Experiences from treatment-predictive KRAS testing; high mutation frequency in rectal cancers from females and concurrent mutations in the same tumor

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Experiences from treatment-predictive KRAS testing; high mutation frequency in rectal cancers from females and concurrent mutations in the same tumor. / Jönsson, Mats; Ekstrand, Anna; Edekling, Thomas; Eberhard, Jakob; Grabau, Dorthe; Borg, David; Nilbert, Mef; Jönsson, Mats; Ekstrand, Anna; Edekling, Thomas; Eberhard, Jakob; Grabau, Dorthe; Borg, David; Nilbert, Mef.

In: BMC Clinical Pathology, Vol. 9, 2009, p. 8.

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

Harvard

Jönsson, M, Ekstrand, A, Edekling, T, Eberhard, J, Grabau, D, Borg, D, Nilbert, M, Jönsson, M, Ekstrand, A, Edekling, T, Eberhard, J, Grabau, D, Borg, D & Nilbert, M 2009, 'Experiences from treatment-predictive KRAS testing; high mutation frequency in rectal cancers from females and concurrent mutations in the same tumor', BMC Clinical Pathology, vol. 9, pp. 8. https://doi.org/10.1186/1472-6890-9-8, https://doi.org/10.1186/1472-6890-9-8

APA

Jönsson, M., Ekstrand, A., Edekling, T., Eberhard, J., Grabau, D., Borg, D., Nilbert, M., Jönsson, M., Ekstrand, A., Edekling, T., Eberhard, J., Grabau, D., Borg, D., & Nilbert, M. (2009). Experiences from treatment-predictive KRAS testing; high mutation frequency in rectal cancers from females and concurrent mutations in the same tumor. BMC Clinical Pathology, 9, 8. https://doi.org/10.1186/1472-6890-9-8, https://doi.org/10.1186/1472-6890-9-8

Vancouver

Jönsson M, Ekstrand A, Edekling T, Eberhard J, Grabau D, Borg D et al. Experiences from treatment-predictive KRAS testing; high mutation frequency in rectal cancers from females and concurrent mutations in the same tumor. BMC Clinical Pathology. 2009;9:8. https://doi.org/10.1186/1472-6890-9-8, https://doi.org/10.1186/1472-6890-9-8

Author

Jönsson, Mats ; Ekstrand, Anna ; Edekling, Thomas ; Eberhard, Jakob ; Grabau, Dorthe ; Borg, David ; Nilbert, Mef ; Jönsson, Mats ; Ekstrand, Anna ; Edekling, Thomas ; Eberhard, Jakob ; Grabau, Dorthe ; Borg, David ; Nilbert, Mef. / Experiences from treatment-predictive KRAS testing; high mutation frequency in rectal cancers from females and concurrent mutations in the same tumor. In: BMC Clinical Pathology. 2009 ; Vol. 9. pp. 8.

Bibtex

@article{b6e8ae00aabc11df928f000ea68e967b,
title = "Experiences from treatment-predictive KRAS testing; high mutation frequency in rectal cancers from females and concurrent mutations in the same tumor",
abstract = "BACKGROUND: KRAS mutations represent key alterations in colorectal cancer development and lead to constitutive EGFR signaling. Since EGFR inhibition represents a therapeutic strategy in advanced colorectal cancer, KRAS mutation analysis has quickly been introduced as a treatment-predictive test. METHODS: We used a real-time PCR based method to determine KRAS mutations in 136 colorectal cancers with mutations identified in 53 (39%) tumors. RESULTS: KRAS mutations were significantly more often found in rectal cancer (21/38, 55%) than in colon cancer (32/98, 33%) (P = 0.02). This finding was explained by marked differences mutation rates in female patients who showed mutations in 33% of the colon cancers and in 67% of the rectal cancers (P = 0.01). Concurrent KRAS mutations were identified in three tumors; two colorectal cancers harbored Gly12Asp/Gly13Asp and Gly12Cys/Gly13Asp and a third tumor carried Gly12Cys/Gly12Asp in an adenomatous component and additionally acquired Gly12Val in the invasive component. CONCLUSION: The demonstration of a particularly high KRAS mutation frequency among female rectal cancer patients suggests that this subset is the least likely to respond to anti-EGFR therapies, whereas the observation of concurrent KRAS mutations imply that repeated KRAS targeting may occur during tumor progression in a subset of colorectal cancers.",
author = "Mats J{\"o}nsson and Anna Ekstrand and Thomas Edekling and Jakob Eberhard and Dorthe Grabau and David Borg and Mef Nilbert and Mats J{\"o}nsson and Anna Ekstrand and Thomas Edekling and Jakob Eberhard and Dorthe Grabau and David Borg and Mef Nilbert",
year = "2009",
doi = "10.1186/1472-6890-9-8",
language = "English",
volume = "9",
pages = "8",
journal = "BMC Clinical Pathology",
issn = "1472-6890",
publisher = "BioMed Central Ltd.",

}

RIS

TY - JOUR

T1 - Experiences from treatment-predictive KRAS testing; high mutation frequency in rectal cancers from females and concurrent mutations in the same tumor

AU - Jönsson, Mats

AU - Ekstrand, Anna

AU - Edekling, Thomas

AU - Eberhard, Jakob

AU - Grabau, Dorthe

AU - Borg, David

AU - Nilbert, Mef

AU - Jönsson, Mats

AU - Ekstrand, Anna

AU - Edekling, Thomas

AU - Eberhard, Jakob

AU - Grabau, Dorthe

AU - Borg, David

AU - Nilbert, Mef

PY - 2009

Y1 - 2009

N2 - BACKGROUND: KRAS mutations represent key alterations in colorectal cancer development and lead to constitutive EGFR signaling. Since EGFR inhibition represents a therapeutic strategy in advanced colorectal cancer, KRAS mutation analysis has quickly been introduced as a treatment-predictive test. METHODS: We used a real-time PCR based method to determine KRAS mutations in 136 colorectal cancers with mutations identified in 53 (39%) tumors. RESULTS: KRAS mutations were significantly more often found in rectal cancer (21/38, 55%) than in colon cancer (32/98, 33%) (P = 0.02). This finding was explained by marked differences mutation rates in female patients who showed mutations in 33% of the colon cancers and in 67% of the rectal cancers (P = 0.01). Concurrent KRAS mutations were identified in three tumors; two colorectal cancers harbored Gly12Asp/Gly13Asp and Gly12Cys/Gly13Asp and a third tumor carried Gly12Cys/Gly12Asp in an adenomatous component and additionally acquired Gly12Val in the invasive component. CONCLUSION: The demonstration of a particularly high KRAS mutation frequency among female rectal cancer patients suggests that this subset is the least likely to respond to anti-EGFR therapies, whereas the observation of concurrent KRAS mutations imply that repeated KRAS targeting may occur during tumor progression in a subset of colorectal cancers.

AB - BACKGROUND: KRAS mutations represent key alterations in colorectal cancer development and lead to constitutive EGFR signaling. Since EGFR inhibition represents a therapeutic strategy in advanced colorectal cancer, KRAS mutation analysis has quickly been introduced as a treatment-predictive test. METHODS: We used a real-time PCR based method to determine KRAS mutations in 136 colorectal cancers with mutations identified in 53 (39%) tumors. RESULTS: KRAS mutations were significantly more often found in rectal cancer (21/38, 55%) than in colon cancer (32/98, 33%) (P = 0.02). This finding was explained by marked differences mutation rates in female patients who showed mutations in 33% of the colon cancers and in 67% of the rectal cancers (P = 0.01). Concurrent KRAS mutations were identified in three tumors; two colorectal cancers harbored Gly12Asp/Gly13Asp and Gly12Cys/Gly13Asp and a third tumor carried Gly12Cys/Gly12Asp in an adenomatous component and additionally acquired Gly12Val in the invasive component. CONCLUSION: The demonstration of a particularly high KRAS mutation frequency among female rectal cancer patients suggests that this subset is the least likely to respond to anti-EGFR therapies, whereas the observation of concurrent KRAS mutations imply that repeated KRAS targeting may occur during tumor progression in a subset of colorectal cancers.

U2 - 10.1186/1472-6890-9-8

DO - 10.1186/1472-6890-9-8

M3 - Journal article

C2 - 19832985

VL - 9

SP - 8

JO - BMC Clinical Pathology

JF - BMC Clinical Pathology

SN - 1472-6890

ER -

ID: 21454905