Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The current TNM classification of the liver was published in 1987 by UICC, which is the same as the staging system in the general Rules for the Clinical and Pathological Study of Primary Liver Cancer by the Liver Cancer Study Group of Japan (3rd Ed.) and was proposed by the Japanese TNM Committee. This was established based upon the data obtained before 1985. Thus, the current TNM classification does not always meet the latest knowledge of advanced hepatic oncology. The disease in which lesions are present both in the left and the right hepatic lobe is defined as Stage 4. Multiple liver cancers of multicentric carcinogenesis which are present in the two hepatic lobe and which are often detected recently, are stage 4 by the current TNM classification. But the postoperative prognosis of this kind of multiple liver cancer is found to be better than that of stage 4 of the advanced type, and equal to stage 3. Some proposals of reversed TNM classification of the liver, made with a small number of experienced cases have been published. However, not all of them would be convincing even with testing of a large number of cases.
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PMID:[TNM classification of liver cancer]. 923 74

Deletions on chromosome arm 8p, as defined by allelic imbalance, are a frequent event in many different types of malignant tumors, including those of the head and neck. These regions are thought to harbor tumor suppressor genes. In order to define a high-density deletion map of this chromosomal arm in oral and oropharyngeal squamous cell carcinomas, we have tested for allelic imbalance in 35 such tumors with 22 short tandem-repeat polymorphisms. Overall, 21 (60%) of the 35 tumors showed allelic imbalance at one or more loci on chromosome arm 8p. Interstitial deletions defined three discrete areas of deletion: at 8p23, 8p22, and 8p12-p21. Tumors of TNM stages II-IV showed a significantly higher frequency of allelic imbalance on 8p than did TNM stage I tumors. Our data suggest that there are least three tumor suppressor loci on chromosome arm 8p that may be implicated in oral carcinogenesis. Furthermore, inactivation of such genes may be associated with high-grade tumors.
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PMID:Deletion mapping defines three discrete areas of allelic imbalance on chromosome arm 8p in oral and oropharyngeal squamous cell carcinomas. 940 50

The expression and coexpression of EGFR, c-erbB-2 and c-erbB-3 in 21 gastric cancers and 20 chronic gastritis was examined using immunohistochemistry on fresh frozen tissues considering clinicopathological variables. Generally, gastric cancer patients showed a higher incidence of EGFR, c-erbB-2 and d-erbB-3 overexpression than the group with chronic gastritis (81% and 43%; 38% and 45%; 35% and 20%, respectively), however, statistically significant differences were found only for EGFR expression (p = 0.01). No association between immunoreactivity of all growth factor receptors and the histopathological structure of gastric cancer was observed. EGFR and c-erbB-3 proteins were detected more frequently in patients with III/IV than in I/II of TNM stages, while c-erbB-2 overexpression was higher in I/II vs. III/IV stages. In chronic gastritis with intestinal metaplasia and or coexisting carcinoma lesions, a higher frequency of the expression of studied proteins was observed in comparison with chronic gastritis without those alternations; however, these differences were statistically insignificant. The percentage of positive cases with coexpression of two proteins was comparable in gastric cancer and chronic gastritis (33% and 35%) but the simultaneous expression of all three receptors was evident only in gastric cancer (19%). Our results indicate that at least one or two members of EGFR related receptors could appear in the early stages of gastric tumorigenesis. The enhancement of c-erbB-2 and c-erbB-3 reactivity seems to cooperate with EGFR activation in the gastric cancer development. Our results indicate the promotional rather than direct transformational role for EGFR supergene family in gastric carcinogenesis.
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PMID:Expression of epidermal growth factor receptor family proteins (EGFR, c-erbB-2 and c-erbB-3) in gastric cancer and chronic gastritis. 970 36

Bax, bcl-2 and their homologues regulate a distal step in an evolutionary very well conserved pathway of apoptotic cell death. It plays a crucial role in the balance between proliferation rate and cell viability. Thus in the last years the attention of the scientific community towards these proteins has remarkably increased, in particular in the oncologic field. We developed an immunohistochemical assay allowing us to evaluate the bax expression in formalin fixed and paraffin embedded lung cancer tissues to investigate bax expression in a cohort of 55 patients affected by non-small cell lung cancer. We detected high expression of bax in 72.7% of our patients. When we statistically analyzed our data we did not find any correlation between bax expression and any clinicopathologic parameters (sex, age, TNM status, tumor grade, histological type). In conclusion, our study shows the frequent overexpression of bax, and this highlights the "apoptotic tendency" of cells during the neoplastic proliferation. But, the role of bax in non-small cell lung cancer pathogenesis still remains unclear and further studies of large numbers of patients, including different stage groups, are needed to better define the involvement of this protein in the complex mechanism of lung carcinogenesis.
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PMID:Frequent high expression of bax pro-apoptotic protein in non-small cell lung cancer. 1021

This study evaluated the potential contribution of the APC gene to malignant transformation in patients with renal cell carcinoma. We tested 36 human renal cell carcinoma samples and 18 adjacent normal kidney tissues for the expression of APC protein, both wild and truncated types, by western blot using antibodies that recognize either the carboxy or the amino epitope of the APC protein. The same tumor samples together with autologous peripheral blood were also analyzed at the DNA level. Using specific oligonucleotide primers for exons 11 and 15, gene instability was followed by polymerase chain reaction/loss of heterozygosity (LOH) (on the basis of restriction fragment length polymorphism). Molecular data were also compared to pathohistological diagnosis, TNM stage, and patient's age using multivariate statistical methods. All normal renal tissues revealed expression of the wild-type APC protein. Neither wild nor mutant type proteins were found in 36% (13/36) of tumor samples; the rest of tumor tissues expressed the wild-type protein (312 kDa). Mutated APC protein, with a molecular weight of 117 kDa, was found in only one tumor sample. From 36 tumor samples 16 (44.4%) were informative for RsaI exon 11 polymorphic site, while only half of these (8/16) demonstrated LOH. From 13 tumor samples that had no detectable protein product by western blot analysis eight were homozygous for the exon 11 polymorphism and were tested for another polymorphic site, MspI/exon 15. The overall proportion of LOH cases for both polymorphisms tested was 52.9% (9/17). Pathohistological diagnosis and molecular data showed no correlation. However, multivariate analysis determined a stage strong positive correlation of age and TNM with the presence of LOH and the absence of the wild-type APC protein. Out results suggest that the APC tumor suppressor gene plays a role in renal carcinogenesis. Alterations in this gene are responsible for tumor evolution and progression, but cannot be considered as a first event in tumor initiation.
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PMID:Loss of heterozygosity and protein expression of APC gene in renal cell carcinomas. 1042 94

p27(Kip1) is a cyclin-dependent kinase inhibitor that negatively regulates cell proliferation. This study was designed to evaluate the roles of p27(Kip1) in gallbladder carcinogenesis and the prognostic value of p27(Kip1) in patients with gallbladder carcinoma. p27(Kip1) expression was examined immunohistochemically in surgically resected specimens of 8 normal epithelia, 8 adenomyomatosis lesions, 6 precancerous adenomas, and 37 carcinomas of the gallbladder. Decreased p27(Kip1) expression (<50% nuclear staining) was observed in 16 of the 37 (43%) gallbladder carcinomas, but not in any specimen of normal epithelium, adenomyomatosis, or adenoma. The fact that all of the adenomas showed normal p27(Kip1) expression suggests that decreased p27(Kip1) expression is probably not an early event in gallbladder carcinogenesis. Decreased p27(Kip1) expression was significantly associated with less marked tumor cell differentiation (P =.017), lymphatic invasion (P =.046), lymph node metastasis (P =.007), and advanced TNM stage (stage IV vs. stage I, P =.026; stage IV vs. stage II, P =.005). This suggests that down-regulation of p27(Kip1) expression is a late event in gallbladder carcinogenesis, possibly promoting tumor progression and metastasis. Kaplan-Meier curves showed that decreased p27(Kip1) expression was significantly associated with shorter overall survival (P =.001) in patients with gallbladder carcinomas who had undergone radical surgery. Cox's proportional hazards model revealed decreased p27(Kip1) expression to be an independent predictor for death (P =.034; risk ratio, 3.9; 95% confidence interval, 1.1-13.7). In conclusion, decreased p27(Kip1) expression significantly correlates with tumor progression and predicts poor prognosis in gallbladder carcinomas.
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PMID:p27(Kip1) expression in normal epithelia, precancerous lesions, and carcinomas of the gallbladder: association with cancer progression and prognosis. 1079 81

Immunotherapy trials using monoclonal antibodies 323/A3 and 17-1A that recognize Ep-CAM, including trials focused on cancer of the lung, currently are underway. Nevertheless, there have been few comprehensive evaluations of the expression of Ep-CAM in specific types of neoplastic processes, including cancer of the lung. The current study of 60 human subjects with squamous cell cancer (SCC) of the lung, selected at random, was undertaken (1) to examine the expression of Ep-CAM in SCC and associated uninvolved bronchial mucosa, bronchial epithelial hyperplasia, and dysplasia, and (2) to correlate the results with established prognostic indicators and survival of patients. In both the uninvolved bronchial mucosa and epithelial hyperplasia, the expression of Ep-CAM in luminal cells was significantly higher compared with its expression in the matched basal cells (P = .003, P < .0001, respectively). When Ep-CAM scores of basal and luminal cells present in uninvolved bronchial mucosa and epithelial hyperplasia were combined, we observed a statistically significant stepwise increase in Ep-CAM expression from uninvolved bronchial mucosa to epithelial hyperplasia to SCC, suggesting its involvement in malignant transformation of SCC. The expression of Ep-CAM was significantly higher in poorly to moderately differentiated SCC compared with well-differentiated SCC (P = .04). An increase in the expression of Ep-CAM with increasing size or local extent of the primary tumor approached statistical significance (P = .09). The expression of Ep-CAM increased significantly with increasing involvement of regional lymph nodes (P = .02). Similarly, the expression of Ep-CAM increased with the increasing TNM stages (P = .04). Kaplan-Meier Survival analysis using the same categorizations showed that increasing tumor size, nodal status, and stage were significantly associated with poor patient survival (P = .04, .01, .01, respectively). There was, however, no statistically significant association between patient survival and staining intensity of carcinomas for Ep-CAM. We conclude that expression of Ep-CAM increased during the progression of SCC of the lung and, therefore, may play a role in the carcinogenesis of this disease.
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PMID:The expression of Ep-CAM (17-1A) in squamous cell cancers of the lung. 1082 96

APC gene mutations play an important role in the initiation step of colorectal carcinogenesis in both familial adenomatous polyposis (FAP) patients and non-FAP patients. Although the APC gene is expressed in most tissues, including the lung, liver, kidney, and mammary gland, its somatic mutations have rarely been found in primary tumors affecting these organs. We have developed a sensitive yeast-based assay for screening almost the entire coding region of the APC gene. By this method, we have been able to detect somatic mutations of the APC gene in 57% of colorectal cancers and none in non-small cell lung cancers. Interestingly, the assay detected somatic APC gene mutations in 18% of breast cancers, in which APC gene mutation was previously considered rare. In the breast cancers, most of the APC mutations were distributed outside the mutation cluster region that has been advocated for colorectal cancers. We also noted a difference in the mutation pattern of the APC between colorectal and breast cancers. In colorectal cancers, all base substitutions were observed at C residues (5 of 5), whereas in breast cancers the majority of them were found at G residues (4 of 5). Furthermore, APC mutations were observed at a significantly high frequency in advanced stages of primary breast cancers (TNM classification, P < 0.05; T category, P < 0.01). Our data suggest that the etiology of the APC mutations and their biological role in carcinogenesis may differ between colorectal and breast cancers.
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PMID:Somatic mutations of the APC gene in primary breast cancers. 1085 22

Breast Cancer (BC) still interest to be discussed, comparison studies from several investigators still in controversial, especially on risk factors of BC, otherwise BC morbidity and mortality were stationary, infact, had a tendency increasing. Epidemiology studies on BC, daily observation for a long period explored that some Indonesian BC cases from different areas were young, plenty of the Indonesian BC cases were admission to hospital in a late stage (TNM III-IV). Western style of life influences on diet, cooking, breast feeding, smoking, etc. Recent studies on bimolecular sciences gave so much hopes on a large scope of human being-non human being, though there were also some threatenings and confusions. On Pathology Molecular, there were so many bimolecular techniques approached to search what was the exactly happening in cellular level of some diseases; so do on carcinogenesis. Searching intracellular abnormalities could be divided into: cellular membrane level, cytoplasmic level, nucleic membrane level, and intranucleus (DNA, RNA) level. Formerly, cytology and histopathology examination had only emphasized the morphological appearances of varied pathological lesions, included Cancer-BC. Recently there were new techniques worldwide well established, well known. Which one we will choose for BC? Benefit?
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PMID:The plausibility and promptness of some pathological aspects of breast cancer. "DHARMAIS" NCCH. 1089 87

The proper staging of colorectal cancer was discussed with emphasis on the most relevant pathological parameters. Standard staging classifications i.e. Dukes', Astler-Coller's and international TNM classifications are defined by a few basic parameters, namely local invasion and lymph node metastasis, along with the histological grade of differentiation. Advances in diagnosis and treatment and modern aspects of tumor biology introduced other prognostic factors regarding proliferative activity of tumor, its local and systemic effects, host defense mechanisms and metastatic potential. Independent prognostic significance was shown and/or new criteria recommended for: resection margin and peritoneal involvement, vascular invasion, tumoral mucin production activity, presence of extranodal (micro) metastasis, extent of presented (extra) mural tumor spread, peritumoral lymphocytic infiltration, character of tumoral invasive margin and presence of peritumoral Crohn's-like lymphoid reaction. The se pathological parameters, discussed in detail, were partly contained in new revision of TNM or other classifications, not widely accepted, such as Jass', Japanese JSCCR, British UKCCCR classification, or new prognostic categories proposed by Harrison and coworkers. Our own first experiences and primary results showed variable agreement most of the mentioned parameters with special respect to reproducibility of Harrison's new prognostic categories. Many newly developed methods and novel tumor markers with some predictive values on clinical outcome are recently recognized, still uncertain for routine clinical usage. We reviewed in brief most important and/or most studied pathobiological predictors, such as: DNA ploidy, markers of proliferative activity, expression of tumor-specific and tumor-associated antigens or receptors. Among many of hereditary and genetic markers we stressed the importance of RER phenotype, mutations of tumor suppressor genes and some oncogenes, allelic loss of 18q, 17p and other chromosomal alleles as prognostic and screening tools or therapeutic targets. In conclusion, more new insights in carcinogenesis and new therapeutic agents will require new classification systems, never considered as definitive.
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PMID:[New prognostic parameters and categories of colorectal carcinoma--correlation with standards]. 1095 90


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