Special Issue "Hepatocyte Growth Factor Pathway in Cancer"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (28 February 2017)
Prof. Dr. Jill M. Siegfried
Professor and Head, Department of Pharmacology, Frederick and Alice Stark Endowed Chair, Masonic Cancer Center, University of Minnesota Medical School, Minneapolis, MN 55455, USA
Website | E-Mail
Interests: lung cancer; HGF; estrogen; EGFR; c-Met; targeted therapy; non-small cell lung cancer; cell signaling
Hepatocyte Growth Factor, the ligand for the c-MET receptor, plays a critical role in normal development, wound healing, and tissue regeneration. It is also important in angiogenesis, invasion, and metastasis in cancer. HGF is produced in the tumor microenvironment, usually secreted by mesenchymal cells, while c-MET is expressed by cells of many lineages, including epithelial, endothelial, and hematopoietic. In many solid tumors and hematological malignancies, mutation, amplification or over-expression of c-MET has been reported, as well as up-regulated levels of HGF. Cross-talk between c-MET and other tyrosine kinase receptors is well-documented, with c-MET serving to amplify signaling of the EGFR pathway and to activate HER3. Up-regulation of c-MET signaling is also found in patients who develop resistance to agents targeting EGFR and VEGFR, mainly through amplification or activating mutation. Preclinical evidence is strong that the HGF/c-MET pathway contributes to many oncogenic processes, and a number of strategies have been developed to inhibit either the ligand or the receptor. Clinical trial results have been disappointing, however, for a number of solid tumors, and combination regimens with agents targeting the HGF/c-MET pathway have not performed, as well as predicted from laboratory and animal studies, or have proven highly toxic.
One of the current challenges is to identify the population of patients who would derive benefit from c-MET pathway interruption. Higher benefit could also justify the risks involved with combination therapies. Recent data suggest that patients with amplification or mutation of c-MET (such as exon 14-skipping mutations), either pre-existing or acquired after failure of another targeted therapy, show the highest dependence on HGF/c-MET signaling. Evidence also suggests that high expression level of c-MET protein confers dependence, but a standardized test of c-MET expression, or another biomarker that would provide guidance for patient selection, is still lacking. This Special Issue will highlight the current state of knowledge about HGF and c-MET in multiple cancers, including results of past clinical trials, agents still in clinical development, and status of biomarkers of sensitivity to these agents.
Prof. Dr. Jill M. Siegfried
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 850 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- receptor cross-talk
- invasion & metastasis
- lung cancer
- gastric cancer
- colorectal cancer