BIOMAT Database Logo BIOMAT Database Logo

p16INK4 and p15INK4B alterations in primary gynecologic malignancy. 1997

Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong, Shatin, N.T.

Chromosome 9 abnormalities have been found in primary tumors and cell lines from human gynecologic malignancy. Alterations of p16INK4 and p15INK4B genes mapped on the band p21 of chromosome 9 have been detected in various human tumors, but the role of these genes as tumor suppressors in vivo appear to be dependent on tumor type. Polymerase chain reaction (PCR)-based analysis was performed to search for lesions of these genes in 202 primary gynecologic malignancies. Homozygous deletions of p16INK4 were detected in 7 of 128 (5%) cervical, 1 of 41 (2%) endometrial, 2 of 27 (7%) ovarian, and 3 of 6 (50%) vulvar carcinomas, while homozygous deletions of p15INK4B were detected in 19 of 128 (15%) cervical, 1 of 41 (2%) endometrial, 9 of 27 (33%) ovarian, and 3 of 6 (50%) vulvar carcinomas, respectively. No mutations were found in exon 2 of p16INK4 from 161 cases of gynecologic malignancy without deletion of p16INK4. All 3 cases of vulvar carcinoma showing homozygous deletions of p16INK4 and p15INK4B were at advanced clinical stage (stage III-IV), while all 7 cases of cervical carcinoma and 2 cases of ovarian carcinoma showing homozygous deletion of p16INK4 were at early stage (stage I-II). The results indicate that homozygous deletions of p16INK4 and/or p15INK4B genes may play a role in a subset of primary gynecologic malignancy.

UI MeSH Term Description Entries
D009154 Mutation Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations. Mutations
D002352 Carrier Proteins Proteins that bind or transport specific substances in the blood, within the cell, or across cell membranes. Binding Proteins,Carrier Protein,Transport Protein,Transport Proteins,Binding Protein,Protein, Carrier,Proteins, Carrier
D004273 DNA, Neoplasm DNA present in neoplastic tissue. Neoplasm DNA
D005260 Female Females
D005833 Genital Neoplasms, Female Tumor or cancer of the female reproductive tract (GENITALIA, FEMALE). Gynecologic Neoplasms,Female Genital Neoplasms,Neoplasms, Female Genital,Neoplasms, Gynecologic,Female Genital Neoplasm,Genital Neoplasm, Female,Gynecologic Neoplasm,Neoplasm, Female Genital,Neoplasm, Gynecologic
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D016133 Polymerase Chain Reaction In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships. Anchored PCR,Inverse PCR,Nested PCR,PCR,Anchored Polymerase Chain Reaction,Inverse Polymerase Chain Reaction,Nested Polymerase Chain Reaction,PCR, Anchored,PCR, Inverse,PCR, Nested,Polymerase Chain Reactions,Reaction, Polymerase Chain,Reactions, Polymerase Chain
D016147 Genes, Tumor Suppressor Genes that inhibit expression of the tumorigenic phenotype. They are normally involved in holding cellular growth in check. When tumor suppressor genes are inactivated or lost, a barrier to normal proliferation is removed and unregulated growth is possible. Antioncogenes,Cancer Suppressor Genes,Emerogenes,Genes, Cancer Suppressor,Genes, Growth Suppressor,Genes, Metastasis Suppressor,Growth Suppressor Genes,Metastasis Suppressor Genes,Tumor Suppressor Genes,Anti-Oncogenes,Genes, Onco-Suppressor,Oncogenes, Recessive,Tumor Suppressing Genes,Anti Oncogenes,Anti-Oncogene,Antioncogene,Cancer Suppressor Gene,Emerogene,Gene, Cancer Suppressor,Gene, Growth Suppressor,Gene, Metastasis Suppressor,Gene, Onco-Suppressor,Gene, Tumor Suppressing,Gene, Tumor Suppressor,Genes, Onco Suppressor,Genes, Tumor Suppressing,Growth Suppressor Gene,Metastasis Suppressor Gene,Onco-Suppressor Gene,Onco-Suppressor Genes,Oncogene, Recessive,Recessive Oncogene,Recessive Oncogenes,Suppressor Gene, Cancer,Suppressor Gene, Growth,Suppressor Gene, Metastasis,Suppressor Genes, Cancer,Suppressor Genes, Growth,Suppressor Genes, Metastasis,Tumor Suppressing Gene,Tumor Suppressor Gene
D050762 Cyclin-Dependent Kinase Inhibitor p15 An INK4 cyclin-dependent kinase inhibitor containing four ANKYRIN-LIKE REPEATS. INK4B is often inactivated by deletions, mutations, or hypermethylation in HEMATOLOGIC NEOPLASMS. CDKN2B Protein,Cyclin-Dependent Kinase Inhibitor 2B,INK4B Protein,INK4b Cyclin-Dependent Kinase Inhibitor,p15 CDK4 Inhibitor,p15INK4B Protein,CDK4 Inhibitor, p15,Cyclin Dependent Kinase Inhibitor 2B,Cyclin Dependent Kinase Inhibitor p15,INK4b Cyclin Dependent Kinase Inhibitor
D018797 Cell Cycle Proteins Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS. Cell Division Cycle Proteins,Cell-Cycle Regulatory Proteins,cdc Proteins,Cell Cycle Regulatory Proteins

Related Publications

Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
p15ink4B and p16ink4 gene inactivation in acute lymphocytic leukemia.
June 1995, Blood,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
Inactivation of the p15INK4B and p16INK4 genes in hematologic malignancies.
October 1996, Leukemia & lymphoma,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
Mutations in the p16INK4/MTS1/CDKN2, p15INK4B/MTS2, and p18 genes in primary and metastatic lung cancer.
April 1995, Cancer research,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
Growth suppression of esophageal cancer cells by p16INK4 and p15INK4B in vitro.
January 1996, The cancer journal from Scientific American,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
Mutations of p16Ink4/CDKN2 and p15Ink4B/MTS2 genes in biliary tract cancers.
July 1995, Cancer research,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
Prognostic importance of p15INK4B and p16INK4 gene inactivation in childhood acute lymphocytic leukemia.
May 1996, Journal of clinical oncology : official journal of the American Society of Clinical Oncology,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
p16INK4/p15INK4B gene inactivation is a frequent event in malignant T-cell lines.
May 1996, European journal of haematology,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
Association of rat p15INK4B/p16INK4 deletions with monosomy 5 in kidney epithelial cell lines but not primary renal tumors.
April 1995, Cancer research,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
Expression of the cyclin-dependent kinase inhibitors p16INK4, p15INK4B and p21WAF1/CIP1 in human breast cancer.
November 1995, International journal of cancer,
Y F Wong, and T K Chung, and T H Cheung, and T Nobori, and S F Yim, and K W Lai, and M Phil, and A L Yu, and M B Diccianni, and T Z Li, and A M Chang
[Unrecognized malignant lymphomas simulating a primary gynecologic malignancy].
October 1984, Schweizerische medizinische Wochenschrift,
Copied contents to your clipboard!