Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor cell suspensions from 100 biopsies of squamous cell carcinomas of the cervix uteri were investigated by impulse cytophotometry (ICP) after staining with pepsin-ethidium bromide. We estimated the ploidy pattern by comparing the ICP curves with normal diploid material. The originally linearly classified curves were transformed in a logarithmical manner. We found 48 diploid populations and 42 polyploid populations, among them 19 tetraploid tumors. In these the 4c-peak was the highest. In 10 cases there were aneuploid stem lines, mainly lying between 2c and 4c; 2 curves had a hypertetraploid pattern. Helpful for interpretation of the whole curve is the introduction of an index: the "relative mean DNA-content" (DNA). In 15 diploid tumors we found a low proliferating rate, characterized by low 4c-peaks. For interpretation of polyploid cell cycles a completed nomenclature of cell cycle phases was introduced. Comparing our material with chromosome analyses in laterature we found more polyploid, e.g. tetraploid tumors. It can be assumed that the estimation of ploidy pattern solely by DNA measurements has another meaning than by chromosome analyses. The higher ploid peaks in DNA distribution curves (e.g. ICP-karyograms) represent not only true polyploid nuclei but also nuclei which are in a blocked premitotic resting phase (G2 for 4c; G'2 for 8c and so on). The ICP is a valuable method for estimating biological pecularities of tumor cell suspensions.
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PMID:Pulse cytophotometric investigations concerning ploidy and proliferation pattern of invasive squamous cell carcinomas of the cervix uteri. 90 6

It is shown that L-cystine-bis-(N,N-beta-chloroethyl)-hydrazide-hydro-bromide possesses strong (50-100%) inhibitory effect in vivo against myeloma P-8, carcinosarcoma Walker, lymphosarcoma Pliss, sarcoma Yoshida, sarcoma Jensen and sarcoma 180 in doses 5-12 mg/kg/day. No suppression of the growth of Ehrlich ascites tumor was observed. The acute toxicity (LD50) of this substance on mice and rats is 71 mg/kg and 47 mg/kg respectively.
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PMID:A new substance effective against transplantable tumors in vivo: L-cystine-bis-(N,N-beta-chloroethyl)-hydrazide. 90 41

Transfer RNA nucleotidyl transferase from Ehrlich tumor cells was inhibited by proflavine sulfate and ethidium bromide but not by actinomycin D, chromomycin, rifamycin SV, rifampin, daunomycin, or alpha-amanitin. Complete inhibition of nucleotidyl transferase activity was attained at a final concentration of 1 mmol/1 proflavine sulfate, while 2 mmol/1 ethidium bromide was required to completely inhibit the enzyme. CMP incorporation into tRNA was more sensitive to both proflavine sulfate and ethidium bromide than was AMP incorporation.
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PMID:Inhibition of transfer ribonucleic acid nucleotidyl transferase (EC 2.7.7.25) from Ehrlich tumor cells by proflavine sulfate and ethidium bromide. 94 58

A number of 2-chloromethyl and 2-bromomethyl derivatives of naphthoquinones, quinolinediones, and naphthazarins were designed and synthesized as potential bioreductive alkylating agents, and the antitumor activity of these compounds was assessed in mice bearing Sarcoma 180 ascites cells. The results indicated that, with the exception of 3-benzamido-2-chloromethyl-1,4-naphthoquinone, which was inactive, all newly synthesized naphthoquinones possessed strong antitumor activity against this neoplasm. 6,7-Bis(bromomethyl)quinoline-5,8-dione had moderate inhibitory activity against Sarcoma 180 at its optimal daily dosage level of 15 mg/kg. 3-Bromo-2-bromomethyl- and 3-bromo-2-chloromethylnaphthazarin produced a moderate extension of the life span of tumor-bearing mice; whereas, in contrast, 6,7-dimethyl analogs of these agents were inactive when employed in daily doses up to 40 mg/kg body weight.
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PMID:Potential bioreductive alkylating agents. 5. Antineoplastic activity of quinoline-5,8-diones, naphthazarins, and naphthoquinones. 115 13

2 Bromo-alpha-ergocryptine, a specific prolactin inhibitor, was administered to 9 patients suffering from galactorrhea-amenorrhea syndrome of varying aetiology. Plasma levels of FSH, LH, prolactin, total estrogens and progesterone were measured by radioimmunoassy before and after treatment initiation. Prior to treatment, plasma prolactin levels were in all cases supraphysiological. FSH and LH levels were, with the exception of one patient, in the low cyclic range. One patient had subnormal gonadotropin levels, presumably reflecting hypophyseal insufficiency following surgical removal of a pituitary adenoma. Mean plasma levels of total estrogens were in the lower normal range. Administration of CB 154 led in all cases to a reduction of plasma prolactin levels. In eight cases, galactorrhea was suppressed during the first month of treatment. Eight patients menstruated and seven ovulated as indicated by the basal body temperature (BBT) or plasma progesterone measurement. The postoperative hypophyseal tumor patient did not, with the exception of galactorrhea suppression, respond to treatment, presumably due to hypophyseal insufficiency. 2 patients conceived during the course of treatment. One patient, who developed galactorrhea-amenorrhea syndrome as a result of psychopharmacological drug administration received 7,5 mg/day CB 154. Prolactin secretion, as indicated by plasma levels, was inhibited but the inhibitation was much slower in onset than that exhibited by the other patients and this patient ovulated only after 5 months of treatment. Upon withdrawal of CB 154 therapy after 6 to 7 months, the patients redeveloped galactorrhea-amenorrhea syndrome, so that a definitive cure could not be demonstrated.
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PMID:Treatment of galactorrhea-amenorrhea syndrome with 2-Br-alpha-ergocryptin (CB 154). Clinical response and pattern of pituitary and steriod hormones before and during therapy. 117 26

8-Bromo-cAMP and substances elevating cAMP levels within cells, such as forskolin, cholera toxin, and Bordetella pertussis-invasive adenylate cyclase (BPAC), suppress the growth of cultured granulosa cells cotransfected by simian virus-40 (SV40) DNA and Ha-ras oncogene concomitantly with the induction of steroidogenesis and without affecting oncogene expression. We, therefore, tested the hypothesis that cAMP can modulate tumorigenesis and metastatic spread of these cells in vivo. The cotransfected cells induced rapid development of tumors when injected sc in nude mice. Tumor development was faster in less differentiated cotransfected cells originating from preantral ovarian follicles than in those obtained from highly differentiated transformed cells originating from preovulatory follicles. Cells transfected by SV40 DNA alone produced only slow-growing small tumors. Metastatic lesions of cotransfected cells were most abundant in lung and less frequent in ovaries, kidney, and spleen. No metastatic lesions were found in the liver. However, metastatic spread was dramatically suppressed when cotransfected cells injected into nude mice were pretreated with the invasive BPAC. In contrast, no suppression of metastases was observed when the cells were pretreated with 8-bromo-cAMP, forskolin, or cholera toxin. Removal of forskolin in cultured cotransfected cells yielded a rapid decrease in cAMP levels. In contrast, high levels of cAMP persist in cell cultures even several hours after 1-h pretreatment and subsequent removal of BPAC from the medium of culture cotransfected cells. It is suggested that the inhibitory effect of BPAC on the metastatic spread of these cells is due to prolonged elevation of cAMP in vivo. The newly established granulosa cell lines transformed by SV40 and the Ha-ras oncogene can serve as a model for further studies of cAMP modulation of carcinogenesis in ovarian malignancies.
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PMID:Adenosine 3',5'-monophosphate suppresses metastatic spread in nude mice of steroidogenic rat granulosa cells transformed by simian virus-40 and Ha-ras oncogene. 131 28

The clinical phenotype of Werner's syndrome (WS) includes short stature, premature cataracts, skin atrophy, osteoporosis, graying and loss of hair, neoplasia, diabetes mellitus, and arteriosclerosis. Cultured cells from patients with this autosomal recessive disorder exhibit chromosomal instability and a markedly reduced replicative lifespan and growth rate. To elucidate the cell cycle alterations associated with the growth deficit, we continuously labeled lymphoid cell lines from five WS patients and from four healthy adult controls with 5-bromodeoxyuridine. Bivariate Hoechst 33258/ethidium bromide flow cytometry revealed a 2.4-h prolongation in the minimal duration of the S phase of WS cells (P less than 0.005). Moreover, the fraction of proliferating cells irreversibly arrested in the S phase (5.4% vs 1.4% in controls) was significantly elevated in WS (P less than 0.001). Other cell cycle compartments were not significantly affected in WS cell lines. As a partial test of the hypothesis that the WS phenotype is due to a defect in DNA topoisomerase I (topo I) or DNA topoisomerase II (topo II) we exposed lymphoid cells from a healthy control to the topo I inhibitor camptothecin or to the topo II inhibitor 4'-(9-acridinylamino)methanesulfon-m-anisidine. The cell kinetic alterations elicited by these compounds differed from that exhibited by untreated WS patients. Thus, a primary defect in topo I or II is unlikely in WS. Our cell cycle results, however, provide important evidence that the biochemical genetic lesion is in fact expressed in lymphoblastoid cell lines, the most readily available cells from such subjects.
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PMID:Impaired S-phase transit of Werner syndrome cells expressed in lymphoblastoid cell lines. 132 51

We have used the polymerase chain reaction (PCR) to detect amplification of the MYCN oncogene in neuroblastoma cell lines and to distinguish primary tumors with a single copy from those with MYCN amplification using DNA extracted from frozen sections. Two primer pairs were used to co-amplify a 428-bp fragment of the MYCN oncogene along with a 268-bp fragment of the beta-globin gene (a single-copy reference standard). After 30 cycles of PCR, the products were resolved by agarose gel electrophoresis. MYCN gene amplification was identified by visual comparison of the relative intensities of MYCN and beta-globin PCR product bands on the ethidium bromide-stained gel. This semiquantitative approach, while inadequate for precise determination of copy number, provided a simple, rapid, nonisotopic method for differentiating tumors with MYCN amplification from those with a single copy. Seventy-four primary tumors were classified as amplified or nonamplified by semiquantitative PCR. Twenty-two of 23 tumors known to carry MYCN gene amplification by Southern analysis were correctly identified by PCR. The single false-negative result was due to a sampling error: DNA was extracted from a block of tissue containing small foci of tumor surrounded by normal tissue. Fifty-one of 51 tumors with a single copy of MYCN were also correctly identified by PCR. We conclude that semiquantitative PCR is a reliable, non-isotopic alternative to Southern blotting for detection of MYCN gene amplification that can be performed rapidly on DNA extracted from frozen sections.
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PMID:Rapid detection of MYCN gene amplification in neuroblastomas using the polymerase chain reaction. 134 70

Complementary DNA (cDNA) that codes for a major androgen-dependent secretory protein of rat coagulating gland and dorsal prostate, dorsal protein 1 (DP1), was isolated by molecular cloning. Recombinant DP1 cDNA clones were identified from a bacteriophage lambda gt11 rat coagulating gland expression library using an affinity purified polyclonal antibody. Amino acid sequence deduced from DNA contained sequences identical with several DP1 cyanogen bromide cleavage fragments. Northern blot hybridization of poly(A) RNA isolated from intact rat dorsal prostate and coagulating gland revealed a predominant messenger RNA (mRNA) species of approximately 3200 nucleotides. Tissue-specific expression of DP1 mRNA was indicated by the absence of DP1 mRNA in ventral prostate and other tissues of the rat. Expression of DP1 mRNA was androgen-dependent, decreasing approximately 80% 7 days after castration and increasing rapidly following androgen replacement. Southern blot analysis of restriction enzyme-digested rat DNA indicated that DP1 is encoded by a single gene and that no major genomic rearrangements accounted for its lack of expression in the dorsal prostate-derived rat Dunning tumor. Sequence comparisons revealed that rat prostate DP1 shares sequence identity with Factor XIIIa and tissue transglutaminase, including the active center, GQCWVF, indicating that DP1 is a member of the transglutaminase gene family.
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PMID:Molecular cloning of rat prostate transglutaminase complementary DNA. The major androgen-regulated protein DP1 of rat dorsal prostate and coagulating gland. 135 90

The human myeloid cell nuclear differentiation antigen (MNDA) is expressed specifically in cells of the granulocyte/monocyte lineage. The MNDA has been isolated by using a monoclonal antibody affinity matrix and reversed-phase high performance liquid chromatography. Its NH2-terminal sequence has been obtained, as well as additional sequence information derived from peptides produced by cyanogen bromide and SV8 protease cleavages. Meaningful similarities were observed in extended regions between the MNDA and the reported beta interferon-inducible proteins, 202 and 204, from Ehrlich ascites mouse tumor cells. An amphipathic, basic alpha-helical region, showing no similarity to the 202 and 204 proteins, exhibited close similarity to a region in the interferon response factor-2, a protein which binds the interferon stimulated response element. The relatively high number of S(T)PXX motifs present in the partial amino acid sequence of the MNDA, described herein, suggests that the MNDA binds DNA and is a transcription factor.
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PMID:Characterization of the human myeloid cell nuclear differentiation antigen: relationship to interferon-inducible proteins. 137 1


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