Abstract
We analyzed the subchromosomal numerical aberrations of 44 surgically resected pancreatic adenocarcinomas by array-based comparative genomic hybridization. The aberration profile ranged widely between cases, suggesting the presence of multiple or complementary mechanisms of evolution in pancreatic cancer, and was associated with lymph node metastasis and venous or serosal invasion. A large number of small loci, previously uncharacterized in pancreatic cancer, showed non-random loss or gain. Frequent losses at 1p36, 4p16, 7q36, 9q34, 11p15, 11q13, 14q32-33, 16p13, 17p11-13, 17q11-25, 18q21-tel, 19p13, 21q22 and 22q11-12, and gains at 1q25, 2p16, 2q21-37, 3q25, 5p14, 5q11-13, 7q21, 7p22, 8p22, 8q21-23, 10q21, 12p13, 13q22, 15q13-22 and 18q11 were identified. Sixteen loci were amplified recurrently. We identified novel chromosomal alterations that were significantly associated with a range of malignant phenotypes. Gain of LUNX, HCK, E2F1 and DNMT3b at 20q11, loss of p73 at 1p36 and gain of PPM1D at 17q23 independently predicted patient outcome. Expression profiling of amplified genes identified Smurf1 and TRRAP at 7q22.1, BCAS1 at 20q13.2-3, and VCL at 10q22.1 as potential novel oncogenes. Our results contribute to a complete description of genomic structural aberrations and the identification of potential therapeutic targets and genetic indicators that predict patient outcome in pancreatic adenocarcinoma.
| Original language | English |
|---|---|
| Pages (from-to) | 392-400 |
| Number of pages | 9 |
| Journal | Cancer Science |
| Volume | 98 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2007 Mar |
Fingerprint
ASJC Scopus subject areas
- Cancer Research
- Oncology
Cite this
Genome-wide array-based comparative genomic hybridization analysis of pancreatic adenocarcinoma : Identification of genetic indicators that predict patient outcome. / Loukopoulos, Panayiotis; Shibata, Tatsuhiro; Katoh, Hiroto; Kokubu, Akiko; Sakamoto, Michiie; Yamazaki, Ken; Kosuge, Tomoo; Kanai, Yae; Hosoda, Fumie; Imoto, Issei; Ohki, Misao; Inazawa, Jyoji; Hirohashi, Setsuo.
In: Cancer Science, Vol. 98, No. 3, 03.2007, p. 392-400.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Genome-wide array-based comparative genomic hybridization analysis of pancreatic adenocarcinoma
T2 - Identification of genetic indicators that predict patient outcome
AU - Loukopoulos, Panayiotis
AU - Shibata, Tatsuhiro
AU - Katoh, Hiroto
AU - Kokubu, Akiko
AU - Sakamoto, Michiie
AU - Yamazaki, Ken
AU - Kosuge, Tomoo
AU - Kanai, Yae
AU - Hosoda, Fumie
AU - Imoto, Issei
AU - Ohki, Misao
AU - Inazawa, Jyoji
AU - Hirohashi, Setsuo
PY - 2007/3
Y1 - 2007/3
N2 - We analyzed the subchromosomal numerical aberrations of 44 surgically resected pancreatic adenocarcinomas by array-based comparative genomic hybridization. The aberration profile ranged widely between cases, suggesting the presence of multiple or complementary mechanisms of evolution in pancreatic cancer, and was associated with lymph node metastasis and venous or serosal invasion. A large number of small loci, previously uncharacterized in pancreatic cancer, showed non-random loss or gain. Frequent losses at 1p36, 4p16, 7q36, 9q34, 11p15, 11q13, 14q32-33, 16p13, 17p11-13, 17q11-25, 18q21-tel, 19p13, 21q22 and 22q11-12, and gains at 1q25, 2p16, 2q21-37, 3q25, 5p14, 5q11-13, 7q21, 7p22, 8p22, 8q21-23, 10q21, 12p13, 13q22, 15q13-22 and 18q11 were identified. Sixteen loci were amplified recurrently. We identified novel chromosomal alterations that were significantly associated with a range of malignant phenotypes. Gain of LUNX, HCK, E2F1 and DNMT3b at 20q11, loss of p73 at 1p36 and gain of PPM1D at 17q23 independently predicted patient outcome. Expression profiling of amplified genes identified Smurf1 and TRRAP at 7q22.1, BCAS1 at 20q13.2-3, and VCL at 10q22.1 as potential novel oncogenes. Our results contribute to a complete description of genomic structural aberrations and the identification of potential therapeutic targets and genetic indicators that predict patient outcome in pancreatic adenocarcinoma.
AB - We analyzed the subchromosomal numerical aberrations of 44 surgically resected pancreatic adenocarcinomas by array-based comparative genomic hybridization. The aberration profile ranged widely between cases, suggesting the presence of multiple or complementary mechanisms of evolution in pancreatic cancer, and was associated with lymph node metastasis and venous or serosal invasion. A large number of small loci, previously uncharacterized in pancreatic cancer, showed non-random loss or gain. Frequent losses at 1p36, 4p16, 7q36, 9q34, 11p15, 11q13, 14q32-33, 16p13, 17p11-13, 17q11-25, 18q21-tel, 19p13, 21q22 and 22q11-12, and gains at 1q25, 2p16, 2q21-37, 3q25, 5p14, 5q11-13, 7q21, 7p22, 8p22, 8q21-23, 10q21, 12p13, 13q22, 15q13-22 and 18q11 were identified. Sixteen loci were amplified recurrently. We identified novel chromosomal alterations that were significantly associated with a range of malignant phenotypes. Gain of LUNX, HCK, E2F1 and DNMT3b at 20q11, loss of p73 at 1p36 and gain of PPM1D at 17q23 independently predicted patient outcome. Expression profiling of amplified genes identified Smurf1 and TRRAP at 7q22.1, BCAS1 at 20q13.2-3, and VCL at 10q22.1 as potential novel oncogenes. Our results contribute to a complete description of genomic structural aberrations and the identification of potential therapeutic targets and genetic indicators that predict patient outcome in pancreatic adenocarcinoma.
UR - http://www.scopus.com/inward/record.url?scp=33846653317&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33846653317&partnerID=8YFLogxK
U2 - 10.1111/j.1349-7006.2007.00395.x
DO - 10.1111/j.1349-7006.2007.00395.x
M3 - Article
VL - 98
SP - 392
EP - 400
JO - Cancer Science
JF - Cancer Science
SN - 1347-9032
IS - 3
ER -