Investigation of the miR16-1 (C>T) + 7 Substitution in Seven Different Types of Cancer from Three Ethnic Groups. (26th October 2009)
- Record Type:
- Journal Article
- Title:
- Investigation of the miR16-1 (C>T) + 7 Substitution in Seven Different Types of Cancer from Three Ethnic Groups. (26th October 2009)
- Main Title:
- Investigation of the miR16-1 (C>T) + 7 Substitution in Seven Different Types of Cancer from Three Ethnic Groups
- Authors:
- Yazici, Hulya
Zipprich, Jennifer
Peng, Tao
Akisik, Elif Z.
Tigli, Hulya
Isin, Mustafa
Akisik, Ebru E.
Terry, Mary Beth
Senie, Ruby T.
Li, Lequn
Peng, Minhao
Liu, Zhiming
Dalay, Nejat
Santella, Regina M. - Other Names:
- Paolo Boffetta Academic Editor.
- Abstract:
- Abstract : Background . MicroRNAs are a type of small noncoding RNA molecules that have been shown to control gene expression in eukaryotes. Aberrant expression and alteration of miRNAs may be responsible for human diseases including cancer. An miR16-1 (C > T ) + 7 gene mutation has been previously found in familial chronic lymphocytic leukemia patients, one of which reported a family history of breast cancer. miR16-1 regulates the expression of bcl-2, which is important in retinoblastoma, and is located in a genomic region that is frequently lost in nasopharyngeal and hepatocellular carcinomas (HCCs). Therefore, miR16-1 may be potentially important in the etiology of several solid tumors. To understand the power of the miR16-1 (C > T ) + 7 mutation as a prognostic and diagnostic risk factor, we investigated the mutation in patients with seven different types of cancer including 188 with breast, 102 with ovarian, and 22 nasopharyngeal carcinomas, 96 HCC, 872 chronic myeloid leukemia (CML), 39 chronic lymphocytic leukemia (CLL), and 46 retinoblastoma cases from three different ethnic groups and of hereditary and sporadic etiology. Methods .5 ′ Nuclease TaqMan SNP genotyping assay was used to detect the miR16-1 geneC > T substitution. Results . The miR16-1 (C > T ) + 7 substitution was not detected in any of the groups studied. Conclusions . Considering the large scale of our study, the representation of different ethnicities and levels of hereditary risk, we conclude thatAbstract : Background . MicroRNAs are a type of small noncoding RNA molecules that have been shown to control gene expression in eukaryotes. Aberrant expression and alteration of miRNAs may be responsible for human diseases including cancer. An miR16-1 (C > T ) + 7 gene mutation has been previously found in familial chronic lymphocytic leukemia patients, one of which reported a family history of breast cancer. miR16-1 regulates the expression of bcl-2, which is important in retinoblastoma, and is located in a genomic region that is frequently lost in nasopharyngeal and hepatocellular carcinomas (HCCs). Therefore, miR16-1 may be potentially important in the etiology of several solid tumors. To understand the power of the miR16-1 (C > T ) + 7 mutation as a prognostic and diagnostic risk factor, we investigated the mutation in patients with seven different types of cancer including 188 with breast, 102 with ovarian, and 22 nasopharyngeal carcinomas, 96 HCC, 872 chronic myeloid leukemia (CML), 39 chronic lymphocytic leukemia (CLL), and 46 retinoblastoma cases from three different ethnic groups and of hereditary and sporadic etiology. Methods .5 ′ Nuclease TaqMan SNP genotyping assay was used to detect the miR16-1 geneC > T substitution. Results . The miR16-1 (C > T ) + 7 substitution was not detected in any of the groups studied. Conclusions . Considering the large scale of our study, the representation of different ethnicities and levels of hereditary risk, we conclude that the miR-16-1 (C > T ) + 7 mutation is not a good diagnostic or prognostic indicator of risk for the cancers tested. … (more)
- Is Part Of:
- Journal of oncology. Volume 2009(2009)
- Journal:
- Journal of oncology
- Issue:
- Volume 2009(2009)
- Issue Display:
- Volume 2009, Issue 2009 (2009)
- Year:
- 2009
- Volume:
- 2009
- Issue:
- 2009
- Issue Sort Value:
- 2009-2009-2009-0000
- Page Start:
- Page End:
- Publication Date:
- 2009-10-26
- Subjects:
- Oncology -- Research -- Periodicals
Tumors -- Periodicals
Neoplasms
Oncology -- Research
Tumors
Periodicals
Periodicals
616.994 - Journal URLs:
- https://www.hindawi.com/journals/jo/ ↗
http://www.pubmedcentral.nih.gov/tocrender.fcgi?journal=859&action=archive ↗ - DOI:
- 10.1155/2009/827532 ↗
- Languages:
- English
- ISSNs:
- 1687-8450
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 10254.xml