Emergence of KRAS mutations and acquired resistance to anti-EGFR therapy in colorectal cancer
Molecular alterations in KRAS are associated with acquired resistance to anti-epidermal growth factor receptor (EGFR) treatment in colorectal cancer; resistant mutations can be identified in the blood of patients, months before clinical evidence of disease progression. Acquired resistance in anti-EG...
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| Veröffentlicht in: | Nature (London) Jg. 486; H. 7404; S. 532 - 536 |
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| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
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London
Nature Publishing Group UK
28.06.2012
Nature Publishing Group |
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| ISSN: | 0028-0836, 1476-4687, 1476-4687 |
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| Abstract | Molecular alterations in
KRAS
are associated with acquired resistance to anti-epidermal growth factor receptor (EGFR) treatment in colorectal cancer; resistant mutations can be identified in the blood of patients, months before clinical evidence of disease progression.
Acquired resistance in anti-EGFR therapy
Antibodies targeting epidermal growth factor receptor (EGFR) have become an established treatment for colorectal cancer, but they are contraindicated in patients carrying mutations in the
KRAS
oncogene. Drug resistance can also arise in initially responsive patients, and two papers in this issue of
Nature
present unequivocal evidence that mutations in
KRAS
underlie acquired resistance to anti-EGFR antibodies in many patients and that
KRAS
mutations can be detected in the serum of patients before the clinical emergence of resistance and relapse. Misale
et al
. show in cell-line models that
KRAS
mutations can confer resistance to cetuximab. And in colorectal cancer patients treated with cetuximab or panitumumab, resistance is associated with
KRAS
mutations selected from pre-existing subclones or acquired during treatment. Diaz
et al
. also find
KRAS
mutations accumulating in patients becoming resistant to panitumumab. Their mathematical models suggest that
KRAS
mutations pre-existed in tumour cells before therapy, which may explain why clinical recurrence is usually seen after about six months of treatment, by which time the resistant subpopulations of tumour cells with
KRAS
mutations has expanded. The apparent inevitability of resistance suggests that combinations of drugs targeting more than one oncogenic pathway will be needed if resistance is to be avoided.
A main limitation of therapies that selectively target kinase signalling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal antibody that binds the extracellular domain of epidermal growth factor receptor (EGFR), is effective in a subset of
KRAS
wild-type metastatic colorectal cancers
1
. After an initial response, secondary resistance invariably ensues, thereby limiting the clinical benefit of this drug
2
. The molecular bases of secondary resistance to cetuximab in colorectal cancer are poorly understood
3
,
4
,
5
,
6
,
7
,
8
. Here we show that molecular alterations (in most instances point mutations) of
KRAS
are causally associated with the onset of acquired resistance to anti-EGFR treatment in colorectal cancers. Expression of mutant
KRAS
under the control of its endogenous gene promoter was sufficient to confer cetuximab resistance, but resistant cells remained sensitive to combinatorial inhibition of EGFR and mitogen-activated protein-kinase kinase (MEK). Analysis of metastases from patients who developed resistance to cetuximab or panitumumab showed the emergence of
KRAS
amplification in one sample and acquisition of secondary
KRAS
mutations in 60% (6 out of 10) of the cases.
KRAS
mutant alleles were detectable in the blood of cetuximab-treated patients as early as 10 months before radiographic documentation of disease progression. In summary, the results identify
KRAS
mutations as frequent drivers of acquired resistance to cetuximab in colorectal cancers, indicate that the emergence of
KRAS
mutant clones can be detected non-invasively months before radiographic progression and suggest early initiation of a MEK inhibitor as a rational strategy for delaying or reversing drug resistance. |
|---|---|
| AbstractList | A main limitation of therapies that selectively target kinase signalling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal antibody that binds the extracellular domain of epidermal growth factor receptor (EGFR), is effective in a subset of KRAS wild-type metastatic colorectal cancers. After an initial response, secondary resistance invariably ensues, thereby limiting the clinical benefit of this drug. The molecular bases of secondary resistance to cetuximab in colorectal cancer are poorly understood. Here we show that molecular alterations (in most instances point mutations) of KRAS are causally associated with the onset of acquired resistance to anti-EGFR treatment in colorectal cancers. Expression of mutant KRAS under the control of its endogenous gene promoter was sufficient to confer cetuximab resistance, but resistant cells remained sensitive to combinatorial inhibition of EGFR and mitogen-activated protein-kinase kinase (MEK). Analysis of metastases from patients who developed resistance to cetuximab or panitumumab showed the emergence of KRAS amplification in one sample and acquisition of secondary KRAS mutations in 60% (6 out of 10) of the cases. KRAS mutant alleles were detectable in the blood of cetuximab-treated patients as early as 10 months before radiographic documentation of disease progression. In summary, the results identify KRAS mutations as frequent drivers of acquired resistance to cetuximab in colorectal cancers, indicate that the emergence of KRAS mutant clones can be detected non-invasively months before radiographic progression and suggest early initiation of a MEK inhibitor as a rational strategy for delaying or reversing drug resistance.A main limitation of therapies that selectively target kinase signalling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal antibody that binds the extracellular domain of epidermal growth factor receptor (EGFR), is effective in a subset of KRAS wild-type metastatic colorectal cancers. After an initial response, secondary resistance invariably ensues, thereby limiting the clinical benefit of this drug. The molecular bases of secondary resistance to cetuximab in colorectal cancer are poorly understood. Here we show that molecular alterations (in most instances point mutations) of KRAS are causally associated with the onset of acquired resistance to anti-EGFR treatment in colorectal cancers. Expression of mutant KRAS under the control of its endogenous gene promoter was sufficient to confer cetuximab resistance, but resistant cells remained sensitive to combinatorial inhibition of EGFR and mitogen-activated protein-kinase kinase (MEK). Analysis of metastases from patients who developed resistance to cetuximab or panitumumab showed the emergence of KRAS amplification in one sample and acquisition of secondary KRAS mutations in 60% (6 out of 10) of the cases. KRAS mutant alleles were detectable in the blood of cetuximab-treated patients as early as 10 months before radiographic documentation of disease progression. In summary, the results identify KRAS mutations as frequent drivers of acquired resistance to cetuximab in colorectal cancers, indicate that the emergence of KRAS mutant clones can be detected non-invasively months before radiographic progression and suggest early initiation of a MEK inhibitor as a rational strategy for delaying or reversing drug resistance. A main limitation of therapies that selectively target kinase signalling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal antibody that binds the extracellular domain of epidermal growth factor receptor (EGFR), is effective in a subset of KRAS wild-type metastatic colorectal cancers1. After an initial response, secondary resistance invariably ensues, thereby limiting the clinical benefit of this drug2. The molecular bases of secondary resistance to cetuximab in colorectal cancer are poorly understood3-8. Here we show that molecular alterations (in most instances point mutations) of KRAS are causally associated with the onset of acquired resistance to anti-EGFR treatment in colorectal cancers. Expression of mutant KRAS under the control of its endogenous gene promoter was sufficient to confer cetuximab resistance, but resistant cells remained sensitive to combinatorial inhibition of EGFR and mitogen-activated protein-kinase kinase (MEK). Analysis of metastases from patients who developed resistance to cetuximab or panitumumab showed the emergence of KRAS amplification in one sample and acquisition of secondary KRAS mutations in 60% (6 out of 10) of the cases. KRAS mutant alleles were detectable in the blood of cetuximab-treated patients as early as 10 months before radiographic documentation of disease progression. In summary, the results identify KRAS mutations as frequent drivers of acquired resistance to cetuximab in colorectal cancers, indicate that the emergence of KRAS mutant clones can be detected non-invasively months before radiographic progression and suggest early initiation of a MEK inhibitor as a rational strategy for delaying or reversing drug resistance. [PUBLICATION ABSTRACT] Molecular alterations in KRAS are associated with acquired resistance to anti-epidermal growth factor receptor (EGFR) treatment in colorectal cancer; resistant mutations can be identified in the blood of patients, months before clinical evidence of disease progression. Acquired resistance in anti-EGFR therapy Antibodies targeting epidermal growth factor receptor (EGFR) have become an established treatment for colorectal cancer, but they are contraindicated in patients carrying mutations in the KRAS oncogene. Drug resistance can also arise in initially responsive patients, and two papers in this issue of Nature present unequivocal evidence that mutations in KRAS underlie acquired resistance to anti-EGFR antibodies in many patients and that KRAS mutations can be detected in the serum of patients before the clinical emergence of resistance and relapse. Misale et al . show in cell-line models that KRAS mutations can confer resistance to cetuximab. And in colorectal cancer patients treated with cetuximab or panitumumab, resistance is associated with KRAS mutations selected from pre-existing subclones or acquired during treatment. Diaz et al . also find KRAS mutations accumulating in patients becoming resistant to panitumumab. Their mathematical models suggest that KRAS mutations pre-existed in tumour cells before therapy, which may explain why clinical recurrence is usually seen after about six months of treatment, by which time the resistant subpopulations of tumour cells with KRAS mutations has expanded. The apparent inevitability of resistance suggests that combinations of drugs targeting more than one oncogenic pathway will be needed if resistance is to be avoided. A main limitation of therapies that selectively target kinase signalling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal antibody that binds the extracellular domain of epidermal growth factor receptor (EGFR), is effective in a subset of KRAS wild-type metastatic colorectal cancers 1 . After an initial response, secondary resistance invariably ensues, thereby limiting the clinical benefit of this drug 2 . The molecular bases of secondary resistance to cetuximab in colorectal cancer are poorly understood 3 , 4 , 5 , 6 , 7 , 8 . Here we show that molecular alterations (in most instances point mutations) of KRAS are causally associated with the onset of acquired resistance to anti-EGFR treatment in colorectal cancers. Expression of mutant KRAS under the control of its endogenous gene promoter was sufficient to confer cetuximab resistance, but resistant cells remained sensitive to combinatorial inhibition of EGFR and mitogen-activated protein-kinase kinase (MEK). Analysis of metastases from patients who developed resistance to cetuximab or panitumumab showed the emergence of KRAS amplification in one sample and acquisition of secondary KRAS mutations in 60% (6 out of 10) of the cases. KRAS mutant alleles were detectable in the blood of cetuximab-treated patients as early as 10 months before radiographic documentation of disease progression. In summary, the results identify KRAS mutations as frequent drivers of acquired resistance to cetuximab in colorectal cancers, indicate that the emergence of KRAS mutant clones can be detected non-invasively months before radiographic progression and suggest early initiation of a MEK inhibitor as a rational strategy for delaying or reversing drug resistance. A main limitation of therapies that selectively target kinase signalling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal antibody that binds the extracellular domain of epidermal growth factor receptor (EGFR), is effective in a subset of KRAS wild-type metastatic colorectal cancers. After an initial response, secondary resistance invariably ensues, thereby limiting the clinical benefit of this drug. The molecular bases of secondary resistance to cetuximab in colorectal cancer are poorly understood. Here we show that molecular alterations (in most instances point mutations) of KRAS are causally associated with the onset of acquired resistance to anti-EGFR treatment in colorectal cancers. Expression of mutant KRAS under the control of its endogenous gene promoter was sufficient to confer cetuximab resistance, but resistant cells remained sensitive to combinatorial inhibition of EGFR and mitogen-activated protein-kinase kinase (MEK). Analysis of metastases from patients who developed resistance to cetuximab or panitumumab showed the emergence of KRAS amplification in one sample and acquisition of secondary KRAS mutations in 60% (6 out of 10) of the cases. KRAS mutant alleles were detectable in the blood of cetuximab-treated patients as early as 10 months before radiographic documentation of disease progression. In summary, the results identify KRAS mutations as frequent drivers of acquired resistance to cetuximab in colorectal cancers, indicate that the emergence of KRAS mutant clones can be detected non-invasively months before radiographic progression and suggest early initiation of a MEK inhibitor as a rational strategy for delaying or reversing drug resistance. A main limitation of therapies that selectively target kinase signaling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal antibody that binds the extracellular domain of EGFR, is effective in a subset of KRAS wild type metastatic colorectal cancers1. After an initial response, secondary resistance invariably ensues, thereby limiting the clinical benefit of this drug2. The molecular bases of secondary resistance to cetuximab in colorectal cancer are poorly understood3-8. Here, we show for the first time that molecular alterations (in most instances point mutations) of KRAS are causally associated with the onset of acquired resistance to anti-EGFR treatment in colorectal cancers. Expression of mutant KRAS under the control of its endogenous gene promoter was sufficient to confer cetuximab resistance but resistant cells remained sensitive to combinatorial inhibition of EGFR and MEK. Analysis of metastases from patients who developed resistance to cetuximab or panitumumab showed the emergence of KRAS amplification in one sample and acquisition of secondary KRAS mutations in 60% (6/10) of the cases. KRAS mutant alleles were detectable in the blood of cetuximab treated patients as early as 10 months prior to radiographic documentation of disease progression. In summary, the results identify KRAS mutations as frequent drivers of acquired resistance to cetuximab in colorectal cancers, indicate that the emergence of KRAS mutant clones can be detected non-invasively months prior to radiographic progression and suggest early initiation of a MEK inhibitor as a rational strategy for delaying or reversing drug resistance. |
| Author | Misale, Sandra Cercek, Andrea Gallicchio, Margherita Chen, Chin-Tung Scala, Elisa Di Nicolantonio, Federica Sartore-Bianchi, Andrea Bencardino, Katia Solit, David Schiavo, Roberta Medico, Enzo Liska, David Buscarino, Michela Janakiraman, Manickam Weiser, Martin Hobor, Sebastijan Veronese, Silvio Vakiani, Efsevia Boscaro, Valentina Siravegna, Giulia Gambacorta, Marcello Siena, Salvatore Bardelli, Alberto Yaeger, Rona Valtorta, Emanuele Zanon, Carlo |
| AuthorAffiliation | 5 Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, USA 7 Falck Division of Medical Oncology, Ospedale Niguarda Ca' Granda, 20162 Milano, Italy 3 Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, USA 4 Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, USA 6 Division of Pathology, Ospedale Niguarda Ca' Granda, 20162 Milano, Italy 8 Dipartimento di Scienza e Tecnologia del Farmaco, University of Torino, 10125 Torino, Italy 9 Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, USA 2 Department of Oncological Sciences, University of Torino Medical School, 10060 Candiolo (Torino), Italy 10 Laboratory of Functional Genomics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy 1 Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy 11 FIRC Institute of Molecular Oncology (IFOM), 20139 Milano, Italy |
| AuthorAffiliation_xml | – name: 4 Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, USA – name: 9 Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, USA – name: 2 Department of Oncological Sciences, University of Torino Medical School, 10060 Candiolo (Torino), Italy – name: 11 FIRC Institute of Molecular Oncology (IFOM), 20139 Milano, Italy – name: 3 Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, USA – name: 1 Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy – name: 8 Dipartimento di Scienza e Tecnologia del Farmaco, University of Torino, 10125 Torino, Italy – name: 10 Laboratory of Functional Genomics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy – name: 5 Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, USA – name: 6 Division of Pathology, Ospedale Niguarda Ca' Granda, 20162 Milano, Italy – name: 7 Falck Division of Medical Oncology, Ospedale Niguarda Ca' Granda, 20162 Milano, Italy |
| Author_xml | – sequence: 1 givenname: Sandra surname: Misale fullname: Misale, Sandra organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy , Department of Oncological Sciences, University of Torino Medical School, 10060 Candiolo (Torino), Italy – sequence: 2 givenname: Rona surname: Yaeger fullname: Yaeger, Rona organization: Department of Medicine, Memorial Sloan-Kettering Cancer Center – sequence: 3 givenname: Sebastijan surname: Hobor fullname: Hobor, Sebastijan organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy – sequence: 4 givenname: Elisa surname: Scala fullname: Scala, Elisa organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy , Department of Oncological Sciences, University of Torino Medical School, 10060 Candiolo (Torino), Italy – sequence: 5 givenname: Manickam surname: Janakiraman fullname: Janakiraman, Manickam organization: Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center – sequence: 6 givenname: David surname: Liska fullname: Liska, David organization: Department of Surgery, Memorial Sloan-Kettering Cancer Center – sequence: 7 givenname: Emanuele surname: Valtorta fullname: Valtorta, Emanuele organization: Division of Pathology, Ospedale Niguarda Ca’ Granda, 20162 Milano, Italy – sequence: 8 givenname: Roberta surname: Schiavo fullname: Schiavo, Roberta organization: Falck Division of Medical Oncology, Ospedale Niguarda Ca’ Granda, 20162 Milano, Italy – sequence: 9 givenname: Michela surname: Buscarino fullname: Buscarino, Michela organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy , Department of Oncological Sciences, University of Torino Medical School, 10060 Candiolo (Torino), Italy – sequence: 10 givenname: Giulia surname: Siravegna fullname: Siravegna, Giulia organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy – sequence: 11 givenname: Katia surname: Bencardino fullname: Bencardino, Katia organization: Falck Division of Medical Oncology, Ospedale Niguarda Ca’ Granda, 20162 Milano, Italy – sequence: 12 givenname: Andrea surname: Cercek fullname: Cercek, Andrea organization: Department of Medicine, Memorial Sloan-Kettering Cancer Center – sequence: 13 givenname: Chin-Tung surname: Chen fullname: Chen, Chin-Tung organization: Department of Surgery, Memorial Sloan-Kettering Cancer Center – sequence: 14 givenname: Silvio surname: Veronese fullname: Veronese, Silvio organization: Division of Pathology, Ospedale Niguarda Ca’ Granda, 20162 Milano, Italy – sequence: 15 givenname: Carlo surname: Zanon fullname: Zanon, Carlo organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy – sequence: 16 givenname: Andrea surname: Sartore-Bianchi fullname: Sartore-Bianchi, Andrea organization: Falck Division of Medical Oncology, Ospedale Niguarda Ca’ Granda, 20162 Milano, Italy – sequence: 17 givenname: Marcello surname: Gambacorta fullname: Gambacorta, Marcello organization: Division of Pathology, Ospedale Niguarda Ca’ Granda, 20162 Milano, Italy – sequence: 18 givenname: Margherita surname: Gallicchio fullname: Gallicchio, Margherita organization: Dipartimento di Scienza e Tecnologia del Farmaco, University of Torino, 10125 Torino, Italy – sequence: 19 givenname: Efsevia surname: Vakiani fullname: Vakiani, Efsevia organization: Department of Pathology, Memorial Sloan-Kettering Cancer Center – sequence: 20 givenname: Valentina surname: Boscaro fullname: Boscaro, Valentina organization: Dipartimento di Scienza e Tecnologia del Farmaco, University of Torino, 10125 Torino, Italy – sequence: 21 givenname: Enzo surname: Medico fullname: Medico, Enzo organization: Department of Oncological Sciences, University of Torino Medical School, 10060 Candiolo (Torino), Italy, Laboratory of Functional Genomics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy – sequence: 22 givenname: Martin surname: Weiser fullname: Weiser, Martin organization: Department of Surgery, Memorial Sloan-Kettering Cancer Center – sequence: 23 givenname: Salvatore surname: Siena fullname: Siena, Salvatore organization: Falck Division of Medical Oncology, Ospedale Niguarda Ca’ Granda, 20162 Milano, Italy – sequence: 24 givenname: Federica surname: Di Nicolantonio fullname: Di Nicolantonio, Federica organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy , FIRC Institute of Molecular Oncology (IFOM), 20139 Milano, Italy – sequence: 25 givenname: David surname: Solit fullname: Solit, David email: solitd@mskcc.org organization: Department of Medicine, Memorial Sloan-Kettering Cancer Center, Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center – sequence: 26 givenname: Alberto surname: Bardelli fullname: Bardelli, Alberto email: alberto.bardelli@ircc.it organization: Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment (IRCC), 10060 Candiolo (Torino), Italy , Department of Oncological Sciences, University of Torino Medical School, 10060 Candiolo (Torino), Italy, FIRC Institute of Molecular Oncology (IFOM), 20139 Milano, Italy |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26036574$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/22722830$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Springer Nature Limited 2012 2015 INIST-CNRS Copyright Nature Publishing Group Jun 28, 2012 |
| Copyright_xml | – notice: Springer Nature Limited 2012 – notice: 2015 INIST-CNRS – notice: Copyright Nature Publishing Group Jun 28, 2012 |
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| DOI | 10.1038/nature11156 |
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| Keywords | Antineoplastic agent Human Treatment resistance Rectal disease Colorectal cancer Monoclonal antibody Malignant tumor Epidermal growth factor receptor Colonic disease K ras Gene Cancerology Treatment C-Onc gene Immunotherapy Genetics Digestive diseases Intestinal disease Mutation Cetuximab Protooncogene Cancer |
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| Snippet | Molecular alterations in
KRAS
are associated with acquired resistance to anti-epidermal growth factor receptor (EGFR) treatment in colorectal cancer; resistant... A main limitation of therapies that selectively target kinase signalling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal... A main limitation of therapies that selectively target kinase signaling pathways is the emergence of secondary drug resistance. Cetuximab, a monoclonal... |
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| SubjectTerms | 631/208/68 631/67/1059/2326 631/67/1504/1885 Alleles Antibodies, Monoclonal - pharmacology Antibodies, Monoclonal - therapeutic use Antibodies, Monoclonal, Humanized Antineoplastic agents Biological and medical sciences Cancer therapies Cell Line, Tumor Cetuximab Cloning Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Disease Progression Drug resistance Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - genetics ErbB Receptors - antagonists & inhibitors Experiments Gastroenterology. Liver. Pancreas. Abdomen Genes, ras - genetics Humanities and Social Sciences Humans Immunotherapy Kinases letter Mass spectrometry Medical sciences Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors multidisciplinary Mutation Mutation - genetics Panitumumab Pharmacology. Drug treatments Promoter Regions, Genetic - genetics Proteins Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins p21(ras) ras Proteins - genetics Science Science (multidisciplinary) Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Tumors |
| Title | Emergence of KRAS mutations and acquired resistance to anti-EGFR therapy in colorectal cancer |
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