Direct Comparison of 2 EGFR Inhibitors Shows There Are Clinically Significant Differences
Fast forward 1.5 years, and we now have the early results of LUX-Lung-7, and they show that these EGFR TKIs are not completely interchangeable...
Fast forward 1.5 years, and we now have the early results of LUX-Lung-7, and they show that these EGFR TKIs are not completely interchangeable...
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.
The following is the edited transcript and figures from a webinar presentation made by Dr. Heather Wakelee, medical oncologist and Associate Professor at Stanford Cancer Center, on Never-Smokers and Gender Differences in Lung Cancer.
EGFR stands for epidermal growth factor receptor, which is a molecule on the surface of many cancer cells that can be activated to activate signals that promote cell growth and cell division. Though this target may play a role for many kinds of cancer, non-small cell lung cancer (NSCLC) is one type in which this target protein is seen in a majority of people's cancers.
The initial or "first line" management of advanced NSCLC has evolved quite a bit over the past 10 years, in that time moving from a much more uniform approach of very similar treatment for just about everyone to a revised approach that is far more individualized. First, we assess key issues like the subtype of NSCLC, focusing largely on whether it is squamous cell or non-squamous NSCLC, because treatment tends to diverge very early based on this factor.
I just wanted to tell people about a remarkable patient I just saw who is delighted to have had a remarkable response to Tarceva a few years after responding to Iressa. She made my day. In truth, her case was remarkably long before this. She was diagnosed with bronchioloalveolar carcinoma (BAC) all the way back in 1995 (I was finishing med school, no kids -- life was simpler then). She had undergone a left lower lobectomy for localized disease initially, but her cancer recurred in late 1998, confirmed on a bronchoscopy, and she began experiencing a cough then.
Among the many challenges in clinical oncology is the fact that a very significant proportion of our patients are quite a bit more debilitated than the vast majority of patients in clinical trials that test our anti-cancer therapies. Approximately a third of the patients with advanced NSCLC have what would be considered a poor performance status (PS) of 2 or 3 (0 to 5 scale, 0 being asymptomatic, and 5 being dead), but they are extremely under-represented on our clinical trials.
We know that cancer cells mutate over time -- in fact, that's how they became cancer cells. In fact, oncologists see the heterogeneity of cancer cells in our daily practice every day. Although there are certainly many reasons why patients have some of their cancer cells respond and others not (blood supply, local microenvironmental factors, etc.), one of the important factors is genetic heterogeneity within the cancer cell population -- some cells die and others don't.
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