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Altered PTEN function caused by deletion or gene disruption is associated with poor prognosis in rectal but not in colon cancer

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Altered PTEN function caused by deletion or gene disruption is associated with poor prognosis in rectal but not in colon cancer. / Bohn, B A; Mina, S; Krohn, A; Simon, R; Kluth, M; Harasimowicz, Silvia; Quaas, A; Bockhorn, M; Izbicki, J R; Sauter, G; Marx, A; Stahl, P R.

In: HUM PATHOL, Vol. 44, No. 8, 01.08.2013, p. 1524-33.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Bohn, BA, Mina, S, Krohn, A, Simon, R, Kluth, M, Harasimowicz, S, Quaas, A, Bockhorn, M, Izbicki, JR, Sauter, G, Marx, A & Stahl, PR 2013, 'Altered PTEN function caused by deletion or gene disruption is associated with poor prognosis in rectal but not in colon cancer', HUM PATHOL, vol. 44, no. 8, pp. 1524-33. https://doi.org/10.1016/j.humpath.2012.12.006

APA

Bohn, B. A., Mina, S., Krohn, A., Simon, R., Kluth, M., Harasimowicz, S., Quaas, A., Bockhorn, M., Izbicki, J. R., Sauter, G., Marx, A., & Stahl, P. R. (2013). Altered PTEN function caused by deletion or gene disruption is associated with poor prognosis in rectal but not in colon cancer. HUM PATHOL, 44(8), 1524-33. https://doi.org/10.1016/j.humpath.2012.12.006

Vancouver

Bohn BA, Mina S, Krohn A, Simon R, Kluth M, Harasimowicz S et al. Altered PTEN function caused by deletion or gene disruption is associated with poor prognosis in rectal but not in colon cancer. HUM PATHOL. 2013 Aug 1;44(8):1524-33. https://doi.org/10.1016/j.humpath.2012.12.006

Bibtex

@article{beb6c93e55f6409f9286ae65ef1a2d25,
title = "Altered PTEN function caused by deletion or gene disruption is associated with poor prognosis in rectal but not in colon cancer",
abstract = "Colorectal cancer is the third most common malignancy worldwide. Anti-epidermal growth factor receptor (EGFR)-targeted therapy shows clinical evidence in this malignancy and improves outcome. The tumor suppressor gene phosphatase and tensin homologue (PTEN) is considered a potential predictor of nonresponse to anti-EGFR agents. The purpose of this study was to assess whether associations between PTEN alterations (PTEN gene deletion or PTEN gene disruption) and clinical outcome could be caused by a prognostic (and not predictive) effect of PTEN inactivation. Therefore, we analyzed 404 colorectal cancers not previously treated with anti-EGFR drugs in a tissue microarray format. PTEN deletion and PTEN gene rearrangements were analyzed by fluorescence in situ hybridization. Heterogeneity analysis of all available large tissue sections was performed in 6 cases with genomic PTEN alteration. Twenty-seven (8.8%) of 307 analyzable colorectal cancer spots showed genomic PTEN alterations including 24 hemizygous and 1 homozygous deletion as well as 2 PTEN gene disruptions. Genomic PTEN alterations were associated with reduced patient survival in rectal cancer in univariate and multivariate analyses (P = .012; hazard ratio, 2.675; 95% confidence interval, 1.242-5.759) but not in colon cancer. Large-section evaluation revealed a homogeneous distribution pattern in all 4 analyzed cases with PTEN deletion and in both cases with a PTEN gene disruption. In conclusion, genomic PTEN gene alterations caused by deletion or gene disruption characterize a fraction of rectal cancers with particularly poor outcome.",
keywords = "Aged, Colonic Neoplasms, Female, Gene Deletion, Humans, In Situ Hybridization, Fluorescence, Kaplan-Meier Estimate, Male, Middle Aged, PTEN Phosphohydrolase, Prognosis, Proportional Hazards Models, Rectal Neoplasms, Tissue Array Analysis, Tumor Markers, Biological",
author = "Bohn, {B A} and S Mina and A Krohn and R Simon and M Kluth and Silvia Harasimowicz and A Quaas and M Bockhorn and Izbicki, {J R} and G Sauter and A Marx and Stahl, {P R}",
note = "Copyright {\textcopyright} 2013 Elsevier Inc. All rights reserved.",
year = "2013",
month = aug,
day = "1",
doi = "10.1016/j.humpath.2012.12.006",
language = "English",
volume = "44",
pages = "1524--33",
journal = "HUM PATHOL",
issn = "0046-8177",
publisher = "W.B. Saunders Ltd",
number = "8",

}

RIS

TY - JOUR

T1 - Altered PTEN function caused by deletion or gene disruption is associated with poor prognosis in rectal but not in colon cancer

AU - Bohn, B A

AU - Mina, S

AU - Krohn, A

AU - Simon, R

AU - Kluth, M

AU - Harasimowicz, Silvia

AU - Quaas, A

AU - Bockhorn, M

AU - Izbicki, J R

AU - Sauter, G

AU - Marx, A

AU - Stahl, P R

N1 - Copyright © 2013 Elsevier Inc. All rights reserved.

PY - 2013/8/1

Y1 - 2013/8/1

N2 - Colorectal cancer is the third most common malignancy worldwide. Anti-epidermal growth factor receptor (EGFR)-targeted therapy shows clinical evidence in this malignancy and improves outcome. The tumor suppressor gene phosphatase and tensin homologue (PTEN) is considered a potential predictor of nonresponse to anti-EGFR agents. The purpose of this study was to assess whether associations between PTEN alterations (PTEN gene deletion or PTEN gene disruption) and clinical outcome could be caused by a prognostic (and not predictive) effect of PTEN inactivation. Therefore, we analyzed 404 colorectal cancers not previously treated with anti-EGFR drugs in a tissue microarray format. PTEN deletion and PTEN gene rearrangements were analyzed by fluorescence in situ hybridization. Heterogeneity analysis of all available large tissue sections was performed in 6 cases with genomic PTEN alteration. Twenty-seven (8.8%) of 307 analyzable colorectal cancer spots showed genomic PTEN alterations including 24 hemizygous and 1 homozygous deletion as well as 2 PTEN gene disruptions. Genomic PTEN alterations were associated with reduced patient survival in rectal cancer in univariate and multivariate analyses (P = .012; hazard ratio, 2.675; 95% confidence interval, 1.242-5.759) but not in colon cancer. Large-section evaluation revealed a homogeneous distribution pattern in all 4 analyzed cases with PTEN deletion and in both cases with a PTEN gene disruption. In conclusion, genomic PTEN gene alterations caused by deletion or gene disruption characterize a fraction of rectal cancers with particularly poor outcome.

AB - Colorectal cancer is the third most common malignancy worldwide. Anti-epidermal growth factor receptor (EGFR)-targeted therapy shows clinical evidence in this malignancy and improves outcome. The tumor suppressor gene phosphatase and tensin homologue (PTEN) is considered a potential predictor of nonresponse to anti-EGFR agents. The purpose of this study was to assess whether associations between PTEN alterations (PTEN gene deletion or PTEN gene disruption) and clinical outcome could be caused by a prognostic (and not predictive) effect of PTEN inactivation. Therefore, we analyzed 404 colorectal cancers not previously treated with anti-EGFR drugs in a tissue microarray format. PTEN deletion and PTEN gene rearrangements were analyzed by fluorescence in situ hybridization. Heterogeneity analysis of all available large tissue sections was performed in 6 cases with genomic PTEN alteration. Twenty-seven (8.8%) of 307 analyzable colorectal cancer spots showed genomic PTEN alterations including 24 hemizygous and 1 homozygous deletion as well as 2 PTEN gene disruptions. Genomic PTEN alterations were associated with reduced patient survival in rectal cancer in univariate and multivariate analyses (P = .012; hazard ratio, 2.675; 95% confidence interval, 1.242-5.759) but not in colon cancer. Large-section evaluation revealed a homogeneous distribution pattern in all 4 analyzed cases with PTEN deletion and in both cases with a PTEN gene disruption. In conclusion, genomic PTEN gene alterations caused by deletion or gene disruption characterize a fraction of rectal cancers with particularly poor outcome.

KW - Aged

KW - Colonic Neoplasms

KW - Female

KW - Gene Deletion

KW - Humans

KW - In Situ Hybridization, Fluorescence

KW - Kaplan-Meier Estimate

KW - Male

KW - Middle Aged

KW - PTEN Phosphohydrolase

KW - Prognosis

KW - Proportional Hazards Models

KW - Rectal Neoplasms

KW - Tissue Array Analysis

KW - Tumor Markers, Biological

U2 - 10.1016/j.humpath.2012.12.006

DO - 10.1016/j.humpath.2012.12.006

M3 - SCORING: Journal article

C2 - 23465274

VL - 44

SP - 1524

EP - 1533

JO - HUM PATHOL

JF - HUM PATHOL

SN - 0046-8177

IS - 8

ER -