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)

The effect of chalone-containing ethanol extract of rat skin (CCE) on the growth in mice of transplanted uterine cervix and skin carcinomas, hepatoma-22a, sarcoma-180 and leukemia L-1210 was studied. When CCE is added to the suspension of tumour cells (10 mg CCE/100 mg tumour tissue/ml saline) the most obvious retention of tumour growth is observed on squamous-cell carcinoma of uterine cervix (72.6%; p less than 0.01). The effect of CCE on the growth of other transplanted tumours, including the skin carcinoma, is not significant. As compared to the uterine cervix carcinoma, the skin carcinoma lacked its primary squamous-cell structure during the tumour progression. The possibility of applicative use of chalones for cancer control is discussed.
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PMID:Study of antiblastomogenic action of epidermal chalones. I. The effect of epidermal chalones on some transplantable mouse tumours. 21 Oct 47

Two rare cases with histologically proven multiple primary neoplasms are described: an association of intracerebral malignant lymphoma with hepatocellular carcinoma in one case and with squamous cell carcinoma of the uterine cervix in the other. Therapeutic problems pertinent to the coexistence of primary intracerebral malignant lymphoma and neoplasms of a different histological type are discussed.
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PMID:Primary intracerebral malignant lymphoma associated with different histological types of carcinoma: report of two cases. 131 11

Restriction-fragment-length polymorphism analysis was performed on several different types of human cancers, including carcinoma of the uterine cervix, neuroblastoma, hepatocellular carcinoma, pheochromocytoma, stomach cancer, and small-cell lung carcinoma (SCLC), to determine the chromosomal loci of putative tumor-suppressor genes in each type of tumor because less of heterozygosity (LOH) is supposed to unmask the recessive mutation of tumor-suppressor gene in the remaining allele. Chromosomal loci showing frequent LOH differed among these tumors, suggesting that there are several tumor-suppressor genes in the human genome and that critical genes for the development of each type of tumor are different. In some cases LOH was observed in the early stage of tumor such as chromosome 3p loss in carcinoma of the uterine cervix, and in other cases it was observed only in the advanced stage of tumor such as chromosomes 4 and 16q loss in hepatocellular carcinoma. These results suggest that there are two different types of tumor-suppressor genes: one is the gene whose inactivation is responsible for malignant transformation of a normal cell and the other is the gene whose inactivation is responsible for the progression of a tumor cell. In SCLC, LOH at three different chromosomal loci, 3p, 13q, and 17p, was simultaneously observed in nearly 100% of tumors. It was observed even in stage I tumors and an untreated tumor, and it occurred prior to N-myc amplification. These results may imply that at least six genetic alterations are necessary to convert a normal cell into a fully malignant cancer cell in SCLC.
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PMID:Chromosomal localization of putative tumor-suppressor genes in several human cancers. 168 40

Pingyangmycin (PYM), produced by Streptomyces pingyangensis n. sp., was found to be identical to bleomycin A5. In the present study, a comparative observation was carried out in 10 human cancer cell lines. As determined by a colony-forming assay, the dose-response curves obtained from cells exposed to PYM for 1 h were of one type only: biphasic exponential. The sensitivities of these cells derived from different types of tumors, however, varied with a broad range of ID50 values (0.03-0.82 microgram/ml). A hepatoma cell line (BEL-7402) and three lines derived from squamous carcinomas of the esophagus (Eca109 and CaEs17) or the nasopharynx (CNE) were relatively sensitive (ID50 less than 0.20 microgram/ml) to PYM which is known to have clinical activity against these diseases. Two gastric adenocarcinoma cell lines (MGc80-3 and BGC-823) and a pulmonary adenocarcinoma cell line (SPC-A-1) appeared to be less sensitive to the drug, with ID50 values of 0.21-0.47 microgram/ml. PYM was 7-fold more effective against LTEP-78 cells derived from pulmonary squamous carcinoma as opposed to SPC-A-1 cells, resulting in a low ID50 value of 0.04 microgram/ml. However, PYM as a single agent has not yet received full evaluation in relation to this type of lung cancer. In contrast with other cell lines of squamous cancer origin, HeLa and CC-801 cells derived from uterine cervix carcinomas which have been evaluated as highly responsive to PYM had the highest ID50 values (greater than 0.70 microgram/ml).
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PMID:[Anticancer spectrum of pingyangmycin in vitro]. 170 47

beta-Sitosterol (SI-0), beta-sitosterol glucoside (SI-1), dioscin (SI-2), methyl protoprosapogenin A of dioscin (SI-3), methyl protodioscin (SI-4) and protodioscin (SI-5) were isolated and characterized from the whole plant of Solanum indicum L. (Solanaceae). Except for beta-sitosterol, these compounds have not been previously isolated from Solanum indicum L. Both CHCl3 soluble (SI-IV) and insoluble (SI-V) fractions of the ethanolic extract (SI-I) showed cytotoxicity on seven cancer cell lines: Colo-205 (colon), KB (nasopharynx), HeLa (uterine cervix), HA22T (hepatoma), Hep-2 (laryngeal epidermoid), GBM8401/TSGH (glioma) and H1477 (melanoma). The purified constituents, SI-2 and SI-4 showed more potent effects by DEA and MTT assay. SI-2,3,4 and 5 also demonstrated cytotoxicity on cultured C6 glioma cells by PRE assay, ans SI-3,4 and 5 showed a tumor inhibitory effect in vivo in C6 glioma cells. In addition, SI-2 had an inhibitory effect on the DNA synthesis of C6 glioma cells at 10 micrograms/ml.
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PMID:Experimental antitumor agents from Solanum indicum L. 176 63

By restriction fragment length polymorphism (RFLP) analysis, it was found that loss of heterozygosity (LOH) at three different chromosomal loci, 3p, 13q, and 17p, occurs simultaneously in nearly 100% of small-cell lung carcinomas (SCLC). This was observed even in stage I tumors and an untreated tumor, and it occurred prior to NMYC amplification. The common region of LOH on chromosome 3p was 3p14-24.1, and this region was also frequently lost in carcinoma of the uterine cervix (100% at D3S2 on 3p14-21) as well as renal cell carcinoma (56% at ERBA beta on 3p22-24.1), suggesting the presence of tumor suppressor gene(s) for these cancers in this region. On chromosome 13, LOH was observed commonly in the region between 13q12 and 13q22, including the RB locus on 13q14, and normal RB protein was not detected in any of 9 SCLC cell lines by immunoprecipitation analysis. The common region of LOH on chromosome 17 was 17p13 and is the same as that in colon carcinoma and osteogenic sarcoma. Since LOH is supposed to unmask the recessive mutation of tumor suppressor gene in the remaining allele, these results may imply that at least six genetic alterations are necessary to convert a normal cell into a fully malignant cancer cell in SCLC. RFLP analysis was performed on several other types of human cancers, including carcinoma of the uterine cervix, neuroblastoma, hepatocellular carcinoma, pheochromocytoma, and stomach cancer to determine the chromosomal loci of putative tumor suppressor genes in each tumor. Chromosomal loci showing frequent LOH were different among these tumors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multiple genetic alterations in small-cell lung carcinoma. 257 37

Data on cancer rates from West Indian populations are scarce, and to the authors' knowledge there are no published data on cancer rates and distributions among Haitians. Proportional distributions of cancers among three groups of patients living in Florida were compared: Haitian born blacks, United States born blacks, and non-Haitian Caribbean born blacks. The incidence rate of cancer of the cervix among the Haitian and United States born black groups was also compared. Increased rates of certain malignancies associated with viral infection or immunodeficiency were found in the Haitian group. These tumors were hepatocellular carcinoma, nasopharyngeal carcinoma, reticulum cell sarcoma, Kaposi's sarcoma, and carcinoma of the uterine cervix. The age-adjusted incidence rate of carcinoma of the cervix was especially high among Haitian women even with a liberal estimate of the female Haitian population from whom the cases were drawn. Except for cancer of the cervix, the numbers of cancers of interest were small, and age-adjusted incidence rates were not calculated. Continued epidemiological study of larger numbers of patients is needed to evaluate these findings further.
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PMID:Cancer among Haitians in Florida. 302 99

The immune system has evolved under Darwinian pressures as a defence against ubiquitous viruses. Immune surveillance against viral antigens protects the normal host. Individuals with inherited or acquired immune-deficiency disorders can become vulnerable to ubiquitous viruses and neoplasms can ensue, such as B-cell lymphoma, hepatocellular carcinoma, squamous-cell carcinoma, Kaposi's sarcoma, and carcinoma of the penis and uterine cervix. Immunodeficiency permits Epstein-Barr virus, hepatitis B virus, papillomavirus, herpes simplex virus, and cytomegalovirus to induce sustained target-cell proliferation. Each virus selects specific cellular targets bearing viral receptors and the infection leads to proliferation of the target cells rather than lysis. Various co-factors, including nutrition, exposure to tumour-promoting agents, parasitic infection, and ultraviolet light, may promote carcinogenesis. Depending on the type and severity of the immune deficiency, gradual proliferation may lead to evolution of a malignant clone. Conversion of polyclonal virally infected proliferating cells to give monoclonal malignancy is probably due to specific cytogenetic rearrangements which allow oncogene activation and endow an altered tumour cell with selective growth advantages over normal diploid cells. Prevention of viral oncogenesis may be possible by treatment of immune-deficient individuals with premalignant disorders. Immunotherapy and antiviral therapy may prevent progression of viral-induced proliferation to malignancy. The purpose of this paper is to discuss and evaluate the role of immune deficiency and viruses in the induction of malignancies commonly occurring in Africans residing in sub-Saharan Africa (Purtilo, 1976). The types of malignancies commonly occurring in this region are believed to be due to ubiquitous viruses. A failure of immune surveillance mechanisms to recognize viral antigens and abrogate proliferation of infected target cells predisposes to malignancy by increasing the chance of a proliferating cell undergoing a cytogenetic or molecular alteration which endows it with malignant characteristics. The immunological surveillance hypothesis has been elaborated during this century by Ehrlich, Thomas, Burnet, and Schwartz (reviewed by Purtilo & Linder, 1983). This hypothesis rests on several assumptions: that neoplastic cells possess unique tumour antigens: tumour antigens provoke an immune response in the host; and the immune response is protective and eliminates the tumour.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Squamous-cell carcinoma, Kaposi's sarcoma and Burkitt's lymphoma are consequences of impaired immune surveillance of ubiquitous viruses in acquired immune deficiency syndrome, allograft recipients and tropical African patients. 610 Feb 88

Enhanced nucleocytoplasmic RNA transport has been demonstrated by incubating normal rat liver nuclei in presence of cytosols originating from the poorly differentiated, fast-growing hepatoma HW-165, in the linear phase of tumor growth. The effect of hepatoma HW-165 cytosol was reduced or suppressed in presence of small amounts of normal liver cytosol: on the other hand, several polypeptides of molecular weight 20,000 to 40,000 daltons were hardly detectable in hepatoma HW-165 cytosol, both arguments indicating that potentially regulatory proteins should be absent or present in reduced concentration in hepatoma HW-165 cytosol. No modification of RNA release was observed in presence of cytosols originating from the thymus of RNA virus (BL/F)-infected rats, whatever be the time after inoculation. Attempts were made to use the nuclear restriction assay, supplemented with plasma or serum of various origins, as a biochemical marker of neoplasia. In a first series of assays, including 80 cancer patients and 12 healthy controls, the RNA transport activity was stimulated by the serum of patients bearing various tumors (lung cancer, cancer of the respiratory tract, uterine cervix...), except in a few cases of mammary carcinoma, where values equivalent to or lower than the controls were obtained.
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PMID:On the altered nucleocytoplasmic transport "in vitro" of rapidly labelled RNA, in the presence of cytosol or serum from tumor-bearing rats. 616 10

Tumors of various histological patterns (squamous-cell carcinoma of uterine cervix SCC. Lewis lung carcinoma, hepatoma-22a, mammary adenocarcinoma-755, sarcoma-180 and hemocytoblastosis La) were transplanted in mice aged 3, 12-18 months. Tumor SCC, hepatoma-22a, sarcoma-180 and adenocarcinoma-755 grew faster in older animals (18 months) than in younger one (3 months), while Lewis lung carcinoma and hemocytoblastosis La developed at the same rate in old and young animals. It is suggested that tumor growth in senescent organism is determined by both hormono-metabolic shifts, degree of immunologic vigor and a number of biological characteristics of tumor.
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PMID:[Effect of age on the growth of transplantable tumors in mice]. 728 93


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