Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blocking of specific SV40-induced resistance of hamsters by the sera collected from 12 individual hamsters infected with SV40 when newborn was studied at different periods of primary virus-induced carcinogenesis. The serum samples were collected at the following periods of primary carcinogenesis: during the latent period (60 days after virus inoculation), at the day of primary tumor appearance, and 19-36 and 45-57 days after primary tumor appearance. For detection of the blocking activity of the collected sera the cells of transplantable SV40 test-tumor were pretreated in vitro with these sera and with control normal hamster sera, and then used for challenge in vivo in SV40-immunized and normal hamsters. With the use of such method, as a rule, no blocking activity of the serum samples collected at any time after the tumor appearance was observed. However, the sera obtained from 7 out of 12 of these hamsters during the latent period significantly decreased the resistance index of animals challenged in transplantation test with the serum pretreated tumor cells. Possible explanations of these findings are discussed.
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PMID:In vivo blocking of SV40 virus-induced antitumor resistance by Syrian hamster sera from early stages of primary SV40 carcinogenesis. 18 66

Since initial studies identifying the important role of vitamin A and its derivatives (retinoids) in maintaining the integrity of epithelial tissues, these compounds have served as paradigms for experimental studies exploring the pharmacologic modification of carcinogenesis. Retinoids have clearly been shown to inhibit chemically induced mammary and urothelial carcinogenesis in experimental animals. Prohibitive toxicity of the parent compound, vitamin A, led to a systematic search for synthetic derivatives with an improved therapeutic index. More than 1500 such compounds have been synthesized, many retaining chemopreventive potential, but with less toxicity. Although several anecdotal reports confirming therapeutic benefits of cis-retinoic acid in patients with acute promyelocytic leukemia and myelodysplastic syndromes appeared in the late 1970s and early 1980s, the remarkable studies of Huang and his colleagues in China in 1988 reporting complete remissions in patients with this uncommon variety of acute myelogenous leukemia with the transisomer of retinoic acid (all-trans-retinoic acid) led to a resurgence of interest in the retinoids as differentiating agents for the prevention and therapy of cancer. Furthermore, molecular studies showing DNA rearrangements of the alpha nuclear receptor for retinoic acid located on chromosome 17 in patients with acute promyelocytic leukemia, a disease invariably associated with a translocation between chromosomes 15 and 17, provided a direct connection between an altered nuclear receptor and the development of a human malignancy. The retinoids also may have important beneficial effects in prevention of recurrent malignancies once the primary tumor has been treated, such as in squamous cell carcinoma of the head and neck. Because retinoids appear to be less effective in inducing differentiation in nonpromyelocytic leukemia cells, investigators have conducted a number of studies to exploit potential synergism between retinoids and other differentiating agents or biologic effectors. Differentiation therapy and chemoprevention are attractive alternative approaches to intensive cytotoxic chemotherapy. It is now clear that retinoids represent one class of compounds with which it may be possible to reverse the progression of malignant disease and prevent carcinogenesis.
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PMID:Retinoids in cancer treatment. 144 94

A new human tumor cell line, NCC-c-CX-1 (CX-1), was established from a uterine cervical cancer xenografted in nude mice. This cell line harbored approximately 50 to 100 copies of human papillomavirus (HPV) type 18 DNA per haploid genome, and contained about 16-fold-amplified c-myc gene with rearrangement. These genomic alterations found in CX-1 cells were also present in both primary tumor and xenografted tumor. Histopathologically, original and xenografted tumors were poorly differentiated cancer and were characterized by neuroendocrine features such as positive neuron-specific enolase and chromogranin A by immunohistochemistry and abundant neurosecretory-type granules in the cytoplasm by electron microscopy. However, the established cell line had lost the neuroendocrine features. This cervical cancer cell line may be a useful model for studying cervical carcinogenesis, especially the interaction between HPV and c-myc oncogene.
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PMID:Newly established uterine cervical carcinoma cell line with co-amplification of human papillomavirus DNA and c-myc gene. 172 14

Results from epidemiological studies have generally indicated an association of dietary saturated animal fats with human breast cancer risk. Some studies, however, have suggested a similar association for some polyunsaturated vegetable fats shown to promote both rodent mammary carcinogenesis and metastasis. This study was performed to evaluate the effects of corn oil on growth and metastasis of MDA-MB-435 human breast cancer cells, which have a propensity for metastasis. Corn oil is rich in the omega-6 fatty acid linoleic acid. Fifty-eight female athymic nude mice (NCr-nu/nu) were fed a high-fat diet (23% wt/wt corn oil; 12% linoleic acid) or a low-fat diet (5% wt/wt corn oil; 2.7% linoleic acid). Seven days after diets were started, tumor cells (1 x 10(6) were injected into a mammary fat pad. The time to appearance of solid tumors and the tumor size were recorded. After 15 weeks, the study was terminated, and autopsies were performed to determine the weight of the primary tumor and the extent of metastasis. The latent interval for tumor appearance in the animals fed the high-fat diet was shorter than that in the low-fat diet group, and the tumor growth rate in the high-fat diet group showed a small but statistically significant increase compared with the low-fat diet group. Primary tumors developed in 27 of the 29 mice on the high-fat diet and in 21 of the 29 on the low-fat diet. Of the mice with palpable primary tumors, 18 of 27 in the high-fat diet group and eight of 21 in the low-fat diet group had macroscopic lung metastases. The extent of metastasis in the high-fat diet group was independent of the primary tumor weight, but only those in the low-fat diet group with primary tumors weighing more than 2 g developed metastases. These results suggest that a high-fat diet rich in omega-6 polyunsaturated fatty acid can enhance metastasis of human breast cancer cells in this mouse model. The findings support the need for further study of the relationship between dietary polyunsaturated fats and breast cancer risk and for experiments to determine the effect on metastasis of only a 50% difference in fat intake--the dietary goal of the proposed clinical trials of low-fat dietary intervention in breast cancer patients.
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PMID:Effect of dietary fat on human breast cancer growth and lung metastasis in nude mice. 173 78

The pharmacology of the antiestrogen tamoxifen is reviewed. The drug is currently used extensively in the treatment of all stages of breast cancer and is being considered as a preventive agent for women at high risk for breast cancer. Extensive laboratory studies demonstrate that tamoxifen is a tumoristatic agent in models of mammary carcinogenesis. Any clinical applications must therefore consider long-term (5-10 years) treatment strategies. Tamoxifen prevents rat mammary carcinogenesis. However, the timing of the carcinogenic insult is unknown among women. Tamoxifen must be considered to be a chemosuppressive agent to prevent the appearance of the primary tumor rather than to prevent the initial carcinogenic insult.
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PMID:Chemosuppression of breast cancer with long-term tamoxifen therapy. 200 27

The effects of carcinogenic nickel [(Ni) CAS: 7440-02-0] and Ni compounds on the natural killer (NK) cell activity of rat peripheral blood mononuclear cells (PBMCs) were studied. Rhabdomyosarcomas were locally induced by one im injection of Ni or Ni subsulfide [(Ni3S2) CAS: 12035-72-2] dust in the hind leg of WAG rats. A weakly tumorigenic dose of 5 mg Ni3S2 (tumor incidence, 2%) induced a transient decrease of PBMC NK activity against YAC-1 cells in vitro (from the 17th to the 23d wk after Ni3S2 inoculation), which could be restored by in vivo injections of partially purified rat fibroblastic interferon (IFN). Injection of 20 mg Ni (tumor incidence, 47.5%) produced a long-lasting depression of NK cell activity (from the 8th to the 23d wk). In vivo chronic IFN treatment of the Ni-injected rats neither restored NK cell activity nor affected the tumor incidence. However, NK cells of Ni-treated animals responded normally to IFN in vitro. Prospective analysis of individual NK cell responses showed that a persistent depression of basal NK cell activity was restricted to rats that subsequently developed a tumor. In these animals the time between carcinogen treatment and clinical detection of the primary tumor was positively correlated with the mean level of NK cell activity (3-4 determinations/rat). Admixture of manganese to Ni inhibited the development of tumors and also prevented the depression of NK cell activity produced by Ni alone. Noncarcinogenic Ni oxide stimulated NK cell activity. These results point out the possible involvement of NK cells in resistance to Ni-induced carcinogenesis.
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PMID:Inhibition of rat natural killer cell function by carcinogenic nickel compounds: preventive action of manganese. 243 44

We have determined the prevalence of amplification of c-myc, N-myc, L-myc, H-ras, Ki-ras, and N-ras oncogenes in 23 cases of squamous cell carcinoma of the oral cavity, using Southern hybridization analysis of DNA extracted from the primary tumor tissues. Nick-translated oncogene probes and oncogene inserts labeled to high specific activities were used. We observed a 5- to 10-fold amplification of one or more of c-myc, N-myc, Ki-ras and N-ras oncogenes in 56% of the tumor tissue samples, with these oncogenes not being amplified in the peripheral blood cells of the same patients. L-myc and H-ras were not amplified in any of our samples. The oncogene amplifications seemed to be associated with advanced stages of squamous cell carcinomas, with the ras and myc family oncogenes being amplified in stages 3 and 4. Hybridization with N-myc detected an additional 2.3 kb EcoRI fragment, along with the normal 2.1 kb fragment. Our data also demonstrated amplification of multiple oncogenes in the same tumor tissue sample. About 60% of the samples with amplified oncogenes showed simultaneous amplification of 2 or more oncogenes. The results showing different oncogene amplifications in similar tumors, as well as multiple oncogene amplifications in the same tumor, suggest that these oncogenes may be alternatively or simultaneously activated in oral carcinogenesis.
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PMID:Oncogene amplification in squamous cell carcinoma of the oral cavity. 250 19

We analyzed the alteration of the hst-1 and int-2 genes in 36 cases of esophageal squamous cell carcinoma, 42 cases of gastric adenocarcinoma, and 52 cases of colorectal adenocarcinoma. Coamplification of the hst-1 and int-2 genes was observed in 19 of 36 esophageal carcinomas (52%), 16 of 34 primary tumor tissues (47%), and 10 of 10 metastatic tumors (100%). The degree of amplification ranged from 4- to 8-fold. The incidence of hst-1 and int-2 gene coamplification was significantly higher in male patients than that in female patients (P less than 0.05). The coamplification of the hst-1 and int-2 genes had a tendency to correlate with clinical stage. The progesterone receptor gene, which is mapped to chromosome 11 at band q21-23, was not amplified in these esophageal carcinomas. Coamplification of the hst-1 and int-2 gene does not seem to imply increased numbers of chromosome 11, and the hst-1 and int-2 genes appear to be in same amplification unit on chromosome 11 at band q13. No coamplification of the hst-1 and int-2 genes was detected in gastric carcinomas and colorectal carcinomas. These results suggest that amplification of chromosomal locus of the hst-1 and int-2 genes might participate in carcinogenesis, in progression, and particularly in metastasis of esophageal carcinomas.
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PMID:High incidence of coamplification of hst-1 and int-2 genes in human esophageal carcinomas. 252 25

We examined the expression of six proto-oncogenes in (i) whole rat liver and isolated liver cell populations during the course of hepatocarcinogenesis induced by a choline-deficient diet containing 0.1% ethionine and (ii) fetal rat liver at different stages of development. The abundance of c-Ki-ras, c-Ha-ras, and c-myc transcripts in polysomal polyadenylated RNA from liver cells increased by 2 weeks after the start of the carcinogenic diet. c-Ki-ras and c-myc expression remained elevated during the 35 weeks of the diet, whereas c-Ha-ras transcripts increased transiently. A primary tumor sampled at 35 weeks after the carcinogenic diet was started contained high levels of both c-Ki-ras and c-myc RNA. The abundance of c-src transcripts was unchanged throughout carcinogenesis; c-abl and c-mos transcripts were not detected in either preneoplastic or neoplastic livers. To determine which cell types within the liver contained proto-oncogene transcripts, we isolated hepatocytes, oval cells, and bile duct cells from normal and preneoplastic livers. The results indicate that proto-oncogenes are expressed differentially in these cell types during hepatocarcinogenesis and that the expression of c-Ki-ras and c-myc is high in oval cells throughout carcinogenesis. In developing livers, c-Ki-ras, c-Ha-ras, and c-myc transcript levels were high at 17 days of gestation but reached the low values characteristic of adult rat livers between 20 days of gestation and 3 days after birth.
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PMID:Expression of c-Ki-ras, c-Ha-ras, and c-myc in specific cell types during hepatocarcinogenesis. 258 Nov 26

We studied the expression of villin, a microfilament-associated, actin-binding protein typical of brush-border microvilli, in a variety of human carcinomas by applying immunofluorescence microscopy to frozen sections and immunoblotting methods to tissue extracts using a rabbit antiserum and a monoclonal antibody specific for villin. All of the 24 primary and metastatic colorectal adenocarcinomas tested were uniformly and strongly positive for villin, with the immunocytochemical labeling concentrated at the luminal cell margin. In poorly differentiated tumor areas, rudimentary tubules were stained. All of the six tubular adenocarcinomas of the stomach studied as well as two adenocarcinomas of the gall bladder and a hepatocellular carcinoma were also villin-positive. Villin was detectable in 12 of 14 adenocarcinomas of the pancreas; in some of these cases, its distribution was heterogeneous. Among 21 renal cell carcinomas investigated, positivity for villin was seen in nine of 13 clear cell tumors (especially those of grade II), and in all four chromophilic cell tumors; however, all four chromophobe cell tumors studied were negative. Four of 11 endometrial but none of nine ovarian carcinomas were (uniformly or focally) villin positive. Of 18 adenocarcinomas of the lung studied, one was uniformly and four focally positive for villin, while the remainder were negative. All of the other epithelial tumors studied, including 12 adenocarcinomas of the breast and seven epithelial or biphasic pleural mesotheliomas, were villin negative. Our results show that the expression of villin in intestinal epithelial cells is consistently maintained in their corresponding carcinomas, even when the organized brush-border structure has been lost. The presence of villin in some endometrial and pulmonary adenocarcinomas--in contrast to its absence in the respective normal epithelia--suggests that this protein is newly expressed during hyperplasia, dysplasia, or carcinogenesis. Determining the presence or absence of villin and its immunocytochemical staining pattern in metastatic adenocarcinomas may be of some help in determining the type and site of the primary tumor.
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PMID:Villin: a cytoskeletal protein and a differentiation marker expressed in some human adenocarcinomas. 289 90


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