GRACE :: Lung Cancer


Targeted Treatment for Lung Cancer After Progression


Dr. Geoffrey Oxnard of Dana-Farber Cancer Institute discusses whether or not patients on targeted therapies, such as EGFR inhibitors, should stay on those therapies after their cancers begin to grow again. February 2014.

CO-1686, a Third Generation Drug for EGFR Positive Lung Cancer Patients


Dr. Heather Wakelee of Stanford University Medical Center talks about a drug still in development for EGFR lung cancer patients, CO-1686. February 2014.

Is It Possible to Test Lung Tumors Without Doing a Biopsy?


Dr. Geoffrey Oxnard of Dana-Farber Cancer Institute talks about exciting new developments which will allow oncologists to test patients’ lung tumors without invasive biopsies. February 2014.

What’s the Status and Potential Utility of Cabozantinib in Lung Cancer?


Dr. Heather Wakelee of Stanford University Medical Center discusses whether or not cabozantinib – a drug already approved for thyroid cancer – can help patients with lung cancer. February 2014.

Squamous Lung Cancer, Part 2: Genomic Testing by Dr. David Spigel


Chart and graph representing genetic mutations across 12 different cancer typesDr. David Spigel, Sarah Cannon Cancer Center, discusses the importance of genomic testing in squamous lung cancer.


Squamous Lung Cancer, Part 2: Genomic Testing Audio Podcast


What you’ll hear in Part 2:

  • Molecular testing (also called genetic or genomic testing) in squamous lung cancer
  • Newly information about genetic targets for squamous lung cancer


Glossary of some terms you’ll hear in Part 2:

Find more cancer definitions at the National Cancer Institute’s Dictionary of Cancer Terms

  • Adenocarcinoma – Cancer that begins in glandular (secretory) cells. Glandular cells are found in tissue that lines certain internal organs and makes and releases substances in the body, such as mucus, digestive juices, or other fluids. Most cancers of the breast, pancreas, lung, prostate, and colon are adenocarcinomas.
  • ALK – A gene that makes a protein called anaplastic lymphoma kinase (ALK), which may be involved in cell growth. Mutated (changed) forms of the ALK gene and protein have been found in non-small cell lung cancer. These changes may increase the growth of cancer cells. Checking for changes in the ALK gene in tumor tissue may help to plan cancer treatment.
  • B-RAF – A gene that makes a protein called B-RAF, which is involved in sending signals in cells and in cell growth. This gene may be mutated (changed) in many types of cancer, which causes a change in the B-RAF protein. This can increase the growth and spread of cancer cells.
  • EGFR – The protein found on the surface of some cells and to which epidermal growth factor binds, causing the cells to divide. It is found at abnormally high levels on the surface of many types of cancer cells, so these cells may divide excessively in the presence of epidermal growth factor. Also called epidermal growth factor receptor, ErbB1, and HER1.
  • Genomics – The study of the complete genetic material, including genes and their functions, of an organism.
  • Oncogenic drivers – That which causes the formation, or supports the progression, of a cancer.
  • Oral therapy – A drug taken by mouth.
  • Personalized medicine – In cancer, personalized medicine uses specific information about a person’s tumor to help diagnose, plan treatment, find out how well treatment is working, or make a prognosis.
  • ROS1 – A receptor tyrosine kinase (RTK) of the insulin receptor family. ROS1 fusions were identified as a potential “driver” mutation in non-small cell lung cancer. (My Cancer Genome)
  • Squamous lung cancer – One of the three sub-types of lung cancer.


Dr. Silvestri on Radiation Pneumonitis and Lung Complications from Targeted Therapies


Here’s the second half of the presentation by Dr. Gerard Silvestri, expert pulmonologist and critical care specialist at the Medical University of South Carolina in Charleston, on pulmonary complications from lung cancer treatment.  In this part, he briefly covers the side effects of some systemic targeted therapies used as a treatment for lung cancer, then covers the important topic of radiation pneumonitis in some detail.

Here is the podcast in video and audio versions, along with the transcript and figures.

Dr. Silvestri Pulm Complics LC Treatment Targeted Rx and RT Pneumonitis Audio Podcast

Dr. Silvestri Pulm Complics LC Treatment Targeted Rx and RT Pneumonitis Transcript

Dr. Silvestri Pulm Complics LC Treatment Targeted Rx and RT Pneumonitis Figs


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ASCO 2012 Lung Cancer Highlights: Question and Answer Session with Drs. Socinski and Neal


We’ve covered a wide range of topics  in our “ASCO 2012 Lung Cancer Highlights” podcast series over the last few weeks.  This webinar and the podcasts from it featured Drs. Mark Socinski from the University of Pittsburgh and Joel Neal from Stanford Cancer Center; following their presentations, they did a question and answer session together, covering a wide range of leading topics in lung cancer from ASCO.  Here’s that Q&A session.

ASCO 2012 LC Highlights QA Session Audio Podcast

ASCO 2012 LC Highlights QA Session Transcript

ASCO 2012 LC Highlights QA Session Figs

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2011 Highlights in Lung Cancer, by Dr. Jared Weiss, Part 1: The EGFR Axis


Apologies for the long wait since our own Dr. Weiss’s upbeat and thoughtful review of the leading stories about lung cancer in 2011.  Dr. Weiss covered a lot of ground in his presentation that was followed by a Q&A session, so we’ve broken that up into several short pieces that cover a few highlights at a time.  In fact, we’re going to make an effort to have podcasts shorter and easier to digest in the future.  

The first part is on EGFR-based therapies, including the EURTAC trial of the EGFR tyrosine kinase inhibitor (TKI) Tarceva (erlotinib) vs. standard doublet chemo in a European, EGFR mutation-positive patient population, followed by work on EGFR TKI/monoclonal antibody combinations: one being the single arm afatinib/Erbitux (cetuximab) for patients with acquired resistance after a good response to earlier EGFR TKI therapy, and the second being Tarceva with either the c-MET antibody MET-MAb or placebo.  

Here’s the audio and video versions of the podcast, along with the transcript and figures for this portion of the program. 

Dr. Weiss Lung Cancer Highlights 2011 Pt 1 EGFR Axis Audio Podcast

Dr. Weiss Lung Cancer Highlights  2011 Pt 1 EGFR Axis Transcript

Dr. Weiss Lung Cancer Highlights 2011 Pt 1 EGFR Axis Figs

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How does the diagnosis of BAC shape systemic therapy considerations today?


It’s not uncommon for a question here to be about the a pathologist’s terminology on a report that equivocates about whether a lesion is bronchioloalveolar carcinoma (BAC) or another form of adenocarcinoma, perhaps “well-differentiated adenocarcinoma”, especially if it has a radiographic appearance of a hazy infiltrate or many small ground glass opacities. Meanwhile, there’s a new classification of lung cancer subtypes that obliterates the term BAC, instead favoring a definition of adenocarcinoma in situ, classifying small non-invasive lesions previously called BAC as a pre-malignant condition. How have the changes over the past few years changed how we should approach BAC?

I would have to say that the new reassignment of BAC as adenocarcinoma in situ hasn’t taken the lung cancer world by storm and that I still think of the clinical entity as BAC. For the preceding decade, the definition the pathologist’s used technically excluded a lesion with even 1% or 5% of the lesion being invasive as being called BAC, even if it acted for all the world like BAC. Clinicians learned not to be too hung up on a pathologist’s technical definitions and tended to define BAC more functionally/operationally. General oncologists and expert lung cancer specialists alike managed BAC based on the overall picture of how it behaved if it looked like a BAC pattern.

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Afatinib vs. Placebo in EGFR-TKI Treated Patients: Efficacy in the Eye of the Beholder


It was almost exactly a year ago that I described the basic results of the global LUX Lung-1 trial that enrolled 585 patients with advanced NSCLC who had gone at least 12 weeks without progression on Tarceva (erlotinib) or Iressa (gefitinib) in a 2:1 fashion to either the oral targeted therapy afatinib (an irreversible inhibitor of the human epidermal receptor (HER) family, of which EGFR and HER2/neu are members, also known as a “pan-HER inhibitor”) or placebo. This trial was intended to enroll patients who had developed acquired resistance to an EGFR tyrosine kinase inhibitor (TKI) like Tarceva or Iressa, but the eligibility criteria were frankly a little too loose to really have enrolled a uniform population of patients who we think of as classic “acquired resistance” patients, who should have an EGFR activating mutation and would often have a very good response in terms of tumor shrinkage, or at least very prolonged stable disease. Requiring just stable disease for at least three months of an EGFR TKI allows the study to become a combination of 1) people with true acquired resistance after a very strong clinical benefit, and 2) people with slowly progressing cancer that didn’t happen to meet criteria for progression within 12 weeks on an EGFR TKI.

To review the highlights, the median age of patients was 58-59 years old, 60% of the patients were women, nearly two thirds were never-smokers, the median duration of response was about 10 months, and the objective response rate to prior EGFR TKI was about 45%. This is lower than the response rate to EGFR TKIs that is typically 60-75% for trials exclusively of patients with an EGFR mutation, and the median duration of response is a little on the low side, so my estimate is that only about one of every three or four patients squeaked into the trial but wasn’t really the target patient for the population that this trial was intending to study. However, this study was designed just before trial results like IPASS made it clear that molecular selection (identifying patients for trials based on the presence of a particular mutation) is clearly superior to clinical selection (identifying a patient based on clinical characteristics like race, sex, and smoking status).

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