go to Japanese home page.....
9
Author: Suzuki, H.; Komiya, A.; Emi, M.; Kuramochi, H.; Shiraishi, T.;
Yatani, R.; Shimazaki, J.
Year: 1996
Title: Three distinct commonly deleted regions of chromosome arm 16q
in human primary and metastatic prostate cancers
Journal: Genes Chromosomes Cancer
Volume: 17
Issue: 4
Pages: 225-33
Label: 97101686
Keywords: Adenocarcinoma/genetics
Cadherins/genetics
Chromosome Mapping
*Chromosomes, Human, Pair 16
Heterozygote
Human
Male
Neoplasm Metastasis/genetics
Polymerase Chain Reaction
Polymorphism, Restriction Fragment Length
Polymorphism, Single-Stranded Conformational
Prostatic Neoplasms/*genetics
*Sequence Deletion
Support, Non-U.S. Gov't
Abstract: Human prostate cancers frequently show loss of heterozygosity
(LOH) at loci on the long arm of chromosome 16 (16q). In this
study, we analyzed prostate cancer specimens from 48 patients
(Stage B, 20 cases; Stage C, 10 cases; cancer death, 18 cases)
for allelic loss on 16q, using either restriction fragment length
polymorphism (RFLP)- or polymerase chain reaction (PCR)-based
methods. Allelic losses were observed in 20 (42%) of 48 cases,
all of which were informative with at least one locus. Detailed
deletion mapping identified three distinct commonly deleted regions
on this chromosome arm: q22.1-q22.3, q23.2-q24.1, and q24.3- qter.
On the basis of a published sex-averaged framework map, the estimated
sizes of the commonly deleted regions were 4.7 (16q22.1- q22.3),
17.2 (16q23.2-q24.1) and 8.4 cM (16q24.3-qter). Allelic losses
on 16q were observed more frequently in the cancer-death cases
(11 of 18; 61%) than in early-stage tumor cases (9 of 30; 30%;
P 0.05). In 7 of 11 patients from whom DNA was available from
metastatic cancers as well as from normal tissues and primary
tumors, the primary cancer foci had no detectable abnormality
of 16q, but the metastatic tumors showed LOH. These results suggest
that inactivation of tumor suppressor genes on 16q plays an important
role in the progression of prostate cancer. We also analyzed exons
5-8 of the E-cadherin gene, located at 16q22.1, in tumor DNA by
means of PCR-single strand conformation polymorphism and direct
sequencing, but we detected no somatic mutations in this candidate
gene.