Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty one patients (59 females, 22 males) with advanced solid tumors were treated with Adriamycin in doses of 40 mg/m2 body surgace daily, in two days cycles, with resting periods of 3 weeks. Overall response rate was 46% (37/81). In breast cancer response rate was 56% (13/23) and in ovarian cancer 48% (13/27). In various other tumors remission was observed in soft tissue sarcomas (3/8), thyroid cancer (1/7), osteogenic sarcoma (1/4), oesophageal cancer (2/4), lung cancer (2/4), bladder cancer (1/2) and hepatoma (1/2). In breast cancer patients, 2-7 month remission duration was observed (M equal to 4.5 month) and in ovarian cancer 1.5-5 month (M equal to 3.2 month). Adriamycin was also applied intrapleurally in 31 patients with malignant pleural effusions with a low response rate (26%). This modified schedule of Adriamycin administration showed a high antitumor activity in breast and ovarian cancer and in soft tissue sarcomas. Squamous cell carcinoma of the esophagus was also sensitive to Adriamycin therapy. The very low rate of myelosuppression and oral ulceration showed the decreased toxicity of this Adriamycin administration schedule.
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PMID:Modified administration schedule of adriamycin in solid tumors. 14 May 42

Sialic acid content in breast or tumor tissue and serum of mouse strains that are either susceptible or resistant to breast cancer was measured at various age periods. Sialic acid content was also studied in normal lung tissue and in lung adenoma and hepatoma. Sialic acid levels during nonmalignant growth of a tissue were measured in breast tissue during pregnancy and lactation, and in regenerating liver, as well as in newborn and postnatal liver. The sialic acid content, when expressed per mg of protein, increased in mammary tumor, lung adenoma, and hepatoma. It also increased in nonmalignant growth of breast tissue during pregnancy and lactation and of regenerating liver and postnatal liver. Increase in sialic acid per mg DNA was observed only in lung tumors, regenerating liver, and postnatal liver. It appears that the changes in sialic acid level are independent of the normal or malignant growth of a tissue and that these changes might be the function of the parameter used to express the sialic acid values, i.e., either the DNA content or protein content of a given tissue.
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PMID:Independence of sialic acid levels in normal and malignant growth. 16 79

In order to estimate end effects of chronic prolonged gammairradiation of dogs, an exposure of 80 animals to irradiation was terminated and they were followed up closely. Out of 80 animals 30 dogs (1st series) were irradiated for 3 years and 50 dogs (II series) for 6 years. The dogs were exposed to irradiation at doses of 21 to 190 rad per year. Out of the total number of animals 22 dogs died. Post-mortem examinations showed neoformations in 13 animals (7 malignant and 12 benign neoformations). The highest number of tumors developed in dogs of the II series (10 out of 11) one-two years after irradiation (6 malignant tumors--malignant pheochromocytoma of adrenals; malignant adenoma of the hypophysis: polymorphocellular sarcoma of the liver; leucomyosarcoma of the uterus; bladder cancer; breast cancer; and 10 benign tumors--pancreatic adenoma; liver angioma; 2 papillary adenomas of the prostate; 3 renal adenomas; lipoma; polyps of the gall-bladder). Animals of the 1st series displayed 3 neoformations (1 malignant tumor--bladder tumor and 2 benign tumorsliver hepatoma and spleen angioma) 4--5 years after irradiation.
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PMID:[Formation of neoplasms in dogs after chronic gamma irradiation at a low-intensity dose]. 64 24

One of the major problems being researched and studied by the World Health Organization is the incidence of harmful side effects in users of steroid contraceptives. A literature search indicates that Anglo-Saxon countries report alarming hyperplastic changes, particularly in the liver, blood clots, hyperlipidemia leading to high blood pressure, porphyria, atypical leiomyomas and cervical hyperplasia. Currently attention is being focused on the relationship between steroid contraceptives and breast cancer. Fazala and Paffenbarger in their study of 1770 women found such benign changes as fibroadenoma, mastopathia fibrosa cystica and papilloma intraductale. In women who had used oral contraceptives for 2-4 yrs, malignancies were 1.9% to 2.5% more frequent than in non-users; in 6 yrs of use, 11 times greater than in non-users. Estrogens, particularly mestranol has been recognized as being harmful to the liver. Length of usage is a definite factor. Beginning with 1960, relatively frequent occurrences of hepotoma in young women on the pill were noted. Caught at an early stage, peliosis hepatis can be reversed if the patient discontinues the use of contraceptives. In some cases, even after a long interval of 6 months to 10 yrs, the disease continued to develop. Liver cell adenoma in the U. S. occurs 1/500,00 to 1/1,000,000. After 5 to 7 yrs of using oral contraceptives, the chance of developing liver cell adenoma is 5 times greater; after 10 yrs of use, 35 times greater. Hepatomas rupture in 43.4% of cases when the patient had been on a contraceptive, while in only 22.2% in cases of non-users. The literature which the author investigated did not establish a clear proof that the hyperplastic changes discussed were due exclusively to usage of oral contraceptives.
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PMID:[Hyperplastic changes and oral contraceptives in Anglo-Saxon countries]. 69 6

This analysis indicated that patients with cancer-related pain account for 71.0% in author's material. After the TCM treatment, the effective rate were 91.6% in hepatocarcinoma-related pain; 86.1% in colon-rectal cancer-related pain; 68.2% in malignant lymphoma-related pain; 100% in irradiation-related pain of esophageal cancer, lung cancer, post-operative breast cancer. Results of "four-step analgesic ladder" showed that 52.1% of pain could be relieved by Step I (TCM therapy); if Step II (indomethacin) or III (phenylbutazone) was added, the rate of pain relief reached as high as 96.5%; and only 3.5% need to be treated by Step IV (Opioids). With less side-effects and addiction of opioids and other narcotics, the "four-step analgesic ladder" therapy seems to be more suitable for cancer pain relief in China.
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PMID:[Comprehensive "4-step analgesic ladder" therapy in treating cancer-related pain-analysis of 486 cases]. 130 38

This report concerns the expression of the gap-junction proteins Connexin (Cx)26, 32 and 43 in different malignant and non-malignant human tissues. Affinity-purified polyclonal antibodies against Cx26, 32 and 43 were used for immunohistochemical as well as immunoblot analysis. Cx32, the major gap-junction protein in rat and mouse liver, was detected in human liver and kidney. By contrast, Cx43 was expressed in epithelial and mesenchymal tissues and Cx26 was detected in different epithelia. Whereas all of the benign tumors studied, and some malignant ones, showed stable expression of gap-junction proteins, breast cancer, renal-cell cancer and sarcomas showed a significant decrease in gap-junction proteins as opposed to normal tissue. Cx43, not detected in human normal liver, was found in human hepatocellular carcinoma and Cx26, not detected in human adult skin, was observed in tissue samples of basal-cell carcinoma. In immunoblot analysis, Cx32 antibodies recognized a 27-kDa protein in human liver and hepatocellular carcinoma. A 43-kDa polypeptide was detected in human kidney, renal-cell carcinoma, normal breast, connective tissue of invasive-duct carcinoma of the breast and hepatocellular carcinoma.
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PMID:Expression of Cx26, Cx32 and Cx43 gap junction proteins in normal and neoplastic human tissues. 131 66

Serum isoferritin levels were detected by ELISA in 96 normal, 11 cases of hepatocellular carcinoma (HCC), 28 breast cancer (BC), 31 lung cancer (LC), 26 breast fibroma, 11 pneumonia and 11 tuberculosis. The results reveal significant differences of serum isoferritin levels between the normals and the patients, and between the malignant cases and benign cases (P < 0.01). Serum isoferritin demonstrates higher sensitivity in detecting HCC, LC and BC and thus is of great value in the differential diagnosis of these cancers.
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PMID:[ELISA of serum isoferritin and its clinical application]. 133 91

We analyzed the expression of plasma glutathione peroxidase (GSHPx-P) messenger RNA (mRNA) in mouse, rat, and human tissues, using a human GSHPx-P cDNA clone as the probe. Unlike the classical cellular glutathione peroxidase (GSHPx-1), GSHPx-P expression appears to be tissue-specific. In the mouse and rat, kidney expresses an mRNA at a high level detected with the human probe. A signal is also detected in mRNA isolated from mouse and rat heart, rat cardiac myocytes, mouse lung, epididymis, and the mammary gland of midpregnant mice. No signal is detected in mRNA isolated from mouse and rat liver, mouse brain, uterus, and testis. In human tissues, an mRNA hybridizing to GSHPx-P cDNA is present in liver, as well as kidney, heart, lung, breast, and placenta. We have shown that human kidney expresses a GSHPx-P mRNA, and not a GSHPx-P-like message, by isolating a cDNA clone from a human kidney library in lambda gt11. From the 412-nucleotide partial sequence of the kidney cDNA, which codes for the 40-170 amino acids of GSHPx-P including the TGA codon for selenocysteine, we found complete sequence identity of the kidney cDNA with GSHPx-P isolated from placenta. The expression of GSHPx-P mRNA in cell lines was also studied. There is some correlation of the expression of GSHPx-P in these cell lines with that in normal tissues. Cell lines that expressed GSHPx-P mRNA or protein included the human hepatocarcinoma HepG2, Hep3B cells, human kidney carcinoma A498 cells, and the human breast cancer SK-BR-3, T47D, MDA-MB-231, and AdrrMCF-7 cells. Cell lines that did not express GSHPx-P included human choriocarcinoma BeWo cells, human breast cancer MCF-7, ZR-75-1, and Hs578T cells, and mouse hepatoma Hepa-1 cells.
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PMID:Expression of plasma glutathione peroxidase in human liver in addition to kidney, heart, lung, and breast in humans and rodents. 133

Frequent loss of heterozygosity at chromosomal loci in a specific tumor type may indicate the presence of a tumor suppressor gene. We have examined loss of heterozygosity on chromosome 8p in paired tumor and constitutional DNA from 346 patients representing seven different types of human cancer. Frequent allelic losses were observed in hepatocellular carcinoma (22 of 46 cases, 47.8%), in colorectal cancer (12 of 26, 46.2%), and in non-small cell lung cancer (14 of 35, 40.0%), in contrast to low frequencies detected in breast cancer (5 of 56, 8.9%) and renal cell carcinoma (2 of 27, 7.4%). Ovarian cancer and gastric cancer showed intermediate frequencies of 33.3% and 22.2%. Subsequent analysis of 120 hepatocellular carcinomas and 94 colorectal cancers with five polymorphic markers along the short arm of chromosome 8 defined commonly deleted regions within the same chromosomal interval, 8p23. 1-8p21.3, suggesting that one or more tumor suppressor genes for both cancers may be present in that region.
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PMID:Frequent loss of heterozygosity for loci on chromosome 8p in hepatocellular carcinoma, colorectal cancer, and lung cancer. 135 16

The c-erbB-2 proto-oncogene encodes a transmembrane protein which is homologous to the epidermal growth factor receptor. This protein can be localized immunohistochemically in formalin-fixed paraffin-embedded material using a monoclonal antibody NCL-CB11; positive membrane staining correlates with gene amplification and protein overexpression in breast cancer. Using this technique we have shown that only 2/26 (8%) of hepatocellular carcinomas, 0/10 (0%) of cholangiocarcinomas and 0/2 (0%) hepatoblastomas overexpressed c-erbB-2 as evidenced by membrane staining. Moreover c-erbB-2 mRNA was not detected in seven hepatocellular carcinomas examined by Northern blot analysis. c-erbB-2 overexpression is, therefore, unlikely to be contributing to the malignant phenotype in hepatocellular carcinoma and cholangiocarcinoma.
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PMID:c-erbB-2 oncogene expression in hepatocellular carcinoma and cholangiocarcinoma. 138 26


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