Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous urography with total body opacification, and tomography as required, often give the most information toward evaluating abdominal masses in children. Ultrasonography is a noninvasive procedure which defines normal structures and differentiates cystic and solid tumors. The combination of these studies gives sufficient information about renal tumors to plan for possible surgery. Arteriography is not necessary for the diagnosis of Wilms' tumor, nor its surgical or medical management. Pseudotumor of the kidney is due to focal cortical hyperplasia. It can be diagnosed by nephrotomography, renal arteriography or renal scanning. The latter method is most accurate and has the lowest morbidity. Aortography is advisable in the evaluation of a patient with pheochromocytoma in an attempt to locate multiple tumors. Determining the extent of abdominal neuroblastoma by angiography and lymphangiography does not appear to influence the mode of therapy, not the survival rate; therefore, invasive diagnostic procedures do not appear to be indicated in neuroblastoma. Angiography is necessary in the evaluation of liver cancer. If one lobe is determined to be free of disease, lobectomy is a possible cure. Splenic cysts and choledochal cysts can be diagnosed by noninvasive methods such as ultrasonography or radioisotope scanning. Arteriography and percutaneous opacification are not necessary to make these diagnoses.
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PMID:The evaluation of abdominal masses in children with emphasis on noninvasive methods. A roentgenographic approach. 16 41

Adriamycin is a new anticancer antibiotic with a wide spectrum of activity against solid tumours. The results obtained with this agent in 159 patients with histologically confirmed advanced metastastic malignancies are reported. Encouraging results were obtained in patients with sarcomas of bone and soft tissue (12/22). Response was also seen in mesothelioma (3/9) and lung cancer (5/15). A variety of other neoplasms was also treated and results obtained in neuroblastoma, testicular tumours, stomach carcinoma, breast cancer and nephroblastoma are reported. Treatment is discussed, with reference to response rates and toxicity. Results in 72 patients with advanced breast cancer, who received adriamycin in combination with other chemotherapeutic agents, are presented. Seventeen patients with primary liver cancer were also treated with adriamycin. To date, this is the only chemotherapeutic agent that appears to significantly improve survival times in patients with this resistant form of cancer. The prophylactic use of adriamycin against osteogenic sarcoma is also discussed.
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PMID:Adriamycin in the treatment of cancer. 125 Dec 78

A thorough understanding of the incidence, clinical presentation, treatment, prognosis, and psychosocial issues surrounding children with solid tumors enables the nurse to actively participate on the health care team. Although significant advances over the past two-and-a-half decades to improve the outcomes of children with cancer have occurred, there remains room for continued improvement, especially among children with advanced-stage nephroblastoma, neuroblastoma, HCC, and teratoma.
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PMID:Solid tumors in children. 752 19

We previously demonstrated that a locus (or loci) linked to the D11S436 marker, which is within the approximately 6-Mb cen-p12 region of human chromosome 11, suppresses the tumorigenic potential of some rat liver epithelial tumor microcell hybrid (MCH) cell lines. To more precisely map this putative liver tumor suppressor locus, we examined 25 loci from human chromosome 11 in suppressed MCH cell lines. Detailed analysis of these markers revealed a minimal area of overlap among the suppressed MCH cell lines corresponding to the chromosomal region bounded by (but not including) microsatellite markers D11S1319 and D11S1958E and containing microsatellite markers D11S436, D11S554, and D11S1344. Direct examination of the kang ai 1 (KA/1) prostatic adenocarcinoma metastasis suppressor gene (which is closely linked to D11S1344) produced evidence suggesting that this locus was not responsible for tumor suppression in this model system. In addition, our data strongly suggested that the putative liver tumor suppressor locus was distinct from other known 11p tumor suppressor loci, including the multiple exotoses 2 locus (at 11p11.2-p12), Wilms' tumor 1 locus (at 11p13), and Wilms' tumor 2 locus (at 11p15.5). The results of this study significantly narrowed the chromosomal location of the putative liver tumor suppressor locus to a region of human 11p11.2-p12 that is approximately 950 kb. This advance forms the basis for positional cloning of candidate genes from this region and, in addition, identified a number of chromosomal markers that will be useful for determining the involvement of this locus in the pathogenesis of human liver cancer.
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PMID:Localization of a putative liver tumor suppressor locus to a 950-kb region of human 11p11.2-p12 using rat liver tumor microcell hybrid cell lines. 929 Jul 4

Fibrolamellar hepatocellular carcinoma (FHCC) is a unique histologic variant of HCC that occurs in a younger subset of patients than classical HCC, and is associated with a better prognosis. Wilms tumor (WT) is a malignant embryonal neoplasm of the kidney and is one of the most common solid tumors of childhood, occurring at an estimated frequency of 1 in 8000 to 10,000 births. Although second malignant neoplasms (SMNs) following therapy for WTs have been reported in the liver, the coexistence of HCC and WT is extremely rare. We present the first report of a synchronous anaplastic WT and FHCC in a previously healthy 4-year-old girl. Despite the presence of focal immunohistochemical positivity for p53 in the WT, molecular analysis failed to reveal a germline or somatic p53 mutation, and was inconclusive in establishing a clonal relation between the two tumors.
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PMID:Synchronous wilms tumor and fibrolamellar hepatocellular carcinoma: report of a case. 1089 Sep 35

To determine the possible role of the epigenetic mechanisms in carcinogenesis of the hepatocellular carcinoma, we methylation-profiled the promoter CpG islands of twenty four genes both in HCC tumors and the neighboring non-cancerous tissues of twenty eight patients using the methylation-specific PCR (MSP) method in conjunction with the DNA sequencing. In comparison with the normal liver tissues from the healthy donors, it was found that while remained unmethylated the ABL, CAV, EPO, GATA3, LKB1, NEP, NFL, NIS and p27KIP1 genes, varying extents of the HCC specific hypermethylation were found associated with the ABO, AR, CSPG2, cyclin a1, DBCCR1, GALR2, IRF7, MGMT, MT1A, MYOD1, OCT6, p57KIP2, p73, WT1 genes, and demethylation with the MAGEA1 gene, respectively. Judged by whether the hypermethylated occurred in HCC more frequently than in their neighboring normal tissues, the hypermethylation status of the AR, DBCCR1, IRF7, OCT6, and p73 genes was considered as the event specific to the late stage, while that the rest that lacked such a distinguished contrast, as the event specific to the early stage of HCC carcinogenesis. Among all the clinical pathological parameters tested for the association with, the hypermethylation of the cyclin a1 gene was more prevalent in the non-cirrhosis group (P=0.021) while the hypermethylated p16INK4a gene was more common in the cirrhosis group (P=0.017). The concordant methylation behaviors of nineteen genes, including the four previously studied and their association with cirrhosis has been evaluated by the best subgroup selection method. The data presented in this report would enable us to shape our understanding of the mechanisms for the HCC specific loss of the epigenetic stability of the genome, as well as the strategy of developing the novel robust methylation based diagnostic and prognostic tools.
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PMID:Methylation profiling of twenty four genes and the concordant methylation behaviours of nineteen genes that may contribute to hepatocellular carcinogenesis. 1467 55

Glypican 3 is a membrane-bound heparan sulfate proteoglycan, which has recently been identified as a marker for liver cancer and germ cell malignancies. Individuals with loss-of-function mutations for the glypican 3 gene exhibit Simpson-Golabi-Behmel syndrome, a rare X-linked overgrowth disorder. Expression of glypican 3 mRNA and protein is normally silenced in most adult organs and may reappear during malignant transformation. In the past few years, immunohistochemical and molecular characteristics of glypican 3 in hepatocellular carcinoma have been elucidated. More recently, glypican 3 has been emerging as a new diagnostic marker for germ cell tumors and especially testicular and ovarian yolk sac tumors. However, in other tumors such as renal cell carcinomas, squamous cell carcinomas, and melanomas, studies disagree on the level of glypican 3 expression. Finally, there is the controversial notion of glypican 3 as a tumor suppressor gene. In this review article, we update current knowledge on glypican 3 expression in normal and neoplastic tissues, evaluate its utility as a tumor marker in clinical practice, and explore its role as a novel oncofetal protein with clinical implications. Our focus is on the diagnostic value of glypican 3 in germ cell tumors and other neoplasms in addition to hepatocellular carcinoma. In conclusion, glypican 3 has been proven to be a useful immunohistochemical marker in distinguishing yolk sac tumors, choriocarcinomas, and Wilms tumors from other malignancies histologically mimicking these primitive tumors. Clinically, we recommend that glypican 3 be used as part of a panel of markers in subtyping testicular germ cell tumors.
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PMID:Discovery and diagnostic value of a novel oncofetal protein: glypican 3. 2529 14

Glypican 3 (GPC3), a heparan sulfate proteoglycan, plays a role in cell growth and differentiation. Mutations of the GPC3 gene are responsible for Simpson-Golabi-Behmel syndrome, which is characterized by anomalies of postnatal overgrowth and an increased risk of developing pediatric malignancies, mostly Wilms tumor and liver cancer. In order to understand the possible role of GPC3 in renal development and Wilms tumor formation, we analyzed messenger RNA (mRNA) and protein levels of GPC3 in sporadic Wilms tumors and compared it to normal kidneys and other common renal epithelial tumors. By using Affymetrix HGU133 oligonucleotide gene expression microarray data from 191 renal tumors and 12 normal kidneys, we found significant overexpression of GPC3 in Wilms tumors (p < 0.01), with 3.5-fold higher expression in comparison to normal kidneys and 6.5-fold higher than any type of renal tumors. The GPC3 gene product in Wilms tumor was further evaluated by immunohistochemistry and quantified by an automated image analysis. Cytoplasmic and membranous GPC3 immunoreactivity was present in 77 % of primary Wilms tumors (23/30), 93 % of metastatic Wilms tumors (13/14), 50 % of metanephric adenomas (4/8), 33 % of congenital mesoblastic nephromas (2/6), 100 % of nephrogenic rests (11/11), and 100 % of fetal kidneys (5/5). GPC3 staining was predominantly identified in blastemal and epithelial components of Wilms tumors, similar to that of fetal non-neoplastic kidney. All adult renal tumors (n = 60) and normal kidneys (n = 15) were GPC3 negative. These findings suggest the utility of GPC3 in differential diagnosis and follow-up of Wilms tumors. Our data also indicate that GPC3 is an oncofetal protein with a potential therapeutic value.
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PMID:Glypican 3 overexpression in primary and metastatic Wilms tumors. 2536 70

Alpha-fetoprotein (AFP) is a glycoprotein and belongs to the gene family of serum albumins. The serum AFP levels were found to be elevated in the sera of liver cancer patients in 1964 and were subsequently developed and used as a liver cancer biomarker. However, elevated serum AFP levels have been observed in patients suffering from other cancer and noncancer diseases. Up to date, a systematic comparison of the serum AFP levels in different diseases has not been reported. In current study, 66,682 clinical lab test results of serum AFP levels from healthy individuals and patients with 47 different types of diseases during the past 5 years were retrieved and analyzed. Based on the mean (SD), median, and p (-Log10p) values, we found that patients suffering from liver, breast, esophagus, cervical, pancreatic, endometrial, gastric, lung, rectum cancers in addition to noncancer diseases cirrhosis, nephrotic syndrome, and gastritis had significantly (p<0.05) increased, whereas patients suffering from multiple myeloma, Wilms' tumor, and other 22 types of noncancer diseases had significantly decreased median serum AFP levels than that of healthy controls. Moreover, patients with liver cancer, cirrhosis, lymphoma, bone fracture, and Wilms' tumor had highest mean serum AFP levels and the biggest SD values. In summary, the increased serum AFP levels were most evident but not specific for liver cancer patients. The potential clinical use of the increased or decreased serum AFP levels for other types of cancer and noncancer diseases and the molecular mechanisms behind our current findings need to be investigated.
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PMID:Serum AFP levels in patients suffering from 47 different types of cancers and noncancer diseases. 3090 50

Serum glycated albumin (GA) level is used along with that of glucose and glycated hemoglobin (HbA1c) as indicators of glycemic control for diabetic patients. Although serum GA levels are affected by blood glucose level, they are also influenced by serum albumin metabolism and other pathological conditions. However, a systematic comparison of the serum GA levels in different types of human diseases has not been reported. In current study, 86,319 clinical lab test results of GA levels from healthy individuals and patients with 57 different types of diseases during the past 5 years in our hospital were retrieved and analyzed. Based on the mean (SD), median, and p (-Log10p) values, we found 29/57 diseases including type 2 diabetes, diabetic nephropathy, uremia, pancreatic cancer, liver cancer, hepatic encephalopathy, and azotemia had significantly (p<0.05, -Log10p>1.30) increased GA levels whereas 18/57 diseases including nephrotic syndrome, preeclampsia, Wilms' tumor, lupus erythematosus, and sepsis had significantly decreased GA levels compared to that of healthy controls. Moreover, the highest -Log10p values (>100) were observed in nephrotic syndrome, type 2 diabetes, preeclampsia, coronary heart disease, uremia, acute cerebral infarction, leukemia, and cerebrovascular disease in a descending order. These data indicated that the serum GA levels could be increased or decreased significantly in a disease-specific manner. Revealing the molecular mechanisms underlying these observations might make the increased or decreased serum GA levels indicators for different types of diseases, especially as an indicator that distinguishes nephrotic syndrome from other types of kidney diseases.
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PMID:Glycated albumin level is significantly decreased in patients suffering nephrotic syndrome. 3090 59


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