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Biomedical subjects

P G Kniazev

Publications and source records attributed to P G Kniazev.

At least 19 recordsLinked to original sources
PubMed1997

[Molecular genetics of human tumors].

The survey dedicated to the 70th anniversary of the Prof. N. N. Petrov Research Institute of Oncology, St. Petersburg, gives a basic idea of molecular pathogenesis of tumor in humans, particular emphasis being placed on the clinical and applied aspects of molecular oncology. The survey is intended for a wide audience including doctors, professors and undergraduate students majoring in medicine and biology.

Blotting, Southern↗
PubMed1996

[Correlation between int-2 oncogene amplification and increased tumor size in breast cancer].

Amplification of the int-2 oncogene was observed in 10 out of 78 (13%) samples of DNA isolated from cells of primary breast tumor. A clinico-morphological examination established a correlation between this molecular-genetical anomaly and tumor size: gene amplification was detected in 1 out 34 (3%) cases of breast tumor under 2 cm and in 9 out 44 (20%) tumors measuring 2 cm and more (p < 0.05). Similarly, a kind of correlation was found between gene amplification and low differentiation of breast cancer cells: enhanced copying ability of the oncogene was registered in 2 out 4 (50%) breast tumors with low cell differentiation, 8 out 69 (12%) tumors with medium cell differentiation, while it was not identified in 5 breast carcinomas with high cell differentiation (p < 0,2).

Breast Neoplasms↗
PubMed1992

[The search for amplification of the ERBB-2 oncogene in human tumors].

The occurrence of ERBB-2 (HER-2/NEU) oncogene amplification was studied in 203 DNA samples obtained from 175 cancer patients. Amplification of ERBB-2 oncogene was established in 14 out of 63 (22%) patients with breast cancer, 1 out of 23 cases of ovarian tumor, 1 out of 19 cases of large bowel cancer and 1 out of 27 patients with cancer of the thyroid. Patients with lung cancer (34), soft tissue sarcoma (6) and malignant melanoma (3) failed to reveal any changes in the above oncogene. A tendency was established for ERBB-2 oncogene amplification to be associated with lymph node involvement in female patients with breast cancer: amplification was observed in 9 out of 28 patients presenting with lymph node metastases and only in 5 out of 29 metastases-free cases. To summarize, ERBB-2 oncogene is fairly often activated in human tumors but a high occurrence of the gene amplification was observed in female patients with breast cancer only.

DNA, Neoplasm↗
PubMed1991

[An increased frequency of allele A6 of the proto-oncogene HRAS1 in cancer patients].

Size and frequency of rare alleles of HRAS1 protooncogene were studied in 258 patients with various neoplasms and 32 healthy donors of the northwestern region of the USSR. Literature data on distribution of rare alleles of certain size in sick and healthy people were compared to our results. On the whole, 1918 HRAS1 alleles from cancer patients and 1104 alleles from donors were considered. The study established a significant increase in the frequency of rare A6 allele in cancer patients.

Alleles↗
PubMed1990

[Frequency and rearrangements of alleles of proto-oncogene c-Ha-ras-1 and their association with development of various malignant tumors in man].

The c-Ha-ras-1 locus in 84 cancer patients was examined for allelic restriction fragment length's polymorphism, as well as for distribution of four common c-Ha-ras-1 alleles (a1, a2, a3 and a4) in lung, ovarian and thyroid cancer patients. In approximately half (8 out of 15) lung and ovarian carcinomas possessing a4 allele, alterations in the Ha-ras locus (deletion, amplification and change in allele length) were detected, as compared to 2 cases of rearrangements out of 40 tumors lacking the a4 allele. An increased a4 allele frequency was found in individuals with lung and ovarian carcinomas, as compared to both controls--summarized literature data, and thyroid cancer patients. On the other hand, homozygosity for the a2 locus, resulting from deletion in another allele, and increased a2 allele frequency in thyroid cancer patients were observed. Thus, a4 and a2 alleles of the c-Ha-ras-1 may perhaps be viewed as genetic markers of predisposition to lung, ovarian and thyroid cancer, respectively, in combination with other clinical parameters.

Alleles↗
PubMed1990

[Alterations of c-myc and c-Ha-ras-1 oncogenes in human ovarian cancer].

Fourteen cases of the ovarian carcinoma (OC) were studied for alterations of c-myc and c-Ha-ras-1 oncogens. Amplification of c-myc was found in four aggressive and widespread OC. An increased frequency of one of the four common alleles of c-Ha-ras-1-allele A4-was determined in OC patients. Rearrangements of c-Ha-ras-1-allelic deletions and change in the allele fragment length-were found in all OC with A4 allele. In contrast, no alterations were detected in tumours without allele A4. Thus allele A4 of c-Ha-ras-1 may be viewed as a genetic marker of predisposition to OC in combination with other clinical parameters. Alterations of c-myc and c-Ha-ras-1 oncogens were observed in 8 out of 14 OC samples suggesting that the development of this type of human neoplasm is due to rearrangements of these genes.

Alleles↗
PubMed1989

[Proto-oncogene expression in human carcinomas of the stomach and in the gastric mucosa of rats exposed to N-methyl-N'-nitro-N-nitrosoguanidine-induced gastric carcinogenesis].

The expression of c-Ha-ras-1, Ki-ras, N-ras, abl, src, fos and myc protooncogenes was analyzed in 13 cases of human gastric carcinomas. The transcriptional activity of both fos and myc protooncogenes was found to be disturbed in 47% and 42% of cases, respectively. An overexpression of fos protooncogenes as well as an appearance in some cases of atypical foc-mRNA transcripts were established. Only an elevation of the number of myc mRNA copies was observed. In one patient with gastric carcinoma a c-Ha-ras-1 overexpression was detected due to its amplification both in tumour tissues and in regional metastasis. The expression of other protooncogenes under investigation was similar to those found in normal gastric mucose. In addition, no differences in expression in protooncogenes mentioned above plus sis protooncogene were established in unchanged, premalignant and malignant stomach tissues in the course of N-methyl-N'-nitro-N-nitrosoguanidin-induced carcinogenesis.

Animals↗
PubMed1987

[Joint amplification of c-myc and c-Ha-ras oncogenes in human breast and thyroid cancer cells].

Both c-myc and c-Ha-ras 1 oncogenes amplification and enhanced expression were revealed in some human mammary and thyroid carcinomas by the molecular genetic analysis. Amplification proves to be a second possible molecular mechanism of the ras family protooncogene activation besides a point mutation. The coexistence of c-myc and c-Ha-ras 1 in some human primary carcinomas suggests a multistep process of carcinogenesis.

Breast Neoplasms↗
PubMed1986

[Virus-specific proteins in cells transformed by the chicken sarcoma virus D6].

The structural proteins and the oncogene product of the avian sarcoma virus (ASV) D6 were analyzed by the radioimmunoprecipitation. ADV D6 was obtained from the chemically induced tumour. ASV D6 contains all the structural proteins found in RSV, but some of them (p19, gp 85) differ from those of RSV. The product of ASV D6 oncogene is pp65src. The protein kinase activity of this src protein is identical to that of wt pp60src. The nature of some other proteins, which can be phosphorylated in this reaction, is discussed.

Animals↗
PubMed1986

[Amplification of myc-specific sequences in human colonic cancer].

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.

Adenocarcinoma↗
PubMed1985

[Identification of the transforming Ha-ras gene in human melanoma, neuroblastoma and breast cancer cells].

Preparations of DNA isolated from malignant melanoma (Ja heterotransplant), neuroblastoma (L-AN-1 cell line) and breast cancer (SK-BR-3 cell line) induced a high incidence of transformation of recipient NIH 3T3 cells in two consecutive cycles of transfection. Transformed NIH 3T3 cells appeared to be highly tumorigenic in newborn BALB/c mice. The analysis of DNA samples isolated from primary and secondary NIH 3T3 transformants identified Alu-repetitive DNA sequences of human genome as well as additional sequences homologous to ras-family oncogene. Transforming c-Ha-ras I gene was identified for the first time in NIH 3T3 cells transformed by preparations of DNA isolated from human malignant melanoma, neuroblastoma and breast cancer.

Animals↗
PubMed1984

[Isolation of nonintegrated forms of proviral DNA of oncogenic viruses using preparative electrophoresis].

Nonintegrated forms of avian sarcoma virus (ASV) D6 proviral DNA have been analyzed in transformed chick embryo fibroblasts (CEF) 72 h after the initial infection. It is shown that nonintegrated proviral DNA in CEF cultures are represented by circular (form I) and linear (form III) forms. The molecular mass of the linear form of ASV D6 proviral DNA is 5.4-5.6 mD. The new method of preparative electrophoresis is proposed for isolation and separation of the nonintegrated forms of ASV D6 proviral DNA. The advantages of this method are considered as compared to the previously used one.

Animals↗