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“Under normal conditions, EGFR [epidermal growth factor receptor] is in an auto-inhibited state. And it’s only when it’s needed that it’s upregulated. But when you have cancers that there is either a mutation in the EGFR or an overexpression, what you see is a dysregulation of normal cellular processes. So you get overexpression or switching on of prosurvival or antiapoptotic responses,” Rowena “Moe” Schwartz, professor of pharmacy practice at James L. Winkle College of Pharmacy at the University of Cincinnati in Ohio, told Lenise Taylor, MN, RN, AOCNS®, BMTCN®, oncology clinical specialist at ONS, during a conversation about the EGFR 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 November 8, 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: The learner will report an increase in knowledge related to EGFR inhibitor drugs.
Episode Notes
To discuss the information in this episode with other oncology nurses, visit the ONS Communities.
To find resources for creating an Oncology Nursing Podcast Club in your chapter or nursing community, visit the ONS Podcast Library.
To provide feedback or otherwise reach ONS about the podcast, email [email protected].
Highlights From This Episode
“It wasn’t until 2004 that the mutations affecting the tyrosine kinase domain of epidermal growth factor receptor was linked to the responses that were seen in gefitinib. And that’s when we really started to understand the way that this was targeting certain patients’ cancers. So that led to the phase three study. People may remember the IPASS study that demonstrated that when patients had an activating mutation of EGFR, that that was a really good biomarker that selected out patients that would respond to therapy.” TS 2:58
“The new player on the market is the bispecific. … This was a bispecific that was developed to hit two different targets. The one target is EGFR. The second target was MET. And the reason MET was targeted is because when you have patients who are on EGFR tyrosine kinase inhibitors, they do so well. But over time, resistance develops. And one of the mechanisms that are thought to be important for resistance is that MET pathway. So it was a development of a bispecific antibody that hit two different targets, EGFR and MET, hoping that you would get less resistance.” TS 7:12
“The other thing that I see with these agents is seeing them combined with chemotherapy. For a long time, it was these drugs were used as the single approach to someone with non-small cell lung cancer who had an EGFR mutation, and they did well. But I think we’re starting to see that because resistance does develop, that there may be roles for combination with chemotherapy, and you’re seeing that in terms of drug approval.” TS 19:10
“I think that people that don’t work in the clinic, say, with non-small cell lung cancer—they think of these as a group and don’t realize the uniqueness of specific agents, what mutations that they hit that affected those that penetrate into the [central nervous system], the drug interactions that are specific for certain agents. So I think that’s one of the common misconceptions.” TS 22:02
“The education, because it evolves so rapidly, is to realize that what you know, if it’s from a year ago, may not be the full picture. And so again, I’m going to call out ONS for the phenomenal resources on the Genomics and Precision Oncology Learning Library to help providers learn. And that is updated, and it is readily available. I think it is phenomenal, and I think it helps people build on their basic understanding of any of these types of therapy, including EGFR inhibitors.” TS 23:24
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“Under normal conditions, EGFR [epidermal growth factor receptor] is in an auto-inhibited state. And it’s only when it’s needed that it’s upregulated. But when you have cancers that there is either a mutation in the EGFR or an overexpression, what you see is a dysregulation of normal cellular processes. So you get overexpression or switching on of prosurvival or antiapoptotic responses,” Rowena “Moe” Schwartz, professor of pharmacy practice at James L. Winkle College of Pharmacy at the University of Cincinnati in Ohio, told Lenise Taylor, MN, RN, AOCNS®, BMTCN®, oncology clinical specialist at ONS, during a conversation about the EGFR 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 November 8, 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: The learner will report an increase in knowledge related to EGFR inhibitor drugs.
Episode Notes
To discuss the information in this episode with other oncology nurses, visit the ONS Communities.
To find resources for creating an Oncology Nursing Podcast Club in your chapter or nursing community, visit the ONS Podcast Library.
To provide feedback or otherwise reach ONS about the podcast, email [email protected].
Highlights From This Episode
“It wasn’t until 2004 that the mutations affecting the tyrosine kinase domain of epidermal growth factor receptor was linked to the responses that were seen in gefitinib. And that’s when we really started to understand the way that this was targeting certain patients’ cancers. So that led to the phase three study. People may remember the IPASS study that demonstrated that when patients had an activating mutation of EGFR, that that was a really good biomarker that selected out patients that would respond to therapy.” TS 2:58
“The new player on the market is the bispecific. … This was a bispecific that was developed to hit two different targets. The one target is EGFR. The second target was MET. And the reason MET was targeted is because when you have patients who are on EGFR tyrosine kinase inhibitors, they do so well. But over time, resistance develops. And one of the mechanisms that are thought to be important for resistance is that MET pathway. So it was a development of a bispecific antibody that hit two different targets, EGFR and MET, hoping that you would get less resistance.” TS 7:12
“The other thing that I see with these agents is seeing them combined with chemotherapy. For a long time, it was these drugs were used as the single approach to someone with non-small cell lung cancer who had an EGFR mutation, and they did well. But I think we’re starting to see that because resistance does develop, that there may be roles for combination with chemotherapy, and you’re seeing that in terms of drug approval.” TS 19:10
“I think that people that don’t work in the clinic, say, with non-small cell lung cancer—they think of these as a group and don’t realize the uniqueness of specific agents, what mutations that they hit that affected those that penetrate into the [central nervous system], the drug interactions that are specific for certain agents. So I think that’s one of the common misconceptions.” TS 22:02
“The education, because it evolves so rapidly, is to realize that what you know, if it’s from a year ago, may not be the full picture. And so again, I’m going to call out ONS for the phenomenal resources on the Genomics and Precision Oncology Learning Library to help providers learn. And that is updated, and it is readily available. I think it is phenomenal, and I think it helps people build on their basic understanding of any of these types of therapy, including EGFR inhibitors.” TS 23:24
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