Trial reportBritish journal of cancer2010
Identification of biological factors predictive of response to imatinib mesylate in aggressive fibromatosis.
Trial report in British journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
- Desmoid Tumors Characteristics, Clinical Management, Active Surveillance, and Description of Our FAP Case Series.Journal of clinical medicine · 2020Review
- Article
- Lymphopenia in Cancer Patients and its Effects on Response to Immunotherapy: an opportunity for combination with Cytokines?Journal for immunotherapy of cancer · 2019Review
- Activated Signaling Pathways and Targeted Therapies in Desmoid-Type Fibromatosis: A Literature Review.Frontiers in oncology · 2019Review
- Towards standardization of next-generation sequencing of FFPE samples for clinical oncology: intrinsic obstacles and possible solutions.Journal of translational medicine · 2017Article
- Retrospective study testing next generation sequencing of selected cancer-associated genes in resected prostate cancer.Oncotarget · 2016Article
- Extra-abdominal fibromatosis: Clinical and therapeutic considerations based on an illustrative case.Oncology letters · 2015Article
- KIT exon 10 variant (c.1621 A > C) single nucleotide polymorphism as predictor of GIST patient outcome.BMC cancer · 2015Article
- Next-generation sequencing reveals clinically actionable molecular markers in myeloid sarcoma.Leukemia · 2015Article
- Desmoid tumour in familial adenomatous polyposis patients: responses to treatments.Familial cancer · 2015Article
- Five years of local control of subscapularis aggressive fibromatosis managed by surgery and imatinib: a case report.Journal of medical case reports · 2014Article
- Article
- Article
- The impact of chemotherapy-associated neutrophil/ lymphocyte counts on prognosis of adjuvant chemotherapy in colorectal cancer.BMC cancer · 2013Article
- Signal transduction pathway analysis in fibromatosis: receptor and nonreceptor tyrosine kinases.Human pathology · 2012Article
Corrections and comments
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Authors and funding
14 authors at 10 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImatinib induces responses and disease stabilisations in non-resectable patients with aggressive fibromatosis (AF). The precise target of imatinib in AF and predictive factors for response to treatment are unknown.
methodsWe investigated factors potentially predictive of response to imatinib in a series of 40 patients with progressive AF included in a phase II trial of imatinib: we tested the presence of KIT exon 10 variant (M541L), the expression of imatinib-sensitive kinases and cell cycle proteins by immunohistochemistry (IHC), and other clinical and biological factors.
resultsOf 10 patients for whom DNA could be extracted, 3 had a KIT exon 10 variant (30%), with no correlation with response or progression-free survival (PFS). The expression of other imatinib targets (PDGFRA/B, macrophage colony-stimulating factor receptor (M-CSFR)) and of downstream components of the cell cycle, cell proliferation and proliferation pathway (cyclin D1, ERK, MEK 1-2) did not correlate with PFS. Pre-treatment lymphopenia (<1500/microl) and tumour size >120 mm correlated with shorter PFS in univariate and multivariate analyses.
conclusionOur findings show that a baseline biological characteristic of the patient is the major parameter influencing response to imatinib in aggressive fibromatosis. Tumour characteristics, including the presence of a KIT exon 10 M541L variant, may influence tumour control but this needs to be confirmed and better explained.
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