Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476089 (endometrial cancer)
11,379 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carboplatin is the one platinum analogue that has received widespread clinical testing both in cancers that are normally targets for cisplatin and in others. It was introduced in 1981 because of its lesser toxicity and equivalent biochemical selectivity and antitumor spectrum relative to cisplatin in preclinical systems. Clinical studies have generally confirmed these expectations and given rise to interesting prospects in current cancer therapeutics. Carboplatin is as effective as cisplatin in ovarian cancer and considerably less toxic. Replacement of cisplatin by carboplatin seems likely in a number of other diseases where cisplatin has played a major role, especially if ongoing phase III studies confirm the regimens are equivalent. Carboplatin may also complement cisplatin's role by its innovative integration into treatment strategies, and by use of it as additional treatment when cisplatin's nonhematologic toxicities are prohibitive. Finally, although it is not likely to possess a different therapeutic spectrum than cisplatin, carboplatin appears to be extending the indications for platinum compounds to new areas such as acute leukemia, endometrial cancer, and breast cancer. In the latter, use of autologous bone marrow reconstitution permits the dose intensity needed for promising therapeutic results. Carboplatin has become the experimental platinum analogue of choice in a wide range of new clinical situations and in combinations with other modalities.
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PMID:Overview of carboplatin: replacing, complementing, and extending the therapeutic horizons of cisplatin. 265 99

This study was carried out to evaluate the effects of neoplastic diseases like carcinoma of the cervix and endometrial carcinoma, and was based on dermatoglyphic traits and their indices of intraindividual diversity (Div), fluctuating asymmetry (FIA) and directional asymmetry (DA). The results were compared with control groups of women and men, whose data have been detailed in our previous publications (Kobyliansky et al., 1999 a-d), and with analogous data of additional cancer groups available in the literature, like acute leukemia, bronchial cancer and breast cancer. The general aims of the study were as follows: (a) to obtain a dermatoglyphic characterization of discrete and quantitative traits and their Div, DA, FIA values in cancer patients, compared to healthy control groups, both female and male; (b) to test the hypothesis that in cancer patients there is an increased level of FIA as a result of an impaired developmental homeostasis; (c) to explore the possibility of using DT (dermatoglyphic traits) data of CW (women with cancer) to predict the probability of the appearance of cervical and endometrial carcinoma in apparently healthy females at a young age. The sample consisted of 94 Israeli-Jewish women of various groups, of which 54 had endometrial carcinoma and 40 had cervical carcinoma. The prints were collected in the Tel-Hashomer Hospital. The control group was a sample of 874 healthy subjects, half of them male and the other female, all from Jewish communities of European extractions (50%) as well as from Africa (50%). All controls were adults (over 18 years of age). Interpretation of prints was performed according to Cummins & Midlo (1961) and Penrose (1968) and included identification of patterns, ridge counts and the measurement of distances and angles in the palms, 79 DT for every individual were assessed. Significant differences were found for some of the studied traits between cancer patients and their healthy control groups. We encountered merely a low sexual dimorphism between the CW and the control males as compared to that between control males and females (with significant differences in 18% of the quantitative traits vs 64% in the control). The indices of diversity and asymmetry proved more suitable for discrimination, yielding the highest discrimination level between CW and control females. This finding suggested other data in the present study which points to a similarity between CW and control males.
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PMID:Relationship between genetic anomalies of different levels and deviations in dermatoglyphic traits. Part 7: Dermatoglyphic peculiarities of females with cervical and endometrial carcinoma. 1137 69

The genes TSC1 and TSC2, encoding hamartin and tuberin, respectively, have been shown to be involved in the development of the autosomal dominantly inherited tumor syndrome tuberous sclerosis (TSC). However, inactivation of these genes has also been demonstrated to be associated with sporadic bladder cancer, ovarian and gall bladder carcinoma, non-small-cell carcinoma of the lung, breast cancer, pancreatic cancer, astrocytoma, xanthoastrocytoma, ependymomas, oral squamous cell carcinoma and endometrial cancer. The hamartin/tuberin protein complex plays a central role in the regulation of the mammalian target of rapamycin (mTOR) signalling network. A wide variety of components of the mTOR cascade have been demonstrated to be involved in many different human cancers. Mutations in several mTOR pathway component genes are known to cause specific monogenic human genetic diseases and this signalling cascade has been shown to be of relevance for Alzheimer's disease, type 2 diabetes, obesity and hypertrophy. Consequently, e.g. clinical trials for the treatment with rapamycin, a negative regulator of mTOR, of hamartomas in TSC have already been initiated. Now the first evidence is provided for an involvement of the TSC genes in acute leukemia.
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PMID:New insights into the role of the tuberous sclerosis genes in leukemia. 1925 Jun 71

BACKGROUND Syncytin-1, a cell membrane-localizing fusogen, is abnormally expressed in several cancers, including endometrial cancer, breast cancer, and leukemia. Although abnormal syncytin-1 expression has been detected in two-thirds of leukemia blood samples, its expression profile in acute leukemia patients has not yet been analyzed. MATERIAL AND METHODS Bone marrow samples from 50 acute myelogenous leukemia (AML) cases and 14 B-cell acute lymphocytic leukemia (B-cell ALL) patients were subjected to flow cytometry to assess leukocyte type distributions and leukocytic syncytin-1 surface expression. RT-PCR was applied to assess leukocytic syncytin-1 mRNA expression. Statistical analysis was applied to compare syncytin-1 expression between AML and B-cell ALL patients across blasts, granulocytes, lymphocytes, and monocytes as well as to determine clinical factors statistically associated with changes in syncytin-1 expression. RESULTS The leukocyte type distributions of the AML and B-cell ALL cohorts highly overlapped, with an observable difference in blast distribution between the 2 cohorts. The AML cohort displayed significantly greater syncytin-1 surface and mRNA expression (p<0.05). Syncytin-1 surface and mRNA expression was significantly increased across all 4 leukocyte types (p<0.05). The percentage of syncytin-1-expressing blasts was significantly greater in AML patients (p<0.05), with blasts showing the largest fold-change in syncytin-1 expression (p<0.05). M5, M5a, and M5b AML patients displayed significantly higher syncytin-1 surface expression relative to all other AML French-American-British (FAB) classifications (p<0.05). CONCLUSIONS These findings suggest leukocytic syncytin-1 expression may play a role in the development and/or maintenance of the AML phenotype and the acute monocytic leukemia phenotype in particular.
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PMID:Upregulation of Leukocytic Syncytin-1 in Acute Myeloid Leukemia Patients. 2739 11