“The signaling and that binding of the MET and the HGF help, in a downstream way, lead to cell proliferation, cell motility, survival, angiogenesis, and also invasion—so all of those key cancer hallmarks. And because of it being on an epithelial cell, it’s a really good marker because it’s found in many, many different types of cancers, so it makes it what we call kind of a nice actionable mutation,” ONS member Marianne Davies, DNP, ACNP, AOCNP®, FAAN, senior oncology nurse practitioner at Yale Comprehensive Cancer Center in New Haven, CT, told Jaime Weimer, MSN, RN, AGCNS-BS, AOCNS®, manager of oncology nursing practice at ONS, during a conversation about the MET inhibitor drug class.

Music Credit: “Fireflies and Stardust” by Kevin MacLeod

Licensed under Creative Commons by Attribution 3.0 

Earn 0.5 contact hours of nursing continuing professional development (NCPD) by listening to the full recording and completing an evaluation at courses.ons.org by May 9, 2026. The planners and faculty for this episode have no relevant financial relationships with ineligible companies to disclose. ONS is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center’s Commission on Accreditation.

Learning outcome: Learners will report an increase in knowledge related to MET inhibitors.

Episode Notes 

• Complete this evaluation for free NCPD. 
• ONS Podcast™ episodes:
• Pharmacology 101 series
• Episode 330: Stay Up to Date on Safe Handling of Hazardous Drugs
• ONS Voice articles:
• Oncology Drug Reference Sheet: Amivantamab-Vmjw
• Oncology Drug Reference Sheet: Cabozantinib
• Oncology Drug Reference Sheet: Capmatinib
• Oncology Drug Reference Sheet: Tepotinib
• Predictive and Diagnostic Biomarkers: Identifying Variants Helps Providers Tailor Cancer Surveillance Plans and Treatment Selection
• ONS books:
• Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice (second edition)
• Clinical Guide to Antineoplastic Therapy: A Chemotherapy Handbook (fourth edition)
• Safe Handling of Hazardous Drugs (fourth edition)
• Telephone Triage for Oncology Nurses (third edition)
• ONS courses: Safe Handling Basics
• ONS Biomarker Database
• ONS Huddle Cards:
• Monoclonal Antibodies
• Targeted Therapy
• ONS Oral Anticancer Medication Learning Library
• ONS Oral Anticancer Medication Toolkit
• ONS and NCODA Oral Anticancer Medication Compass
• Oral Chemotherapy Education Sheets
• IV Chemotherapy Education Sheets
• Drugs@FDA

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Highlights From This Episode

“The MET receptor was actually identified back in 1984. And it was actually identified as an oncogene in osteosarcoma. And so basically what that MET receptor does—it’s a tyrosine kinase pathway, and the ligand that it attaches to is something called HGF/SF. That’s hepatocyte growth factor/scatter factor. And so this MET pathway tyrosine kinase pathway is really important in tumor cell growth and migration. And it’s expressed specifically on epithelial cells, so that’s going to really help us in identifying how it can be a pathway for cancer treatments.” TS 1:35

“But in the particular classes, there kind of are some unique things that are with these MET inhibitors. For example, crizotinib, we found early on, causes some vision changes. Patients would report things like floaters or a little bit of blurry vision. For the capmatinib, things like elevation of amylase and lipase, fluid retention and bloating, and hypersensitivity reactions and photosensitivity.” TS 7:36

“Other things to teach for the TKI is the self-management strategies in terms of nausea management and dietary changes for the risk of peripheral edema. Having them do things like maybe doing daily weights, or at least weights every other day, and sometimes doing limb measurements so it can help us really quantify the amount of fluid retention they have. And then from a nursing perspective, meeting with these patients, is to do really good skin inspection. When people have peripheral edema, they’re at risk for skin breakdown, and that can lead obviously to infection.” TS 16:06

“The biggest [misconception] is that people assume that all MET mutations are going to be equally responsive to the same targeted therapies, that all of the abnormalities are the same and react the same, and they really don’t. We’re really diving down and carving that pie thinner and thinner in terms of each individual MET abnormality, in terms of what drugs responds it to and what that means for patient outcomes and prognosis.” TS 25:21