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Cancers
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Revolutionizing Cancer Therapy: Unleashing the Power of MET Inhibitors
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Revolutionizing Cancer Therapy: Unleashing the Power of MET Inhibitors

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 7314

Special Issue Editor

Prof. Dr. Sang Hyub Lee

E-Mail Website
Guest Editor
Department of Internal Medicine and Liver Research Institute, Seoul National University Hospital, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
Interests: oncology; pancreatic cancer; gastrointestinal cancer

Special Issue Information

Dear Colleagues,

We would like to discuss the HGF-MET signaling pathway, which involves the interaction between the Mesenchymal Epithelial Transition Factor (MET) receptor and its ligand, the Hepatocyte Growth Factor (HGF). This pathway plays a crucial role in various cellular processes, such as cell proliferation, motility, morphogenesis, angiogenesis, and tissue regeneration. Dysregulation of the MET signaling system is associated with various malignancies.

MET-TKI inhibitors, as agents targeting the MET-HGF signaling pathway, have shown promising results in various cancer types with resistance to conventional chemotherapy. Continuous research findings have been reported, demonstrating their efficacy in cancer subtypes resistant to first-line treatment. Beyond second-line regimens, studies are also exploring the use of MET inhibitors in neoadjuvant and combination regimens for multiple cancer types, with ongoing research anticipated in the future.

In this Special Issue, we aim to focus on the promising target agent, MET inhibitors, and invite contributions from multidisciplinary expert groups engaged in research related to targeting the MET-HGF signaling pathway for various cancer treatments. This Special Issue seeks to present studies that apply next-generation sequencing (NGS) technology to the development of target agents, not only contributing to the treatment of lung cancer, but also exploring the potential for diverse cancer types, including gastric cancer, hepatocellular carcinoma, and pancreatic cancer.

We believe that this Special Issue will make significant contributions to the development of promising therapies for various cancer types, utilizing MET-TKI inhibitors as a potential targeted therapy. We welcome research papers that explore the efficacy and safety of MET inhibitors, and we anticipate that this Special Issue will foster advancements in the field of oncology and inspire future investigations in cancer treatment.

We invite researchers and experts to submit their original research, reviews, and for consideration in this Special Issue. Together, we can advance the understanding and application of MET inhibitors in cancer treatment and contribute to the development of innovative therapies for various malignancies.

Prof. Dr. Sang Hyub Lee
Guest Editor

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 submissions that pass pre-check are 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 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 semimonthly 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 2900 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.

Keywords

  • epithelial–mesenchymal transition
  • mesenchymal–epithelial transition
  • MET gene mutation
  • MET exon14 skipping
  • hepatocyte growth factor
  • tumor microenvironment
  • savolitinib
  • crizotinib
  • cabozatinib
  • tepotinib

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Published Papers (2 papers)

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Review

37 pages, 3636 KiB  
Review
Relationship of Signaling Pathways between RKIP Expression and the Inhibition of EMT-Inducing Transcription Factors SNAIL1/2, TWIST1/2 and ZEB1/2
by Andrew Bustamante, Stavroula Baritaki, Apostolos Zaravinos and Benjamin Bonavida
Cancers 2024, 16(18), 3180; https://doi.org/10.3390/cancers16183180 - 17 Sep 2024
Cited by 1 | Viewed by 2335
Abstract
Untreated primary carcinomas often lead to progression, invasion and metastasis, a process that involves the epithelial-to-mesenchymal transition (EMT). Several transcription factors (TFs) mediate the development of EMT, including SNAIL1/SNAIL2, TWIST1/TWIST2 and ZEB1/ZEB2, which are overexpressed in various carcinomas along with the under expression [...] Read more.
Untreated primary carcinomas often lead to progression, invasion and metastasis, a process that involves the epithelial-to-mesenchymal transition (EMT). Several transcription factors (TFs) mediate the development of EMT, including SNAIL1/SNAIL2, TWIST1/TWIST2 and ZEB1/ZEB2, which are overexpressed in various carcinomas along with the under expression of the metastasis suppressor Raf Kinase Inhibitor Protein (RKIP). Overexpression of RKIP inhibits EMT and the above associated TFs. We, therefore, hypothesized that there are inhibitory cross-talk signaling pathways between RKIP and these TFs. Accordingly, we analyzed the various properties and biomarkers associated with the epithelial and mesenchymal tissues and the various molecular signaling pathways that trigger the EMT phenotype such as the TGF-β, the RTK and the Wnt pathways. We also presented the various functions and the transcriptional, post-transcriptional and epigenetic regulations for the expression of each of the EMT TFs. Likewise, we describe the transcriptional, post-transcriptional and epigenetic regulations of RKIP expression. Various signaling pathways mediated by RKIP, including the Raf/MEK/ERK pathway, inhibit the TFs associated with EMT and the stabilization of epithelial E-Cadherin expression. The inverse relationship between RKIP and the TF expressions and the cross-talks were further analyzed by bioinformatic analysis. High mRNA levels of RKIP correlated negatively with those of SNAIL1, SNAIL2, TWIST1, TWIST2, ZEB1, and ZEB2 in several but not all carcinomas. However, in these carcinomas, high levels of RKIP were associated with good prognosis, whereas high levels of the above transcription factors were associated with poor prognosis. Based on the inverse relationship between RKIP and EMT TFs, it is postulated that the expression level of RKIP in various carcinomas is clinically relevant as both a prognostic and diagnostic biomarker. In addition, targeting RKIP induction by agonists, gene therapy and immunotherapy will result not only in the inhibition of EMT and metastases in carcinomas, but also in the inhibition of tumor growth and reversal of resistance to various therapeutic strategies. However, such targeting strategies must be better investigated as a result of tumor heterogeneities and inherent resistance and should be better adapted as personalized medicine. Full article
(This article belongs to the Special Issue Revolutionizing Cancer Therapy: Unleashing the Power of MET Inhibitors)
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17 pages, 1060 KiB  
Review
Savolitinib: A Promising Targeting Agent for Cancer
by Tae Seung Lee, Jun Yeol Kim, Myeong Hwan Lee, In Rae Cho, Woo Hyun Paik, Ji Kon Ryu, Yong-Tae Kim and Sang Hyub Lee
Cancers 2023, 15(19), 4708; https://doi.org/10.3390/cancers15194708 - 25 Sep 2023
Cited by 7 | Viewed by 4532
Abstract
Savolitinib is a highly selective small molecule inhibitor of the mesenchymal epithelial transition factor (MET) tyrosine kinase, primarily developed for the treatment of non-small cell lung cancer (NSCLC) with MET mutations. It is also being investigated as a treatment for breast, head and [...] Read more.
Savolitinib is a highly selective small molecule inhibitor of the mesenchymal epithelial transition factor (MET) tyrosine kinase, primarily developed for the treatment of non-small cell lung cancer (NSCLC) with MET mutations. It is also being investigated as a treatment for breast, head and neck, colorectal, gastric, pancreatic, and other gastrointestinal cancers. In both preclinical and clinical studies, it has demonstrated efficacy in lung, kidney, and stomach cancers. Savolitinib is an oral anti-cancer medication taken as a 600 mg dose once daily. It can be used as a monotherapy in patients with non-small cell lung cancer with MET mutations and in combination with epidermal growth factor receptor (EGFR) inhibitors for patients who have developed resistance to them. Furthermore, savolitinib has shown positive results in gastric cancer treatment, particularly in combination with docetaxel. As a result, this review aims to validate its efficacy in NSCLC and suggests its potential application in other gastrointestinal cancers, such as pancreatic cancer, based on related research in gastric and renal cancer. Full article
(This article belongs to the Special Issue Revolutionizing Cancer Therapy: Unleashing the Power of MET Inhibitors)
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