-core Intel Xeon W processor, Turbo Boost up to 4.3GHz
128GB 2666MHz DDR4 ECC memory
Radeon Pro Vega 64 with 16GB of HBM2 memory
*Display *
Retina display
27-inch (diagonal) Retina 5K display
5120‑by‑2880 resolution with support for one billion colors
500 nits brightness
Wide color (P3)
*Size and Weight *
25.6 inches
(65.0 cm)
20.3 inches
(51.6 cm)
Height: 20.3 inches (51.6 cm)
Width: 25.6 inches (65.0 cm)
Stand depth: 8 inches (20.3 cm)
Weight: 21.5 pounds (9.7 kg)3
Electrical and Operating Requirements
Line voltage: 100–240V AC
Frequency: 50Hz to 60Hz, single phase
Operating temperature: 50° to 95° F (10° to 35° C)
Relative humidity: 5% to 95% noncondensing
Operating altitude: tested up to 16,400 feet (5000 meters)
Limited Warranty and Service
Your iMac Pro comes with 90 days of complimentary technical support and a one-year limited warranty. Purchase AppleCare+ for Mac to extend your coverage to three years from your computer's purchase date and add up to two incidents of accidental damage coverage, each subject to a service fee of $99 for screen damage or external enclosure damage, or $299 for other repairable damage, plus applicable tax.
In the Box
iMac Pro
Space Gray Magic Keyboard with Numeric Keypad
Space Gray Magic Mouse 2
Lightning to USB Cable
Power cord
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Motion Booth Captures the Moment & the Commotion
The Motion Booth is a dynamic digital experience that kicks the traditional photo booth to the curb. We combine outgoing personalities with the wonders of modern technology, to create a revolutionary experience! Frame-by-frame, the Motion Booth will capture your every move and produce a video on the spot. Those memories can then be shared instantly by sending an email or printing a photo to create your own commotion.


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Become a leader in your community. Join the Ready, Set, Go! team today. Learn about the the RSG! Program benefits
The RSG! Program tenets help residents be Ready with preparedness understanding, be Set with situational awareness when fire threatens, and to Go, acting early when a fire starts.
RSG! Program Accepting Submissions for Contractors
RSG! Program Seeking Individuals with WUI Expertise to Assist with DHS FEMA FP&S Grant
The Ready, Set, Go! (RSG) Program, managed by the International Association of Fire Chiefs (IAFC), is accepting submissions for contractor positions to assist with facilitating targeted wildland fire community risk reduction.
The Ready, Set, Go! (RSG) Program, managed by the International Association of Fire Chiefs (IAFC), seeks to develop and improve the dialogue between fire departments and the residents they serve. Launched nationally in March 2011 at the Wildland-Urban Interface (WUI 2011) Conference, the program helps fire departments to teach individuals who live in high risk wildfire areas – and the wildland-urban interface – how to best prepare themselves and their properties against fire threats.
Join As A Ready, Set, Go! Department
Find A Ready, Set, Go! Program By State
Explore Ready, Set, Go! Resources
The Ready, Set, Go! Program for Residents
Contact the Ready, Set, Go! Program Team
Ready, Set, Go! Discussion Forums


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Posted: Sep 11, 2009
Sept. 11, 2009
IRVINE, Calif. - UCSB senior Julian deRubira was named Big West Conference Male Athlete of the Week for his performance in the Gauchos season-opening Lagoon Run on Saturday.
A native of Aliso Viejo, Calif., deRubira won the 8K race in a time of 24:33, crossing the finish line six seconds ahead of teammate Scott Smith for the individual title in the dual meet against Cal Poly.
UCSB returns to action on Saturday, Sept. 19 when it travels to the UC Riverside Invitational.


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CLOSED: Notice to Contractors - SP 42-610-34 and SP 42-070-003. Bidding on Mar 19, 2013
Sealed Proposals will be received until 2:00 p.m. on March 19, 2013 by E.J. Moberg, Lyon
County Auditor/Treasurer, of Lyon County at the County Government Center at 607 West Main,
Marshall, MN 56258, on behalf of the Board of Commissioners for the construction of the
projects listed below. Proposals will be opened and read publicly in Commissioner Room # 7 of
the Lyon County Government Center in Marshall, Minnesota, immediately after the hour set for
receiving bids.
Minimum wage rates to be paid by the Contractors have been predetermined and are subject to
the Work Hours Act of 1962, P.L. 87-581 and implementing regulations.
The Minnesota Department of Transportation hereby notifies all bidders: in accordance with
Title VI of the Civil Rights Act of 1964 (Act), as amended and Title 49, Code of Federal
Regulations, Subtitle A Part 21, Non-discrimination in Federally-assisted programs of the
Department of Transportation, it will affirmatively assure that in any contract entered into
pursuant to this advertisement, disadvantaged business enterprises will be afforded maximum
opportunity to participate and/or to submit bids in response to this invitation, and will not be
discriminated against on the grounds of race, color, disability, age, religion, sex or national
origin in consideration for an award;
in accordance with Title VI of the Civil Rights Act of 1964 as amended, and Title 23, Code of
Federal Regulations, Part 230 Subpart A-Equal Employment Opportunity on Federal and
Federal-Aid Construction Contracts (including supportive services), it will affirmatively assure
increased participation of minority groups and disadvantaged persons and women in all phases of
the highway construction industry, and that on any project constructed pursuant to this
advertisement equal employment opportunity will be provided to all persons without regard to
their race, color, disability, age, religion, sex or national origin;
in accordance with the Minnesota Human Rights Act, Minnesota Statute 363A.08 Unfair
Discriminatory Practices, it will affirmatively assure that on any project constructed pursuant to
this advertisement equal employment opportunity will be offered to all persons without regard to
race, color, creed, religion, national origin, sex, marital status, status with regard to public
assistance, membership or activity in a local commission , disability, sexual orientation, or age;
in accordance with the Minnesota Human Rights Act, Minnesota Statute 363A.36 Certificates of
Compliance for Public Contracts, and 363A.37 Rules for Certificates of Compliance, it will
assure that appropriate parties to any contract entered into pursuant to this advertisement possess
valid Certificates of Compliance.
If you are not a current holder of a compliance certificate issued by the Minnesota Department of
Human Rights and intend to bid on any job in this advertisement you must contact the
Department of Human Rights immediately for assistance in obtaining a certificate.
The following notice from the Minnesota Department of Human Rights applies to all contractors:
"It is hereby agreed between the parties that Minnesota Statute, section 363A.36 and Minnesota
Rules, parts 5000.3400 to 5000.3600 are incorporated into any contract between these parties
based on this specification or any modification of it. A copy of Minnesota Statute 363A.36 and
Minnesota Rules, parts 5000.3400 to 5000.3600 is available upon request from the contracting
"It is hereby agreed between the parties that this agency will require affirmative action
requirements be met by contractors in relation to Minnesota Statute 363A.36 and Minnesota
Rules 5000.3600. Failure by a contractor to implement an affirmative action plan or make a
good faith effort shall result in revocation of its certificate or revocation of the contract
(Minnesota Statute 363A.36, Subd. 2 and 3)."
A minimum goal of 2.4% Good Faith Effort to be subcontracted to Disadvantaged Business
SP 042-610-034 and SP 042-070-003
Concrete Surfacing, Aggregate Base and Aggregate Shouldering
Comprising Approximately
Open Graded Aggregate Base Mod. 28,660.0 Tons
Aggregate Shouldering Cl. 5 Mod. 10,930.0 Tons
Concrete Pavement 7.0" (P) 93,520.0 S.Y.
Type SP 12.5 Wear Course Mix 2,B (15% RAP) 1,061.0 Tons
Specifications may be examined at the office of the Public Works Director, 504 Fairgrounds
Road, Marshall, MN. Plans and Specifications may be downloaded from the Lyon County
website, www.lyonco.org, (see further details on website) or by calling the Lyon County
Highway Department at 507-532-8205 to request a paper copy for a charge of $85.00 (includes
shipping and tax). All Proposals must be on forms furnished by the Public Works Director.
Sealed Bids should be mailed to E.J. Moberg, Lyon County Auditor/Treasurer, 607 West
Main Street, Marshall, MN 56258 and must be clearly marked as a sealed bid for SP 042-
610-034 and SP 042-070-003. Each Proposal must be accompanied by a certified check or bid
bond, payable to the Treasurer of Lyon County, for at least 5% of the amount of the Bid. The
County reserves the right to reject any or all bids.


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HARRIONBURG, Va. – UMBC women's basketball ran into Ohio University on the wrong day,
as the Bobcats drained 13-of-21 shots from beyond the arc in the opening half and cruised to an 84-36 victory in day two of the James Madison Invitational on Monday afternoon at the Convocation Center.
The Bobcats connected on 19-of-35 shots from three-point range in the contest, including five apiece from junior guard Mariah Byard and sophomore guard Kiyanna Black. The duo combined for 35 points and were two of four Ohio players that finished with double-digit points in the contest.
UMBC sophomore guard Liz McNaughton (Fairfax, Va./Fairfax) led the Retrievers in scoring for the first time in her career, knocking down five of her eight shots and finishing with 11 points, while classmate Bridget O'Donnell (Belle Mead, N.J./Montgomery) and junior guard Janelle Saling (Lathrop, Mo./Lathrop/Highland CC) each chipped in 10 points. Saling shot 44 percent from beyond the arc in the tournament.
UMBC spotted Ohio (5-7) nine points out of the gate before sophomores McNaughton and O'Donnell awakened the Retrievers with the squad's first eight points. Saling, who hit four-of-eight from beyond the arc in yesterday's contest, continued to hit from the outside, as a trey from her and one from freshman forward Sara Tarbert (Delta, Pa./Kennard-Dale) cut UMBC's deficit to five, 19-14, with 10:03 to go in the first half. The Bobcats did not lose their stroke though, as they opened the game up with a12-0 run, triggered by eight of Black's game-high 18 points.
Ohio finished the half with 13 of its 16 field goals coming from long range to take a 51-22 advantage at the break. The Bobcats did not cool off much in the second half, hitting six more three-pointers in the period, while the Retrievers hit 25 percent of its shots in the stanza and made 13 of its 22 turnovers.
The Bobcats held a 48-25 advantage on the boards, including 19 offensive rebounds, and converted UMBC's 22 turnovers in 28 points.
The Retrievers close out non-conference play with a 1-11 overall mark and look for a fresh start in the New Year, as UMBC opens America East play against Binghamton on Jan. 4. Tip-off is set for 1 p.m. at the RAC Arena.
Game Notes
-UMBC drops its first-ever meeting against Ohio.
-Ohio's 19 three-point field goals marked a Convocation Center record for three-point field goals made in a women's game, breaking the previous record of 12 from Feb. 15, 2007. The 19 was also a season-high against the Retrievers and marked a school record for the Bobcats.
-Ohio's 51 first half points matched the most allowed in the opening half of a game this season for the Retrievers.
-UMBC's 36 points was a season-low and marked its lowest point total since Dec. 7 2012. The Retrievers 14 second half points also marked a season-low.
-Bridget O'Donnell's 10 points was her first double-digit scoring performance since the season-opener, while Liz McNaughton's 11 points matched a career-high.


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On behalf of the faculty and staff, I extend a warm welcome to Paradise Valley Community College (PVCC). We have been providing quality higher education experiences for the residents of north Phoenix and the greater northern Maricopa county community for over 30 years.
Our motto – The Power of Learning – reflects our focus as a learning-centered college. In recognition of the college's exemplary student success and degree/certificate completion rates, I am pleased to share that PVCC was recognized in 2013, 2015, and 2017 by the Aspen Institute as ranking in the "Top 150" of all community colleges nationwide.
Whether your goals are to transfer to a four-year university, prepare for a career, or enhance your skills, PVCC offers an associate degree or certificate program that is right for you – at the right time and in the right format.
We offer courses that meet the busy schedules of our students – in traditional face-to-face format, online, and hybrid (combined online and face-to-face). At PVCC, students have the opportunity to Start Almost Anytime, as we offer multiple starting dates each semester.
PVCC offers courses at two locations – in north Phoenix (32nd Street and Union Hills) and at our Black Mountain Campus (60th Street and Carefree Highway), serving the residents in the far north valley
I invite you to discover The Power of Learning at PVCC. I would also like to invite you to visit my President's blog What's on my Mind. We wish you success in the attainment of your goals and welcome you to Paradise Valley Community College!
Paul A. Dale