ArticlePloS one2014
Gain of ALK gene copy number may predict lack of benefit from anti-EGFR treatment in patients with advanced colorectal cancer and RAS-RAF-PI3KCA wild-type status.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The autocrine loop of ALK receptor and ALKAL2 ligand is an actionable target in consensus molecular subtype 1 colon cancer.Journal of experimental & clinical cancer research : CR · 2022Pooled it
- CCN1 is a therapeutic target upregulated in EML4-ALK mutant lung adenocarcinoma reversibly resistant to alectinib.Cell death & disease · 2025Article
- Progress in clinical diagnosis and treatment of colorectal cancer with rare genetic variants.Cancer biology & medicine · 2024Review
- The association of blood ctDNA levels to mutations of marker genes in colorectal cancer.Cancer reports (Hoboken, N.J.) · 2023Article
- Prognostic value of ALK overexpression and molecular abnormalities in high-grade serous ovarian carcinoma.Cancer biomarkers : section A of Disease markers · 2023Article
- Article
- ALK: a tyrosine kinase target for cancer therapy.Cold Spring Harbor molecular case studies · 2017Review
- Potential biomarkers for anti-EGFR therapy in metastatic colorectal cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- ALK gene copy number gains in non-small-cell lung cancer: prognostic impact and clinico-pathological correlations.Respiratory research · 2016Article
- Anaplastic lymphoma kinase protein expression predicts micrometastases and prognosis for patients with hepatocellular carcinoma.Oncology letters · 2016Article
- Overexpression ofOncology letters · 2015Article
- Analysis of ALK gene in 133 patients with breast cancer revealed polysomy of chromosome 2 and no ALK amplification.SpringerPlus · 2015Article
- Cost-effectiveness of RAS screening before monoclonal antibodies therapy in metastatic colorectal cancer based on FIRE3 Study.Cancer biology & therapy · 2015Article
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Authors and funding
13 authors.
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Abstract
introductionAlthough cetuximab and panitumumab show an increased efficacy for patients with KRAS-NRAS-BRAF and PI3KCA wild-type metastatic colorectal cancer, primary resistance occurs in a relevant subset of molecularly enriched populations. PATIENTS AND
methodsWe evaluated the outcome of 68 patients with advanced colorectal cancer and RAS, BRAF and PI3KCA status according to ALK gene status (disomic vs. gain of ALK gene copy number--defined as mean of 3 to 5 fusion signals in ≥ 10% of cells). All consecutive patients received cetuximab and irinotecan or panitumumab alone for chemorefractory disease.
resultsNo ALK translocations or amplifications were detected. ALK gene copy number gain was found in 25 (37%) tumors. Response rate was significantly higher in patients with disomic ALK as compared to those with gain of gene copy number (70% vs. 32%; p = 0.0048). Similarly, progression-free survival was significantly different when comparing the two groups (6.7 vs. 5.3 months; p = 0.045). A trend was observed also for overall survival (18.5 vs. 15.6 months; p = 0.885).
conclusionGain of ALK gene copy number might represent a negative prognostic factor in mCRC and may have a role in resistance to anti-EGFR therapy.
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