Recurrent deletions of specific chromosomal sites in 1p, 3p, 6q, and 9p in human malignant mesothelioma

Takahiro Taguchi, Suresh C. Jhanwar, Jill M. Siegfried, Steven M. Keller, Joseph R. Testa

Research output: Contribution to journalArticle

149 Citations (Scopus)

Abstract

Detailed cytogenetic analyses were carried out on primary tumor specimens and cell lines from 23 patients with pleural malignant mesothelioma (MM). Clonal abnormalities were identified in 20 of 23 MM. In 3 cases, karyotypic data were compiled from harvests of both short-term cultures (1-3 days), and primary cultures grown on murine feeder layers for several weeks. The karyotypes obtained with these 2 different culture methods were very similar, although polyploid versions of abnormal clones were found only in the long-term cultures. In addition, while short-term cultures from 9 tumor biopsies usually exhibited near-diploid clones, cell lines derived from 11 tumors tended to have higher ploidies. Each of the cytogenetically abnormal MM displayed multiple clonal alterations. The 2 most frequent changes were chromosomal losses of specific regions in 1p (17 cases) and 9p (16 cases). The shortest regions of overlap of these losses were at 1p21-p22 and 9p21-p22, respectively. Other common abnormalities included losses of 3p21 (13 cases) and 6q15-q21 (9 cases), and numerical losses of chromosomes 14, 16, 18, and 22 (each observed in 10-13 tumors). In many of the MM examined, most or all of these recurrent changes occurred in combination, suggesting the involvement of a pathogenetic cascade in this cancer. The pattern of recurrent chromosomal losses suggests that these regions represent the locations of tumor suppressor genes whose loss/inactivation may have a pivotal role in MM tumorigenesis.

Original languageEnglish (US)
Pages (from-to)4349-4355
Number of pages7
JournalCancer Research
Volume53
Issue number18
StatePublished - Sep 15 1993
Externally publishedYes

Fingerprint

Neoplasms
Clone Cells
Feeder Cells
Chromosomes, Human, Pair 16
Chromosomes, Human, Pair 14
Polyploidy
Ploidies
Cytogenetic Analysis
Tumor Cell Line
Tumor Suppressor Genes
Diploidy
Karyotype
Carcinogenesis
Malignant Mesothelioma
Biopsy
Cell Line

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Taguchi, T., Jhanwar, S. C., Siegfried, J. M., Keller, S. M., & Testa, J. R. (1993). Recurrent deletions of specific chromosomal sites in 1p, 3p, 6q, and 9p in human malignant mesothelioma. Cancer Research, 53(18), 4349-4355.

Recurrent deletions of specific chromosomal sites in 1p, 3p, 6q, and 9p in human malignant mesothelioma. / Taguchi, Takahiro; Jhanwar, Suresh C.; Siegfried, Jill M.; Keller, Steven M.; Testa, Joseph R.

In: Cancer Research, Vol. 53, No. 18, 15.09.1993, p. 4349-4355.

Research output: Contribution to journalArticle

Taguchi, T, Jhanwar, SC, Siegfried, JM, Keller, SM & Testa, JR 1993, 'Recurrent deletions of specific chromosomal sites in 1p, 3p, 6q, and 9p in human malignant mesothelioma', Cancer Research, vol. 53, no. 18, pp. 4349-4355.
Taguchi T, Jhanwar SC, Siegfried JM, Keller SM, Testa JR. Recurrent deletions of specific chromosomal sites in 1p, 3p, 6q, and 9p in human malignant mesothelioma. Cancer Research. 1993 Sep 15;53(18):4349-4355.
Taguchi, Takahiro ; Jhanwar, Suresh C. ; Siegfried, Jill M. ; Keller, Steven M. ; Testa, Joseph R. / Recurrent deletions of specific chromosomal sites in 1p, 3p, 6q, and 9p in human malignant mesothelioma. In: Cancer Research. 1993 ; Vol. 53, No. 18. pp. 4349-4355.
@article{befd5590061c47549af4621f06bb0b7c,
title = "Recurrent deletions of specific chromosomal sites in 1p, 3p, 6q, and 9p in human malignant mesothelioma",
abstract = "Detailed cytogenetic analyses were carried out on primary tumor specimens and cell lines from 23 patients with pleural malignant mesothelioma (MM). Clonal abnormalities were identified in 20 of 23 MM. In 3 cases, karyotypic data were compiled from harvests of both short-term cultures (1-3 days), and primary cultures grown on murine feeder layers for several weeks. The karyotypes obtained with these 2 different culture methods were very similar, although polyploid versions of abnormal clones were found only in the long-term cultures. In addition, while short-term cultures from 9 tumor biopsies usually exhibited near-diploid clones, cell lines derived from 11 tumors tended to have higher ploidies. Each of the cytogenetically abnormal MM displayed multiple clonal alterations. The 2 most frequent changes were chromosomal losses of specific regions in 1p (17 cases) and 9p (16 cases). The shortest regions of overlap of these losses were at 1p21-p22 and 9p21-p22, respectively. Other common abnormalities included losses of 3p21 (13 cases) and 6q15-q21 (9 cases), and numerical losses of chromosomes 14, 16, 18, and 22 (each observed in 10-13 tumors). In many of the MM examined, most or all of these recurrent changes occurred in combination, suggesting the involvement of a pathogenetic cascade in this cancer. The pattern of recurrent chromosomal losses suggests that these regions represent the locations of tumor suppressor genes whose loss/inactivation may have a pivotal role in MM tumorigenesis.",
author = "Takahiro Taguchi and Jhanwar, {Suresh C.} and Siegfried, {Jill M.} and Keller, {Steven M.} and Testa, {Joseph R.}",
year = "1993",
month = "9",
day = "15",
language = "English (US)",
volume = "53",
pages = "4349--4355",
journal = "Cancer Research",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "18",

}

TY - JOUR

T1 - Recurrent deletions of specific chromosomal sites in 1p, 3p, 6q, and 9p in human malignant mesothelioma

AU - Taguchi, Takahiro

AU - Jhanwar, Suresh C.

AU - Siegfried, Jill M.

AU - Keller, Steven M.

AU - Testa, Joseph R.

PY - 1993/9/15

Y1 - 1993/9/15

N2 - Detailed cytogenetic analyses were carried out on primary tumor specimens and cell lines from 23 patients with pleural malignant mesothelioma (MM). Clonal abnormalities were identified in 20 of 23 MM. In 3 cases, karyotypic data were compiled from harvests of both short-term cultures (1-3 days), and primary cultures grown on murine feeder layers for several weeks. The karyotypes obtained with these 2 different culture methods were very similar, although polyploid versions of abnormal clones were found only in the long-term cultures. In addition, while short-term cultures from 9 tumor biopsies usually exhibited near-diploid clones, cell lines derived from 11 tumors tended to have higher ploidies. Each of the cytogenetically abnormal MM displayed multiple clonal alterations. The 2 most frequent changes were chromosomal losses of specific regions in 1p (17 cases) and 9p (16 cases). The shortest regions of overlap of these losses were at 1p21-p22 and 9p21-p22, respectively. Other common abnormalities included losses of 3p21 (13 cases) and 6q15-q21 (9 cases), and numerical losses of chromosomes 14, 16, 18, and 22 (each observed in 10-13 tumors). In many of the MM examined, most or all of these recurrent changes occurred in combination, suggesting the involvement of a pathogenetic cascade in this cancer. The pattern of recurrent chromosomal losses suggests that these regions represent the locations of tumor suppressor genes whose loss/inactivation may have a pivotal role in MM tumorigenesis.

AB - Detailed cytogenetic analyses were carried out on primary tumor specimens and cell lines from 23 patients with pleural malignant mesothelioma (MM). Clonal abnormalities were identified in 20 of 23 MM. In 3 cases, karyotypic data were compiled from harvests of both short-term cultures (1-3 days), and primary cultures grown on murine feeder layers for several weeks. The karyotypes obtained with these 2 different culture methods were very similar, although polyploid versions of abnormal clones were found only in the long-term cultures. In addition, while short-term cultures from 9 tumor biopsies usually exhibited near-diploid clones, cell lines derived from 11 tumors tended to have higher ploidies. Each of the cytogenetically abnormal MM displayed multiple clonal alterations. The 2 most frequent changes were chromosomal losses of specific regions in 1p (17 cases) and 9p (16 cases). The shortest regions of overlap of these losses were at 1p21-p22 and 9p21-p22, respectively. Other common abnormalities included losses of 3p21 (13 cases) and 6q15-q21 (9 cases), and numerical losses of chromosomes 14, 16, 18, and 22 (each observed in 10-13 tumors). In many of the MM examined, most or all of these recurrent changes occurred in combination, suggesting the involvement of a pathogenetic cascade in this cancer. The pattern of recurrent chromosomal losses suggests that these regions represent the locations of tumor suppressor genes whose loss/inactivation may have a pivotal role in MM tumorigenesis.

UR - http://www.scopus.com/inward/record.url?scp=0027853058&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027853058&partnerID=8YFLogxK

M3 - Article

C2 - 8364929

AN - SCOPUS:0027853058

VL - 53

SP - 4349

EP - 4355

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 18

ER -