UMLS:C0596263 - FACTA Search

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Query: UMLS:C0596263 (carcinogenesis)
64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary carcinomas are rarely encountered in the laryngeal ventricle of Morgagni. They are classified into the subgroup of supraglottic laryngeal carcinoma in the TNM classification system of malignant tumors. However, detailed investigations have not hitherto been made on the possible occurrence of carcinomas in this region of the larynx. To find out whether the laryngeal ventricle could be the site of carcinogenesis, the author examined squamous metaplasia in the mucosal epithelium of 60 human laryngeal ventricles which were taken from 38 larynges removed operatively from patients with laryngeal carcinoma (14 cases), hypopharyngeal carcinoma (20 cases), carcinoma of the upper esophagus (two cases), tracheal carcinoma (one case) or thyroid carcinoma (one case). The patients consisted of 31 males and 7 females, with an age distribution of 44 to 80, average 62.7. The laryngeal ventricles were selected for investigation only when they did not show any carcinomatous invasion macroscopically. Macroscopic observations were performed after gross staining with pyronin Y, which permits differentiation of squamous metaplasia from respiratory epithelia. Tissues were embedded in paraffin, sectioned serially and stained with hematoxylin and eosin. The clinical records of the patients were also made. The results are summarized as follows: 1. Squamous metaplasia of the stratified ciliated epithelium was found in 38 out of 60 specimens (63%) of the laryngeal ventricles examined. 2. The metaplasia seemed to be precipitated by smoking or exposure to radiation, along with aging. 3. The incidence and extent of metaplasia of the ventricular mucosa depended on the disease entity which had necessitated total laryngectomy, and the metaplasia was most prominent in cases with the supraglottic type of laryngeal carcinoma. 4. The metaplastic epithelium was occasionally associated with hyperplasia or dysplasia of the epithelium. 5. Microinvasive carcinoma was found in one laryngeal ventricle with severe metaplasia. These findings suggested a possible de novo carcinogenic process in the laryngeal ventricle through squamous metaplasia of the respiratory epithelium. From this observation, the author proposes to call carcinoma of this region of the larynx the ventricular type of laryngeal carcinoma.
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PMID:[Squamous metaplasia of the mucosa of the human laryngeal ventricle: a clinicopathological study with reference to the possibility of de novo carcinogenesis]. 156 15

In a case-referent study on the possible role of selenium in human mammary carcinogenesis, serum selenium was found to be 79 +/- 12 micrograms/l in 66 cases and 81 +/- 12 micrograms/l in 93 referents. An internal trend in serum selenium was observed among cases (TNM stage I 81 +/- 11 micrograms/l and TNM stage II 76 +/- 13 micrograms selenium/l), indicating disease-mediated changes. The evaluation of selenium as a risk indicator in human breast cancer was therefore restricted to TNM stage I patients (n = 36). Multiple logistic regression analyses including variables associated with selenium levels revealed no association between selenium levels and breast cancer risk.
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PMID:Selenium in human mammary carcinogenesis: a case-referent study. 184 79

We have reviewed retrospectively the records of 157 patients, less than or equal to 30 years of age with nasopharyngeal carcinoma (NPC) from 218 such cases identified in the tumor registry files of three major teaching hospitals in Taipei, Taiwan. These cases were diagnosed between 1 January 1982 and 31 December 1985, with a minimum follow-up of 2 years. The average age was 25, with a male/female ratio of 1.67. The TNM (tumor size, nodes, metastases) classification of 127 patients showed T1, 22%; T2, 33.1%; T3, 23.6%; T4, 21.3%; N0, 26%; N1, 16.5%; N2, 27.6%; N3, 30%; and M1, 13.4%. Antibody titer to Epstein-Barr virus capsular antigen (EBVCA) were elevated in 45 of 48 patients tested. Of the 29 patients who had hepatitis B (HB) viral survey done 34.5% were positive for HB surface antigen (HBsAg). Of 13 patients with elevated EBVCA antibody who were also tested for HB, six were HBsAg carrier. Actuarial survival rates of 2 and 3 years are 70 and 62%, respectively, among the 90 patients who were followed regularly or to death. HBsAg carriers and patients with M1 disease had a shorter survival time. We concluded that patients less than 30 years of age seemed to have an increased incidence of NPC, compared to that in an earlier report. Our patients frequently presented with advanced stage and poor prognosis. The high rate of HB carrier raises the possibility that HBV may play a role in the carcinogenesis and tumor growth in some NPC patients. Future prospective studies are needed.
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PMID:Nasopharyngeal carcinoma in young patients. 184 56

A study was undertaken to determine whether the variation in the increased expression of three oncogenes (Ha-ras, Ki-ras and myc) could be correlated with various clinicopathological parameters of squamous cell carcinoma (SCC) of the head and neck region. No correlation was found with sex, age, site of primary tumour, level of differentiation of the tumour, previous X-ray treatment, or fate. The one exception was myc expression with TNM staging of SCC. A significant increase was found for myc expression in TNM Stage III and IV as compared to the combined stages of I and II. Elevated expression of Ha-ras, Ki-ras and myc oncogenes was found in pleomorphic salivary adenoma (PSA), but at a lower level than SCC. It is proposed that in a percentage of cases the elevated expression of these oncogenes in PSA corresponds to a relatively early event in the multistep process of carcinogenesis.
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PMID:Clinical relevance of oncogene expression in head and neck tumours. 301 19

Alterations in the p53 tumor suppressor gene are the most frequent genetic abnormalities in human cancers. The p53 protein is present in normal cells, and is assumed to induce G1 arrest or apoptosis in the presence of DNA lesion. The mutant protein lacks this property. Squamous cell carcinomas of the head and neck (SCCHN) are related to carcinogens in tobacco and alcohol, and provide a good model of multiple-step carcinogenesis in association with DNA damage and p53-related tumorigenesis. Stabilization of the mutant p53 protein allows immunohistochemical analyses (IHC) to be routinely used to demonstrate the mutant p53 protein in tissue samples, whereas normal p53 protein is undetectable. Ninety-nine squamous cell carcinomas, 8 in situ carcinomas, 31 preneoplastic lesions and 79 normal carcinogen-exposed mucosas of the head and neck from a total of 107 patients were examined for the expression of p53 tumor suppressor gene protein. Samples were collected before treatment, and stained with p53 specific mono- and polyclonal antibodies (DO-7, Pab 1801 and 240, CM1) using an indirect immunoperoxidase technique. Proliferating cell nuclear antigen (PCNA) provided semiquantitative estimates of proliferation. The main localizations were the pharynx (64/107) and the larynx (21/107). Positive IHC detection of p53 was observed in 9% of normal-appearing carcinogen-exposed mucosas, 37% of hyperplasias, 68% of dysplasias, 75% of in situ carcinomas, and 56/99 (56.5%) of primary tumor samples. Mucosas from 15 control patients under 10 years of age were negative. There was no correlation between p53 IHC and localization, differentiation or TNM staging.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunohistochemical detection of p53 protein in preneoplastic lesions and squamous cell carcinoma of the head and neck. 761 Aug 36

Mutational activation and overexpression of the family of ras proto-oncogenes have been associated with many human tumors. The role of mutations of H-ras, K-ras, and N-ras, as well as expression of the respective protein products (p21s) in normal mucosa, dysplastic mucosa, and squamous cell carcinomas (SCCs) of the head and neck has not been fully described. In our study, 51 tumors (40 paraffin embedded and 11 fresh frozen) were examined to determine if mutational activation of ras is an important molecular event in head and neck SCC. Analyses of codons 12, 13, and 61 of H-ras, K-ras, and N-ras revealed no mutations, suggesting that mutational activation of ras is not important in the majority of head and neck SCCs. Immunocytochemistry (ICC) was used to define the expression of H-ras, K-ras, and N-ras in normal mucosa, dysplastic mucosa, and SCC of the head and neck and to determine if expression of ras family members correlated with early or late events in the development of SCC. Expression of p21N-ras in nine samples of histologically normal head and neck mucosa revealed moderate staining in the basal proliferative layers with progressively less staining as cells matured. The most superficial layers of normal mucosa failed to express p21N-ras. A low level of p21H-ras was expressed in all layers of normal mucosa while K-ras was not expressed. ICC of SCC tumor sections revealed cytoplasmic expression of N-ras in nine of nine tumors, H-ras in five of nine tumors, and K-ras in one of nine tumors. Expression of H-ras, K-ras, and N-ras in head and neck SCC was not related to histologic differentiation or TNM staging; however, p21N-ras was overexpressed in seven of nine tumors. Furthermore, the pattern of N-ras expression in dysplastic lesions revealed expression in all layers of the mucosa in contrast to normal mucosa, which expresses p21N-ras primarily in the basal proliferative layer. The change in p21N-ras expression pattern in dysplastic mucosa and its overexpression in the majority of tumors suggest that loss of control of N-ras expression may be an early step in carcinogenesis of head and neck SCC.
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PMID:ras mutations and expression in head and neck squamous cell carcinomas. 796 62

Carcinogenesis in the human colon is associated with a marked increase of urokinase type plasminogen activator and a decrease of tissue type plasminogen activator. This study was performed to determine the concentrations of urokinase type plasminogen activator and tissue type plasminogen activator in normal tissue and carcinomas along the upper part of the gastrointestinal tract. Activity and antigen levels of both activators were determined in homogenates of endoscopically obtained biopsies from normal and carcinomatous tissues. Although the concentrations of tissue type plasminogen activator and urokinase type plasminogen activator in normal squamous epithelium of the oesophagus were low compared with those in columnar epithelium from the stomach, the urokinase type plasminogen activator/tissue type plasminogen activator antigen ratio of the different locations showed hardly any difference. Significant but heterogeneous increases were found in urokinase type plasminogen activator concentrations of biopsy specimens originating from carcinomas of both epithelial cell types. A decrease in tissue type plasminogen activator concentrations, as found in human colon carcinomas, could only be shown in carcinomas of columnar epithelium origin but not in squamous cell carcinomas of the oesophagus. The increase of urokinase type plasminogen activator and urokinase type plasminogen activator/tissue type plasminogen activator antigen ratio and the decrease of tissue type plasminogen activator in the carcinomas did not show a significant correlation with known prognostic determinants as differentiation grade, TNM classification, intestinal metaplasia, inflammation, and ulceration. The heterogeneous increase of urokinase type plasminogen activator in oesophageal and stomach carcinomas, together with the recently described association of urokinase type plasminogen activator in tissue extracts of breast carcinomas with aggressiveness and prognosis, may be relevance to prognostic studies, may be of relevance to prognostic studies in oesophageal and gastric cancer.
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PMID:Plasminogen activators in normal tissue and carcinomas of the human oesophagus and stomach. 843 57

In addition to the commonly used pathologic staging systems such as the TNM classification, the grading and demographic features have been reported to affect survival following surgical extirpation of renal cell carcinoma (RCC). These features, especially the pathologic stage, are well established as prognostic factors. However, several cellular and molecular variables, although potentially important in the ultimate outcome, are not taken into consideration by these criteria. Thus patients with different prognoses may be classified as belonging to the same stages. Attempts are now made to use cytogenetic and molecular findings to predict long-term survival of RCC patients. Chromosome 16 q and 14 q aberrations may play an important role in the future by identifying the high-risk groups of patients with papillary and nonpapillary RCC, resp. In nonpapillary RCC, mutations of the von Hippel-Lindau gene have been implicated as the initial step of carcinogenesis. However, the subsequent steps remain to be elucidated and the search for genetic markers associated with tumor progression is under way. The distinction between patients with high and low risk of progression will become increasingly important as more effective adjuvant therapies are available.
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PMID:[Traditional and future criteria for progression in renal cell carcinoma. Molecular biology and clinical aspects]. 871 34

Genotoxical agents as PAH, nitrosamines, aromatic amines located in tobacco smoke are responsible for disorders of structure and function of DNA chromosomes, proteins and also initiation of carcinogenesis. DNA adducts are recognized as measure of the biological effective dose of exposure to environmental genotoxicant. So far most studies on DNA adducts after human exposure to tobacco smoke have ben carried out on white blood cells, lungs and oral cavities tissue. The aim of this work was estimation of relationship between state of neoplastic disease (TNM system) and number of aromatic DNA adducts. The subject were 37 patients with primary larynx tumor. In every case histopathological investigation revealed squamous cell carcinoma. There were 33 total and 4 partial laryngectomies performed. From tumour and nontumour larynx tissue DNA was isolated. Analysis of DNA adducts was performed by the 32P-postlabelling method. The results were characterized by individual differentiation. The highest level of DNA adducts was found in larynx tumour cells. In case of strong smokers (30-40 cigarettes per day) the level of aromatic adducts was higher then in non- or ex-smokers. In both tissues (tumour and non-tumour) the highest level of aromatic adducts was in T3 stage, the lowes in cause of T2 stage. In tissues with T4 stage the level of DNA adducts was intermediate. One has been observed decrease tendency in level of DNA adducts which is connected with increase of TNM stage.
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PMID:[Estimation of aromatic DNA adduct levels in laryngeal tumors in relation to cancer staging]. 871 63

The p53 gene is known as an anti-oncogene that manifests its function by controlling the cell cycle and is responsible for apoptosis of cells with unrepaired DNA. An accelerated p53 protein synthesis is the first response of a cell following DNA damage. However, mutations of the p53 gene can disturb protein synthesis or may be responsible for synthesis of a changed protein unable to control the cell cycle. Laryngeal tissue specimens from 120 patients were tested by immunohistopathological staining to detect mutated wild-type p53 protein. It was found that p53-positive specimens correlated with TNM staging and histopathological grading. Another indication of entering the cell cycle and undertaking an active proliferation by laryngeal cells was shown by detection of proliferating cell nuclear antigen (PCNA) and Ki67 nuclear antigen, which appeared in proliferating cells (late G1, S-G2 and M phase), but was absent in resting cells. Scoring of the staining for p53 protein, PCNA and Ki67 correlated with each other. DNA from 40 specimens was then isolated, amplified by polymerase chain reaction and analysed by single-strand conformation polymorphism and DNA sequencing for mutation in the p53 gene. Fifteen DNA samples were found to be positive, while mutations were detected in exons 5-8 in 13 samples. The majority of mutations were found in tissue specimens from T3 and T4 tumors. A possible explanation is almost half was attributable to genotoxic effects of tobacco smoking. Changes in the p53 gene and its products may also reflect early changes in laryngeal carcinogenesis and be of prognostic value.
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PMID:Alteration of p53 gene structure and function in laryngeal squamous cell cancer. 906 48

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