Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The biological behavior of early-stage invasive carcinoma of the uterine cervix is not always predictable. Therefore it is important to identify new biological markers which could more accurately predict the evolution of the disease. Amplification and/or overexpression of the c-myc gene were frequently observed in advanced-stage cervical cancers and were shown to be associated with tumor progression. More interesting was the study on 93 patients with early-stage carcinoma showing that c-myc gene overexpression was significantly related to a higher risk of relapse. A combination of c-myc expression and nodal status provided a very accurate indication of the risk of relapse. Indeed, in the subgroup of patients with negative nodes, the 3-year disease-free survival rate was 93% (95% confidence interval CI: 79-98%) when c-myc was expressed at a normal level, whereas this rate was only 51% (95% CI: 26-63%) when c-myc was overexpressed. Moreover the c-myc overexpression was related to a 6.1-times higher risk of distant metastases, suggesting that activation of this proto-oncogene may lead to metastatic ability of tumor cells. These data clearly show that patients with c-myc overexpression are high risk patients who thus might benefit from intensive treatment.
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PMID:The c-myc proto-oncogene in invasive carcinomas of the uterine cervix: clinical relevance of overexpression in early stages of the cancer. 217 73

Ras p21 and myc p62 expression has been examined immunohistochemically in seventy specimens of bronchial carcinomas. Both ras and myc oncoproteins were found to be overexpressed at a higher frequency in non small cell carcinomas (squamous cell carcinomas and adenocarcinomas) compared to the small cell carcinoma specimens; however only myc p62 overexpression was found to be statistically significant. Also, ras p21 oncoprotein expression was frequently overexpressed in adenocarcinomas compared to squamous cell carcinomas (p less than 0.05). Overexpression of c-myc p62 was found to correlate with poorly differentiated squamous cell carcinomas compared to the well and moderately differentiated tumors. The results of this study indicate that both the ras and myc oncogenes are important in the progression of bronchial carcinomas.
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PMID:Expression of ras p21 and myc p62 oncoproteins in small cell and non small cell carcinoma of the lung. 217 69

Normal and neoplastic thyroid tissues express a variety of oncogenes, growth factors, and growth factor receptors. The increased expression of a mutated form or forms of c-myc and c-ras appears to be associated with some epithelial and medullary thyroid carcinomas. In some cases the presence of these oncogenes correlates with less favorable histologic appearance. The possibility of cooperation between oncogene products (myc and ras) in neoplastic development is raised by studies on transformed thyroid cells in culture. Moreover, a tissue-specific oncogene associated with papillary carcinoma recently has been described. The role of excessive growth factor or growth factor receptor expression in thyroid carcinoma also has been discussed and may, as with other tumor types, be linked to specific oncogene products (e.g., c-erb-B encoding for the EGF receptor). However, the regulation of oncogenes in various stages of differentiation of thyroid tissues is not well understood. In addition to describing these associations with thyroid carcinoma and putative unchecked growth factor action in the development of neoplasia, more direct demonstrations of a causal relationship are necessary. Thus, one needs to overexpress oncogenes/growth factors in normal cell lines (as has been described in this review) and observe whether cellular transformation or dedifferentiation or both occur. The ability to specifically block oncogene or growth factor expression in neoplastic cell lines at the RNA or protein level (with antisense oligonucleotides or monoclonal antibodies, respectively) should provide important information about the pathogenetic importance of these factors. It may be anticipated that reversing the overexpression of certain oncogenes can lead to normal cellular proliferation, morphology, and differentiation. The knowledge obtained from investigating the associations of oncogenes and growth factors with thyroid cancer should provide insight into the mechanisms involved in cell growth and differentiation and in the biochemical steps involved in neoplastic transformation. New insights into these processes may lead to specific therapeutic measures designed to block aberrant expression of the cellular products involved in neoplasia. A more complete understanding of the role of oncogenes in thyroid cancer also may lead to the development of specific tumor markers that may be useful in the early diagnosis of thyroid cancer and the follow-up of therapeutic maneuvers. If specific markers can be identified, analysis of fine-needle aspiration specimens of the thyroid or imaging techniques (using for example, oncogene-specific monoclonal antibodies) could be added to the diagnostic armamentarium for thyroid disease.
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PMID:Oncogenes and growth factors in thyroid carcinogenesis. 217 2

The role of cellular proto-oncogene activation in shortwave UV light in the B range (UV-B)--induced skin carcinogenesis was investigated. Epidermal papillomas and carcinomas were induced on the depilated skin surface of Sencar mice with single-dose UV-B irradiation (7 x 10(4) J/m2). The tumors thus initiated were present in 18.8% of treated animals and were primarily benign papillomas, while a few (6 of 17) progressed to form squamous cell carcinomas. A 5- to 10-fold stimulation of cHa-ras gene expression in both papillomas and carcinomas was observed. Other cellular proto-oncogenes such as cKi-ras, c-myc, or c-fos specific messenger RNAs were not detected in these UV-B--induced skin tumors. Subsequent Southern blot analysis revealed a threefold to fivefold amplification of cHa-ras gene in skin papillomas and carcinomas. However, only the carcinoma and not the papilloma DNA induced foci in the classic NIH-3T3 transformation assay, suggesting that activation of cHa-ras gene alone is not sufficient to exhibit this phenotypic expression of transformed cells. The NIH-3T3 transformants exhibited (1) anchorage independent growth on soft agar, (2) tumor induction in athymic mice, and (3) overexpression and amplification of the cHa-ras gene. We propose that overexpression of a ras gene by gene amplification plays a role in the UV-B--induced skin carcinogenesis process.
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PMID:cHa-ras proto-oncogene. Amplification and overexpression in UV-B-induced mouse skin papillomas and carcinomas. 217 60

Subcellular distribution of c-myc oncogene product and EGF receptor in oral squamous cell carcinomas was examined by using immunohistochemical method. Immunohistochemy for c-myc oncogene showed three staining patterns. Reactive products were demonstrable in the nucleus, in the perinuclear cytoplasm with granular appearance and in the entire cytoplasm. Concomitant stainings of each reactive pattern were observed. Occasionally, the reactive product was strongly deposited on the chromatin under mitotic phase. EGF receptor positive cases were found in only 4 of 28 cases. Though reactive products were usually found in the cytoplasm, the cell surface staining was detected in the only one case. In this case, cells under mitotic phase were strongly stained. The fact that the strong staining both of c-myc and EGF receptor in cells under mitotic phase suggested the close relation between the expression of these genes and the proliferation of carcinoma cells.
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PMID:Immunohistochemical localization of c-myc oncogene product and EGF receptor in oral squamous cell carcinoma. 217 34

Previous articles have reported that the c-myb proto-oncogene was activated in various types of tumours of the hematopoietic system suggesting that this gene plays a role in the development of these malignancies. However no studies of the c-myb gene have as yet been performed in solid primary tumours. In the present study we have analysed in breast cancer the c-myb gene with the aim to determine its involvement in tumour progression. Expression of the c-myb oncogene was analysed from 169 carcinoma specimens obtained from untreated patients with non-inflammatory breast cancer (NBC) (112 patients) and inflammatory breast cancer (IBC) (57 patients). A 3.5 kb c-myb transcript band was detected in 108 (64%) tumours. c-myb expression was found to be associated with good prognostic factors (lowest histopathologic grade (P = 0.01), oestrogen and progesterone receptor status (P less than 10(-4)) and pS2 gene expression (P less than 10(-4)) and negatively correlated with breast cancers of poorer prognosis, namely IBC (P = 0.03) and NBC with multiple involved nodes (P = 0.15). Other genes (c-myc, c-erbB2, c-fos and epidermal growth factor receptor) were also studied. The c-myb gene expression was found to be inversely correlated (P less than 0.03) with only c-erbB2 overexpression in NBC. When data were analysed with a logistic regression model using a stepwise procedure, c-myb expression was found to be associated only with the oestrogen receptor status (P less than 10(-4)). In conclusion, our data indicate that analysis of c-myb expression in breast cancer could allow the characterization of a new class of oestrogen-dependent tumours.
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PMID:Strong association between c-myb and oestrogen-receptor expression in human breast cancer. 218 74

The biological behaviour of invasive carcinoma of the uterine cervix is not always predictable. It is therefore important to establish new biological markers which could be useful in determining a more reliable prognosis. We have analyzed the c-Ha-ras and c-myc proto-oncogenes in a large series (154 cases) of cervical cancers at various clinical stages. Alterations of c-Ha-ras (deletion, mutation) and c-myc (amplification) were frequently observed in cervical cancers and were shown to be associated with tumor progression. Furthermore, c-myc overexpression, when detected in early cervical cancers, provides a means of identifying patients at high risk of early recurrence.
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PMID:[c-myc and c-Ha-ras proto-oncogenes in cervical cancer: prognostic value]. 219 30

The distribution of the c-myc oncogene product p62 was examined by immunohistochemistry using the monoclonal antibody Mycl-9E10 in a series of 50 colorectal resections for carcinoma. The specimens were specially handled to ensure rapid fixation in formalin, and a significant improvement was shown in the quality and localization of staining compared with routinely handled specimens. Non-neoplastic mucosa showed the presence of nuclear staining of epithelial cells in 93 per cent of the samples, whilst all carcinomas showed cytoplasmic staining and infrequent nuclear staining. Adenomas showed an intermediate pattern, with significantly more frequent cytoplasmic distribution than non-neoplastic mucosa, but less than carcinomas. The results show that whilst fixation conditions are important in the immunolocalization of the c-myc protein product, there may be a consistent difference between non-neoplastic mucosa and carcinoma in the manner of association of p62 with the nucleus.
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PMID:Immunohistochemical demonstration of altered intracellular localization of the C-Myc oncogene product in human colorectal neoplasms. 219 34

Rat embryo cells or Rat-1 fibroblasts were transfected with either an activated c-myc or a c-Ha-ras from the T24/EJ bladder carcinoma, or they were cotransfected with both. A gene conferring neomycin or hygromycin resistance was also cotransfected so that independent cell lines could be selected by growth in medium containing the antibiotic. Certain isolates from cells transfected with only one type of oncogene were further transformed by exposure to 600 cGy of 250-kVp X-rays. Successful transfection and transformation were characterized by altered morphology, increased plating efficiency, shorter doubling time, longer life span, foci formation, anchorage-independent growth, and Southern and Northern hybridization analysis. The thermal response of these cells at different stages of oncogenic transformation was examined by exposing exponentially growing cells to 45 degrees C for 0 to 45 min and measuring cellular survivals using colony formation assay. We found that cells transfected with myc oncogene, singly or in combination with ras, were more sensitive to thermal stress. Aside from that, the cells' thermal sensitivity was not affected by the degree or the nature of transformation.
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PMID:Thermal response of oncogene-transfected rat cells. 219 14

Structural alterations of protooncogene sequences may be involved in the pathogenesis of human neoplasms. We screened 54 thyroid tumors (36 benign and 18 malignant) for gene rearrangements of the protooncogenes c-myc, c-myb, c-fos, c-erb-B1, c-erb-B2, c-erb-A, N-ras, K-ras, and H-ras. Only mutations of H-ras were observed. None of the 15 colloid adenomas examined had detectable H-ras rearrangements. Of the remaining tumors, we observed mutations of H-ras in 4 benign and 4 malignant neoplasms. Gene amplification was found in 5 tumors. An aggressive recurrent papillary carcinoma had a marked amplification of one of the H-ras alleles. The amplified allele was truncated, in that the 3' variable tandem repeat was not a part of the amplification unit, and contained a codon 12 point mutation leading to a valine for glycine substitution. We also observed the association of low copy gene amplification with a codon 12 valine for glycine mutation in a follicular adenoma. Two tumors contained H-ras EcoRI polymorphisms not present in the DNA of normal thyroid from the same individuals, and one follicular carcinoma showed loss of an H-ras allele. Ras protooncogenes may become transforming by quantitative mutations, leading to increased expression, or qualitative mechanisms, through activating point mutations. Both of these appear to coexist in thyroid neoplasms, and it may be that a combination of both mechanisms is capable of inducing a more complete spectrum of neoplastic phenotypes.
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PMID:H-ras protooncogene mutations in human thyroid neoplasms. 219 80


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