GRACE :: Lung Cancer

erlotinib

Are EGFR TKIs (Such as Tarceva) Effective in Lung Cancer Patients Who Are Wild Type EGFR?

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For patients with wild type EGFR, meaning there is no EGFR mutation, drugs like Tarceva (erlotinib) can have a small benefit, but Dr. Joan Schiller wants research to do better. February 2014


How Do You Help Your EGFR Patients Make Treatment Decisions When Their Cancers Grow?

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Dr. Geoffrey Oxnard of Dana-Farber Cancer Institute describes how he helps his EGFR lung cancer patients make decisions about next steps in treatment when their cancers grow.


Should Small Cell Lung Cancer Patients Who Respond to Chemo Receive Consolidation Radiotherapy?

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Dr. Nasser Hanna outlines the possible benefits of consolidation chest radiation for small cell lung cancer patients who respond well to chemotherapy.

CREST Trial Design


What Went Wrong? The Failure of MetMab with Tarceva in Advanced Non-Small Cell Lung Cancer

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“Dead negative,” is how Dr. Nasser Hanna describes results of a phase 3 study that examined how patients with high MET expression did on the drug MetMab (onartuzumab).

OAM4971g: Overall Survival Results


Not all EGFR Activating Mutations are Created Equal: Time to Stop Pooling Them Together

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It’s been a decade since EGFR gene mutations were first identified as highly correlated with a high probability of response to EGFR tyrosine kinase inhibitors (TKIs) like Iressa (gefitinib) and Tarceva (erlotinib), and more recently Gilotrif (afatinib).   We’ve learned that there are an array of EGFR mutations, and that the two most common ones, an exon 19 deletion or an L858R substitution on exon 21 (an exon is a specific expressed portion of a gene), each somewhere around 40-45% of  the EGFR mutations seen, are actually the ones consistently associated with a dramatic and often long-lasting response to EGFR TKIs. In contrast, the other 10-12% of EGFR mutations, most commonly on exon 18 or exon 20, are a heterogeneous group with a less clear benefit from EGFR TKIs.  

For about the last 5 years, the lung cancer community has reached a pretty clear consensus that the exon 19 deletions and exon 21, L858R substitutions represent so-called “activating mutations”, and patients with these specific mutations in their tumors are the ones that have, in trial after trial, been shown to have a markedly higher response rate (RR) and longer progression-free survival (PFS) with EGFR TKIs than with standard chemotherapy.  Over that time, they have been pooled together and largely presumed to be very comparable. More recent research presented at ASCO 2014, however, rekindles questions that go back many years and cast doubt on whether we should really pool these two mutations together. 

Back in 2006, two different publications came out — one from Boston’s Dana Farber Cancer Institute (on the top of the figure below), and another from New York’s Memorial Sloan-Kettering Cancer Center (bottom of figure below) — each independently reported that while both mutations were associated with very good responses to Iressa or Tarceva, the exon 19 patients seemed to do better, potentially in terms of both PFS and overall survival (OS).  

Exon 19 vs. Exon 21 2006

(click on image to enlarge)

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