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Targeting HER2 in colorectal cancer: The landscape of amplification and short variant mutations in ERBB2 and ERBB3
Cancer, 2018-04, Vol.124 (7), p.1358-1373
Ross, Jeffrey S.
Fakih, Marwan
Ali, Siraj M.
Elvin, Julia A.
Schrock, Alexa B.
Suh, James
Vergilio, Jo‐Anne
Ramkissoon, Shakti
Severson, Eric
Daniel, Sugganth
Fabrizio, David
Frampton, Garrett
Sun, James
Miller, Vincent A.
Stephens, Philip J.
Gay, Laurie M.
2018
Details
Autor(en) / Beteiligte
Ross, Jeffrey S.
Fakih, Marwan
Ali, Siraj M.
Elvin, Julia A.
Schrock, Alexa B.
Suh, James
Vergilio, Jo‐Anne
Ramkissoon, Shakti
Severson, Eric
Daniel, Sugganth
Fabrizio, David
Frampton, Garrett
Sun, James
Miller, Vincent A.
Stephens, Philip J.
Gay, Laurie M.
Titel
Targeting HER2 in colorectal cancer: The landscape of amplification and short variant mutations in ERBB2 and ERBB3
Ist Teil von
Cancer, 2018-04, Vol.124 (7), p.1358-1373
Ort / Verlag
United States: Wiley Subscription Services, Inc
Erscheinungsjahr
2018
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
BACKGROUND In contrast to lung cancer, few precision treatments are available for colorectal cancer (CRC). One rapidly emerging treatment target in CRC is ERBB2 (human epidermal growth factor receptor 2 [HER2]). Oncogenic alterations in HER2, or its dimerization partner HER3, can underlie sensitivity to HER2‐targeted therapies. METHODS In this study, 8887 CRC cases were evaluated by comprehensive genomic profiling for genomic alterations in 315 cancer‐related genes, tumor mutational burden, and microsatellite instability. This cohort included both colonic (7599 cases; 85.5%) and rectal (1288 cases; 14.5%) adenocarcinomas. RESULTS A total of 569 mCRCs were positive for ERBB2 (429 cases; 4.8%) and/or ERBB3 (148 cases; 1.7%) and featured ERBB amplification, short variant alterations, or a combination of the 2. High tumor mutational burden (≥20 mutations/Mb) was significantly more common in ERBB‐mutated samples, and ERBB3‐mutated CRCs were significantly more likely to have high microsatellite instability (P<.002). Alterations affecting KRAS (27.3%) were significantly underrepresented in ERBB2‐amplified samples compared with wild‐type CRC samples (51.8%), and ERBB2‐ or ERBB3‐mutated samples (49.0% and 60.8%, respectively) (P<.01). Other significant differences in mutation frequency were observed for genes in the PI3K/MTOR and mismatch repair pathways. CONCLUSIONS Although observed less often than in breast or upper gastrointestinal carcinomas, indications for which anti‐HER2 therapies are approved, the percentage of CRC with ERBB genomic alterations is significant. Importantly, 32% of ERBB2‐positive CRCs harbor short variant alterations that are undetectable by routine immunohistochemistry or fluorescence in situ hybridization testing. The success of anti‐HER2 therapies in ongoing clinical trials is a promising development for patients with CRC. Cancer 2018;124:1358‐73. © 2018 Foundation Medicine, Inc. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. Greater than 6% of colorectal cancer cases harbor activating alterations in ERBB2 or ERBB3, representing a significant population of patients who may benefit from therapies targeting human epidermal growth factor receptor 2 (HER2) and the ERBB pathway. The success of anti‐HER2 therapies in ongoing clinical trials is a promising development for patients with colorectal cancer.
Sprache
Englisch
Identifikatoren
ISSN: 0008-543X
eISSN: 1097-0142
DOI: 10.1002/cncr.31125
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5900732
Format
–
Schlagworte
1-Phosphatidylinositol 3-kinase
,
Adolescent
,
Adult
,
Aged
,
Aged, 80 and over
,
Amplification
,
Antineoplastic Combined Chemotherapy Protocols - therapeutic use
,
Biomarkers, Tumor - genetics
,
Breast carcinoma
,
Cancer
,
Child
,
Clinical trials
,
colorectal adenocarcinoma
,
Colorectal cancer
,
Colorectal carcinoma
,
Colorectal Neoplasms - drug therapy
,
Colorectal Neoplasms - genetics
,
Colorectal Neoplasms - pathology
,
comprehensive genomic profiling
,
Dimerization
,
Epidermal growth factor
,
ErbB protein
,
ErbB-2 protein
,
ErbB-3 protein
,
ERBB2, ERBB3
,
Female
,
Fluorescence
,
Fluorescence in situ hybridization
,
Follow-Up Studies
,
Gene Amplification
,
Gene Expression Regulation, Neoplastic
,
Genes
,
Genomics
,
human epidermal growth factor receptor 2 (HER2)
,
Humans
,
Immunohistochemistry
,
Immunotherapy
,
lapatinib
,
Lung cancer
,
Male
,
Medical research
,
Microsatellite Instability
,
Middle Aged
,
Mismatch repair
,
Molecular Targeted Therapy
,
Monoclonal antibodies
,
Mutation
,
Original
,
pertuzumab
,
Prognosis
,
Receptor, ErbB-2 - genetics
,
Receptor, ErbB-3 - genetics
,
Rectum
,
Stability
,
Targeted cancer therapy
,
TOR protein
,
trastuzumab
,
tumor mutational burden
,
Young Adult
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