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

The spectrum of progestin therapy has changed and expanded during the last few years. 1. The drug-therapy of choice in endometriosis is the medication of progestins for at least six months, for instance ethinyl-testosterone. If a patient wants additional children the "more gentle" dydrogesterone should be considered. 2. In the treatment of dysmenorrhea combination pills should be given, sequentials should be avoided. In the case of incompatibility of estrogens or in danger of oversuppression syndrome dydrogesterone should be applicated. 3. Dysfunctional bleedings should lead to an intense search for their cause. The treatment consists in an estrogen-progestin combination for 9 days and in cyclic continuation of this therapy for at least a further three months. In the case of hemorrhagic diathesis progestin treatment should be continued. 4. Cyclic adequate progestins have proofed to be successful in handling of hirsutism. The choice of the preparation depends on the patient's wish for children. 5. The progestin test is still the first step in diagnosis of amenorrhea. 6. Progestin therapy is indicated in progressive endometrial carcinoma. Some medical centres treat carcinoma of the mamma successfully with progestins. 7. Nowadays fast and early hormonal pregnancy tests are available. The progestin-pregnancy-test is limited to cases of premenopause. 8. The so-called short luteum phase has received considerable attention as a possible cause of infertility. In these cases a substitutional therapy of progestins should follow. Clomiphene or HCG-therapy is advisable. In short luteum phase and premenstrual spottings potent progestins should be given. 9. High dosage of progestins are in common use in the treatment of abortus imminens. 10. Combination pills and sequentials are widely used, the possible methods of a pure progestin contraception are: minipills, three-month-injections, implanted silastic capsules with progestional compounds, progestin impregnated intrauterine devices, vaginal silastic rings impregnated with progestional compounds. 11. Carcinogenesis of progestins was not detectable. 12. Some progestins are teratogenic.
 ...
PMID:[Current status of gestagen administration. 2. Gestagen therapy in the area of reproduction]. 55 11

One of the difficulties in characterization of the oncogenes involved in thyroid carcinogenesis is the production of cell lines. Arising from a poorly differentiated thyroid papillary carcinoma we have established a cell line synthesizing the thyroglobulin and human chorionic gonadotropin (alpha and beta subunits) (HCG) hormones. These cells will allow research of the oncogenes involved or potentially involved in thyroid papillary carcinomas and evaluation of the role of the autocrine secretion of HCG.
 ...
PMID:[Description of cell line established from human thyroid papillary cancer and secreting human chorionic gonadotropin hormone]. 129 27

The expression of blood group-related and tumor-associated antigens was examined in pancreatic adenocarcinomas and in the normal pancreas of hamsters to determine if this expression correlated with the host blood group and/or stage of carcinogenicity, respectively. Pancreatic tumors were induced by 4 weekly treatments of hamsters with N-nitrosobis(2-oxopropyl)amine (BOP) and analyzed immunohistochemically during different stages of tumor progression with polyclonal antibodies (PoAbs) and monoclonal antibodies (MoAbs) against A, B, O and Lewis (Le) isoantigens, including X, Y and CA 19-9 monosialoganglioside (gastrointestinal cancer antigen, GICA), as well as with PoAbs detecting human carcinoembryonic antigen (CEA), alpha-fetoprotein (AFP) and the beta-subunit of human chronic gonadotropin (beta-HCG). The red blood cells of both control and tumor-bearing hamsters expressed AB and Le(a+b+)-like blood group types, as detected by polyvalent antisera. However, none of the MoAbs reacted with the hamster red blood cells. In the pancreas, all PoAbs against blood group antigens reacted with hyperplastic ducts and ductules at very early stages of carcinogenesis, as well as with neoplastic lesions, but not with normal pancreatic cells, except for the acinar cells, which were stained with PoAb-B, PoAb-Lea and PoAb-Leb. None of the MoAbs showed any affinity for the normal pancreatic cells; however, they reacted to various degrees with induced hyperplastic and neoplastic tissue. Reactivities of several MoAbs with malignant cells were greater than those with hyperplastic lesions: MoAb-B was highly reactive with all induced lesions, MoAb-A less reactive, and MoAb-H and MoAb-Ley (which has 6 sugar chains) detected only some cancer cells. Neither of the two MoAb-Lex (with 5 carbohydrate chains) reacted with carcinoma cells, although they did bind to a few hyperplastic cells. Neither MoAb-Lea and MoAb CA 19-9, nor PoAbs against CEA, AFP and beta-HCG, reacted with any normal, hyperplastic or malignant cells. These results demonstrate the differential reactivity of these PoAbs and MoAbs in normal and malignant pancreatic tissue and show that blood group antigens, especially the B isoantigens, are specific markers for induced pancreatic duct tumors in hamsters.
 ...
PMID:Blood-group antigen expression during pancreatic cancer induction in hamsters. 331 27

The heterogeneity of gastrin-containing G cells present in human gastric mucosa has been examined immunohistochemically. Calcitonin gene-related peptide (CGRP), calcitonin and human chorionic gonadotropin (hCG)-immunoreactivity were detected in about 500, 20 and 10 cells pro 1,000 G cells, respectively, these findings supporting the "one cell, multi-hormone theory". Gastrin, calcitonin immunoreactive tumor cells were demonstrated in 13%, 3% of the antral adenocarcinomas and 17% and 10% of antral endocrine tumors, but they were not found in fundic adenocarcinomas and endocrine tumors. Cell hybridization between the tumor cell and the G-cell might be a possible mechanism for the occurrence of gastric and calcitonin in the gastric tumors. HCG-immunoreactive tumor cells were detected in 27% of antral adenocarcinomas, and in 24% of the fundic adenocarcinomas, and the production of hCG by gastric tumor cells might be based on the gene expression during carcinogenesis, regardless of the tumor localization.
 ...
PMID:[Heterogeneity of gastrin-containing G-cells and its expression in gastric adenocarcinomas and endocrine tumors]. 349 29

Comparative genomic hybridization was used to screen the DNA extracted from histologically defined tissue sections from consecutive stages of colorectal carcinogenesis for chromosomal aberrations. No aberrations were detected in normal epithelium (n = 14). Gain of chromosome 7 occurred as a single event in low-grade adenomas (n = 14). In high-grade adenomas (n = 12), and overrepresentation of chromosomes 7 and 20 was present in 30% of the cases analyzed. The transition to colon carcinomas (n = 16) was characterized by the emergence of multiple chromosomal aberrations. Chromosomes 1, 13, and 20 and chromosome arms 7p and 8q were frequently gained, whereas chromosome 4 and chromosome arms 8p and 18q were recurrently underrepresented. The same tissue sections that were used for CGH were analyzed by means of DNA-ploidy measurements and immunohistochemical staining to quantify proliferative activity and p21/WAF-1 and TP53 expression. We observed that crude aneuploidy and increased proliferative activity are early events in colorectal carcinogenesis, followed by TP53 overexpression and the acquisition of recurrent chromosomal gains and losses during the progression from high-grade adenomas to invasive carcinomas.
 ...
PMID:Comparative genomic hybridization reveals a specific pattern of chromosomal gains and losses during the genesis of colorectal tumors. 870 49

Breast cancer is more frequent in nulliparous women, while its incidence is significantly reduced by full-term pregnancy. The fact that the protection conferred by pregnancy is observed in women from different countries and ethnic groups, regardless of the endogenous incidence of this malignancy, indicates that this protection does not result from extrinsic factors specific to a particular environmental, genetic, or socioeconomic setting, but rather from an intrinsic effect of parity on the biology of the breast. Using an experimental system we have shown that treatment of young virgin rats with human chorionic gonadotropin (hCG), like full-term pregnancy, efficiently inhibits the initiation and progression of chemically induced mammary carcinomas. Treatment of young virgin rats with hCG induced a profuse lobular development of the mammary gland, reduced the proliferative activity of the mammary epithelium, and induced the synthesis of inhibin, a secreted protein with tumor-suppressor activity. HCG treatment also increased the expression of the programmed cell death (PCD) genes testosterone repressed prostate message 2 (TRPM2), interleukin 1-beta-converting enzyme (ICE), p53, c-myc, and bcl-XS, induced apoptosis, and downregulated cyclins. PCD genes were activated through a p53-dependent process, modulated by c-myc, and with partial dependence on the bcl-2 family-related genes. The possibility that this hormonal treatment activates known or new genes was tested by differential display technique. We have identified a series of new genes, hormone-induced-1 (HI-1) among them. The characterization of their functional role will contribute to clarify the mechanisms through which hCG inhibits the initiation and progression of mammary cancer. Of great significance was the observation that PCD genes remained activated even after lobular formations had regressed due to the cessation of hormone administration. We postulate that this mechanism plays a major role in the long-lasting protection exerted by hCG from chemically induced carcinogenesis, and might be also involved in the lifetime reduction in breast cancer risk induced in women by full-term pregnancy. The implications of these observations are two-fold: on one hand, they indicate that hCG, as pregnancy, may induce early genomic changes that control the progression of the differentiation pathway, and on the other, that these changes are permanently imprinted in the genome, regulating the long-lasting refractoriness to carcinogenesis. The permanence of these changes, in turn, makes them ideal surrogate markers of hCG effect in the evaluation of this hormone as a breast cancer preventive agent.
 ...
PMID:Hormonal approach to breast cancer prevention. 1076 7

The cell line U937, which has been used extensively for studies of myeloid differentiation, bears the t(10;11)(p13;q14) translocation which results in a fusion between the MLLT10 (myeloid/lymphoid or mixed-lineage leukemia [trithorax, Drosophila, homolog]; translocated to 10; alias AF10) gene and the Ap-3-like clathrin assembly protein, PICALM (Clathrin assembly lymphoid myeloid leukaemia). Apart from this translocation, very little is known about the other genetic alterations in this cell line that may represent significant events in disease progression. In this study, conventional G-banding, CGH and M-FISH have been used to characterise fully all of the cytogenetic alterations present in the U937 cell line. M-FISH analysis confirmed the presence of the t(10;11) and an apparently normal copy of both chromosomes 10 and 11. A t(1;5) translocation was observed as well as several unbalanced rearrangements. CGH detected amplifications resulting from duplications of 2q, 6p and 13q. These changes could result in fusion gene products involved in carcinogenesis or the positions of putative oncogenes and tumour suppressor genes. A good correlation between conventional G-banding, CGH and M-FISH was observed.
 ...
PMID:The characterisation of the lymphoma cell line U937, using comparative genomic hybridisation and multi-plex FISH. 1170 46

Rat is widely used in biomedical and pharmaceutical research but its genome has been significantly less studied than that of the mouse. This represents a major limitation for studying cytogenetic and molecular mechanisms in the rat model. As Muridae species underwent an intense chromosome evolution it is not possible to directly transpose knowledge of the mouse genome to that of the rat. For establishing a comparative karyotype between rat and mouse, painting probes of both species were prepared by PARM-PCR (Priming Authorizing Random Mismatches PCR) from a low copy number of sorted chromosomes, the mouse and rat specific painting probes being then hybridized on rat and mouse metaphases, respectively. The availability of rodent species chromosome painting probes as well as the information obtained by the comparative karyotype and comparative gene mapping data are of great interest to improve knowledge on species evolution but also to better understand carcinogenesis process, as illustrated by our data concerning the cytogenetic characterization of radon-induced rat lung tumors. Detailed methods for obtaining painting probes by PARM-PCR from sorted mouse and rat chromosomes and for their hybridization in homologous or heterologous conditions are described. Usefulness of chromosome painting is illustrated by the characterization of chromosomal abnormalities in a radon-induced rat lung tumor. Advantages and limitations of this technique as compared to classical cytogenetics, FISH and CGH are discussed.
 ...
PMID:Comparative karyotype using bidirectional chromosome painting: how and why? 1174 Nov 54

Secretion of human chorionic gonadotropin (hCG) during pregnancy induces differentiation of the mammary gland, thereby making breast tissue less susceptible to carcinogenesis. HCG binds to specific hCG receptors on mammary epithelial cells inducing changes in gene expression that can inhibit cell proliferation and, therefore, interfere with tumorigenesis. Since breast cancer cells also contain a relatively high level of the hCG receptor, hCG has potential as a therapeutic agent. We postulated that hCG might also enhance the radiosensitivity of breast cancer cells and, therefore, be useful as an adjunctive therapy. In the present study, MCF-7 breast cancer cells grown in cell culture were treated with hCG (0.2-5 IU/ml) for 24 h prior to exposing the cells to 0 Gy, 3 Gy, 4 Gy, or 5 Gy of radiation. Following irradiation, the MCF-7 cells were incubated either in the presence or absence of hCG. Cell survival was monitored with an MTT assay 1 day, 4 days, and 7 days after irradiation. All of the concentrations of hCG tested enhanced radiosensitivity of MCF-7 cells. The maximum enhancement occurred with MCF-7 cells that had been exposed to 2 IU/ml of hCG for at least 24 h prior to irradiation with 4 Gy. The use of higher concentrations of hCG or a higher dose of radiation did not increase the enhancement effect. Treatment of MCF-7 cells with hCG for only 24 h was sufficient to achieve the maximum effect. However, maintaining the cells in hCG beyond 24 h increased the effectiveness of the lowest hCG concentration. Using a linear-quadratic equation to analyze the data, we determined that the use of hCG would result in an 8-10% reduction in MCF-7 cell survival at a dose of 2 Gy, a typical dose used in conventional cancer therapy.
 ...
PMID:Enhancement of radiosensitivity of the MCF-7 breast cancer cell line with human chorionic gonadotropin. 1200 Feb 19

The oncogenic HPVs immortalize primary genital keratinocytes in vitro and there is evidence that such lines represent suitable models to examine HPV-induced carcinogenesis. Early in vivo studies and more recent CGH analyses have revealed amplification of chromosome 5p in advanced stage carcinoma of the uterine cervix (CaCx). In the present study, a panel of established CaCx-derived cell lines were analysed by M-FISH to identify recurrent karyotypic abnormalities. Amplification of 5p was observed in 11 of 13 CaCx cell lines harbouring HR (high-risk) HPV. The region of 5p undergoing amplification was confirmed using human band-specific paints. The F-box protein Skp2 is present at 5p13 and its protein is present at increased levels in many cancers of an advanced stage. The HPV16-harbouring cell line W12 shows progressive morphological abnormality with in vitro passage, culminating in an invasive phenotype. The expression of Skp2 at different stages of this progression was investigated utilizing Western blot and TaqMan quantitative PCR. At medium to late passage, gain of 5p as an isochromosome was observed. Increased expression of Skp2 and a reduction in the expression of its target p27 correlated with increasing passage in this line.
 ...
PMID:Amplification of chromosome 5p correlates with increased expression of Skp2 in HPV-immortalized keratinocytes. 1271 29


1 2 3 4 5 Next >>