Mutational analysis of the p73 Gene in human breast cancers

In primary breast cancer, mutations of the p53 tumor suppressor gene lead to loss of growth‐suppressive properties and poor outcome. Recently, a p53‐related gene, termed p73, has been cloned and its gene product possesses a function similar to p53. p73 has been mapped at chromosome 1p36.3, a region...

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Bibliographic Details
Published in:International journal of cancer 1999-06, Vol.84 (3), p.321-325
Main Authors: Shishikura, Tomotane, Ichimiya, Shingo, Ozaki, Toshinori, Nimura, Yoshinori, Kageyama, Hajime, Nakamura, Yohko, Sakiyama, Shigeru, Miyauchi, Mitsuru, Yamamoto, Naohito, Suzuki, Masato, Nakajima, Nobuyuki, Nakagawara, Akira
Format: Article
Language:English
Subjects:
Adult
Aged
Aged, 80 and over
Biological and medical sciences
Breast Neoplasms - genetics
DNA-Binding Proteins - genetics
Female
Genes, p53
Genes, Tumor Suppressor
Gynecology. Andrology. Obstetrics
Humans
Loss of Heterozygosity
Mammary gland diseases
Medical sciences
Middle Aged
Mutation
Nuclear Proteins - genetics
RNA, Messenger - analysis
Tumor Protein p73
Tumor Suppressor Proteins
Tumors
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Summary:In primary breast cancer, mutations of the p53 tumor suppressor gene lead to loss of growth‐suppressive properties and poor outcome. Recently, a p53‐related gene, termed p73, has been cloned and its gene product possesses a function similar to p53. p73 has been mapped at chromosome 1p36.3, a region frequently deleted in breast cancer, neuroblastoma and other malignancies. To elucidate the functional significance of p73 in the oncogenesis of breast cancer, we have studied genetic alterations of p73 in tissue specimens obtained from 87 patients with primary breast cancer. Thirteen percent of informative cases showed loss of heterozygosity (LOH) at the p73 gene. However, there was no correlation between the p73 LOH and clinical features such as histo‐pathological types, metastatic behavior or expression of estrogen or progesterone receptor. The levels of p73 transcript in primary breast cancer were not significantly different from those in normal breast tissue. Moreover, PCR‐SSCP analysis failed to detect any missense or frameshift mutations in the p73 gene. Our observations suggest that allelic loss, expression levels and mutations of the p73 gene may not contribute to oncogenesis of primary breast cancers. Int. J. Cancer (Pred. Oncol.) 84:321–325, 1999. © 1999 Wiley‐Liss, Inc.
ISSN:0020-7136
1097-0215
DOI:10.1002/(SICI)1097-0215(19990621)84:3<321::AID-IJC21>3.0.CO;2-S