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1941. [Amplification of myc-specific sequences in human colonic cancer].
作者: O M Serova.;T V Shpatar'.;S N Fedorov.;P G Kniazev.;L B Novikov.
来源: Vopr Onkol. 1986年32卷8期89-92页
DNA samples obtained from tumors and adjacent mucosa of the large bowel of a patient with large bowel multiple neoplasia were examined after Southern. The procedure established amplification of v-myc oncogene-related DNA sequences in 1 out of 5 tumors tested. Restriction fragments of amplified myc-specific sequences and matching c-myc and N-myc loci of the human genome differed in size.
1942. [Assessment of the risk of developing ovarian cancer based on individual and family anamnestic data].
A study of individual and family histories of 200 ovarian cancer patients and 200 healthy controls was concerned with evaluation of 274 factors of risk. It yielded 36 most informative ones. An 80% credibility of screening results was demonstrated when a combination of characteristics was used. Decision rule is recommended as a test for formation of a group at high risk.
1943. [Comparative evaluation of the cytogenetic effect of cyclophosphamide on lymphosarcoma cells and the bone marrow of intact and irradiated rats].
The paper deals with a comparative evaluation of cytogenetic action of cyclophosphamide on tumor and bone marrow cells in intact and radiation--exposed Pliss' lymphosarcoma-bearing mice. In both study groups, the level of cells with drug--induced chromosome damage was shown to be higher in tumor. No significant difference was established between the 2 groups in the effect of cyclophosphamide on similar tissues.
1944. [A case of Lewandowski-Lutz's epidermodysplasia verruciformis].
作者: Iu S Butov.;N G Korotkiĭ.;V Iu Udzhukhu.;S N Golovin.;Iu I Dolinskiĭ.
来源: Vestn Dermatol Venerol. 1986年4期34-6页 1946. [Type of acetylation in children with Hodgkin's disease].
Examination of a healthy European population showed 60% to be "slow" acetylators and 40% "rapid" ones. A similar distribution was established in pediatric controls. Among children with Hodgkin's disease, there were 4.1 times more slow acetylators. N-acetyltransferase activity was found to increase with tumor advancement. Conversion of acetylation pattern was observed in pediatric patients with Hodgkin's disease.
1947. [Mechanism of the leukemogenic action of ionizing radiation].1949. [Cellular and molecular mechanisms of radiation carcinogenesis].1950. [Specific chromosomal changes (aberrations)--supplementary marker of malignant degeneration in oncomorphologic studies].
The paper deals with some methods studying chromosome set in tumour cells. The latest data on tumour chromosome aberrations are reported. The latter are subdivided by the authors into non-specific and specific, characteristic only of certain variants of tumour differentiation, and are of diagnostic significance. The authors put forward further tasks of combined oncomorphologic and cytogenetic studies of specific chromosome aberrations as a valuable marker for the diagnosis of malignancy.
1951. [Clinical stages of myelocytic leukemia in children].1952. [A case of familial neurofibromatosis].1953. [Transactivation of the long terminal repeat promoter of the bovine leukemia virus in infected cells].
作者: V V Bychko.;P P Pumpen.;O N Aprelikova.;V M Mikhaĭlov.;N V Tomilin.
来源: Dokl Akad Nauk SSSR. 1986年286卷1期221-3页 1954. [Polynucleotide sequences in the DNA from leukemic cells forming RNAse-resistant complexes with polyuridylic acid].
RNAase-resistant complexes of poly(U): poly (dA) were obtained by hybridization of [3H] poly (U) with cellular DNA. Depending on the mode by hybrids treatment with RNAase, two types of (dA)-sites i. el, dA and poly (dA) sites with different homogeneity were identified. The amount of these sequences in the DNA isolated from normal cells of intact animals and from several types of leukemic cells was determined. Full identity of the dA-sites in normal tissue DNAs of the same animals and a statistically significant increase in their content in leukemic cells were demonstrated. Differences between DNAs of normal and leukemic cells vary widely, depending on the leukemia type.
1955. [Relation between hemoglobins S and C and protein products of various oncogenes].1956. [Characteristic features of protein synthesis in the extracellular matrix during tumor growth].
Changes in the biosynthesis of basic extracellular proteins (e.g., collagen proteins, fibronectins, proteoglycans) in the course of neoplastic growth are reviewed. Some peculiarities of quantitative changes in the biosynthesis and modifications of the primary structure of the above macromolecules are discussed in terms of neoplastic cell differentiation. The main emphasis is laid on the mechanisms underlying the disturbances in the biosynthetic activity of extracellular matrix proteins in neoplastic cells at different steps of protein synthesis and extracellular degradation of protein molecules.
1957. [Type of inheritance and probability of having a child with the sclerocystic ovary syndrome].1958. [Structural-functional state of the genetic apparatus of blood leukocytes in breast cancer patients during cytostatic therapy].
Functional state of genetic apparatus was studied in leukocytes of patients with carcinoma of mammary gland at the III-IV stage by measuring incorporation of 3H-thymidine into DNA as well as by monitoring impairment of DNA structure using immunofluorescent procedure and antibodies to DNA. The studies were carried out before, in the middle period and at the end of the antitumour chemotherapy. The structure-functional state of genetic apparatus was injured in circulating leukocytes in blood of oncological patients.
1959. [Radiation carcinogenesis as a general biological problem].
The initial steps of radiation carcinogenesis have been briefly surveyed. Actuality of their further research is shown on the molecular level. There is a discussion going on about the close connection of such research with basic directions in the development of biology, such as: genome destabilization, gene repression and activation, regulation of growth activity factors, the role of biomembranes in the processes, and synergism in the action of factors on live systems.
1960. [Initiation of the mouse sarcoma virus oncogene v-K-ras during the chemical treatment of proto-oncogene C-ras].
On the basis of the results obtained in the laboratories of Weinberg, Barbacid et al. describing the responsibility of one or another mutation in one of coding triplets of the ras family gene both for chemical and viral cancerogenesis, we draw the conclusion that it is impossible to distinguish these two causes of cancer appearance. It is shown that the cause of mice viral sarcoma v-K ras development from the cellular protooncogene C-ras may consist in the chemical reaction of one of coding triplet nucleotides with cancerogenic substance.
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