publication . Other literature type . Article . 2015 . Embargo end date: 13 Feb 2020

Therapy-induced tumour secretomes promote resistance and tumour progression

Andrew L. Ji; Hubing Shi; Weiping Shu; Thomas Wiesner; Marcus C. Bosenberg; Sakari Vanharanta; Sakari Vanharanta; Yilong Zou; Anna C. Obenauf; Xiangju Kong; ...
Open Access
  • Published: 25 Mar 2015
  • Publisher: Apollo - University of Cambridge Repository
  • Country: United Kingdom
Abstract
Tumour cells respond to an effective, targeted drug treatment with BRAF, ALK or EGFR kinase inhibitors by inducing a complex network of secreted signals that promote tumour growth, dissemination and metastasis of drug-resistant cancer cell clones, and increase the survival of drug-sensitive tumour cells, potentially contributing to incomplete tumour regression. Targeted kinase inhibitors such as have proved clinically effective in melanoma with BRAF mutations and in lung adenocarcinoma with EGFR mutations or ALK translocations, but drug resistance almost always follows. This study by Joan Massague and colleagues shows that tumour cells responding to kinase inhib...
Subjects
free text keywords: Cell Line, Tumor, Clone Cells, Animals, Humans, Mice, Melanoma, Adenocarcinoma, Lung Neoplasms, Neoplasm Metastasis, Disease Progression, Proto-Oncogene Proteins B-raf, Receptor Protein-Tyrosine Kinases, Proto-Oncogene Proteins c-fos, Protein Kinase Inhibitors, Signal Transduction, Cell Proliferation, Cell Movement, Cell Survival, Down-Regulation, Enzyme Activation, Drug Resistance, Neoplasm, Female, Proto-Oncogene Proteins c-akt, Metabolome, Tumor Microenvironment, ErbB Receptors, Anaplastic Lymphoma Kinase, Article, Multidisciplinary, Metastasis, medicine.disease, medicine, Protein kinase B, Cancer cell, Biology, Cancer research, Targeted therapy, medicine.medical_treatment, Vemurafenib, medicine.drug
Funded by
NIH| MOUSE GENETICS
Project
  • Funder: National Institutes of Health (NIH)
  • Project Code: 2P30CA008748-43
  • Funding stream: NATIONAL CANCER INSTITUTE
,
FWF| The impact of stochastic (epi)mutations on the aging genome
Project
  • Funder: Austrian Science Fund (FWF) (FWF)
  • Project Code: J 3013
  • Funding stream: Schrödinger-Programm
38 references, page 1 of 3

Engelman, JA, Settleman, J. Acquired resistance to tyrosine kinase inhibitors during cancer therapy. Current opinion in genetics & development. 2008; 18: 73-79 [OpenAIRE] [PubMed] [DOI]

Holohan, C, Van Schaeybroeck, S, Longley, DB, Johnston, PG. Cancer drug resistance: an evolving paradigm. Nature reviews. Cancer. 2013; 13: 714-726 [OpenAIRE] [PubMed] [DOI]

Chapman, PB. Improved survival with vemurafenib in melanoma with BRAF V600E mutation. The New England journal of medicine. 2011; 364: 2507-2516 [OpenAIRE] [PubMed] [DOI]

Sosman, JA. Survival in BRAF V600-mutant advanced melanoma treated with vemurafenib. The New England journal of medicine. 2012; 366: 707-714 [OpenAIRE] [PubMed] [DOI]

Shaw, AT, Engelman, JA. ALK in lung cancer: past, present, and future. Journal of clinical oncology: official journal of the American Society of Clinical Oncology. 2013; 31: 1105-1111 [OpenAIRE] [PubMed] [DOI]

Zhou, C. Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, open-label, randomised, phase 3 study. The Lancet. Oncology. 2011; 12: 735-742 [PubMed] [DOI]

Villanueva, J. Acquired resistance to BRAF inhibitors mediated by a RAF kinase switch in melanoma can be overcome by cotargeting MEK and IGF-1R/PI3K. Cancer cell. 2010; 18: 683-695 [OpenAIRE] [PubMed] [DOI]

Nazarian, R. Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation. Nature. 2010; 468: 973-977 [OpenAIRE] [PubMed] [DOI]

Poulikakos, PI. RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E). Nature. 2011; 480: 387-390 [OpenAIRE] [PubMed] [DOI]

Wagle, N. Dissecting therapeutic resistance to RAF inhibition in melanoma by tumor genomic profiling. Journal of clinical oncology: official journal of the American Society of Clinical Oncology. 2011; 29: 3085-3096 [OpenAIRE] [PubMed] [DOI]

Lito, P. Relief of profound feedback inhibition of mitogenic signaling by RAF inhibitors attenuates their activity in BRAFV600E melanomas. Cancer cell. 2012; 22: 668-682 [OpenAIRE] [PubMed] [DOI]

Shi, H. Melanoma whole-exome sequencing identifies V600EB-RAF amplification-mediated acquired B-RAF inhibitor resistance. Nature Communications. ; 3 (1): 724-728

Wilson, TR. Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors. Nature. 2012; 487: 505-509 [OpenAIRE] [PubMed] [DOI]

Straussman, R. Tumour micro-environment elicits innate resistance to RAF inhibitors through HGF secretion. Nature. 2012; 487: 500-504 [OpenAIRE] [PubMed] [DOI]

Johannessen, CM. A melanocyte lineage program confers resistance to MAP kinase pathway inhibition. Nature. 2013; 504: 138-142 [OpenAIRE] [PubMed] [DOI]

38 references, page 1 of 3
Any information missing or wrong?Report an Issue