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Pneumonic BAC: The Subtype Very Unlike Other Forms of BAC

January 2, 2009 - 1:22 pm     Print This Post Print This Post     view / write comments

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 Dr West

   One of the issues with BAC is that I’ve referred to it as potentially very indolent, but as we’ve learned more about BAC, it’s become clear that there is a great degree of heterogeneity in BAC cases.  We’re learning that the cases that are more often slowly progressing and sometimes exceptionally responsive to EGFR inhibitors like tarceva and iressa are far more likely to be non-mucinous BAC.  These typically have the appearance of innumerable small nodules throughout the lungs.  There is a form that is the opposite: with sweeping areas of consolidation (also known as opacity) throughout entire areas of lung, typically mucinous, and essentially never responsive to EGFR inhibitors based on what we know right now.  This form is called pneumonic BAC, and it is typically very aggressive and unfortunately seems to be resistant to most of our treatments. 

   It’s called pneumonic BAC because it looks for all the world like pneumonia on an x-ray or CT, and I suspect that just about every patient who is ultimately diagnosed with pneumonic BAC is treated for at least weeks and often months with antibiotics.  The classic example is that it involves much or sometimes all of a lobe of the lung:

Pneumonic BAC

Because it’s mucinous BAC, these patients often describe coughing up large amounts of frothy sputum.

   The case above shows involvement in both lungs, so surgery wouldn’t generally be performed (although it’s sometimes done even palliatively to relieve the productive cough and shortness of breath, since blood runs through this part of the lung and gets no oxygen), but in cases that have involvement of an entire lobe that go to surgery, we sometimes review the cases in a tumor board.  Unfortunately, these are cases in which we often see them develop recurrences within months.  It’s not clear whether chemo leads to a lower risk of recurrence. 

    As I mentioned above, the limited analysis we’ve done of mucinous vs. non-mucinous BAC in trials of EGFR inhibitors like iressa and tarceva have shown that responses seem to be essentially limited to the patients with non-mucinous BAC.  My colleagues from Memorial Sloan Kettering Cancer Center in NYC have been doing molecular testing on a lot of lung tumors they’re treating, and they’ve told me that these pneumonic BAC cases very often have K-Ras mutations, which goes with a lack of benefit from EGFR inhibitors.

    We don’t know whether any systemic therapy works for these patients, but I’ll describe a clinical case in the next few days that illustrates typical course.  In the meantime, the take home message is that while some BAC lesions grow incredibly slowly and are responsive to many treatments, others are very different.  I think very few oncologists know the difference, but the pneumonic BAC cases are ones that are typically very aggressive and respond rarely if ever to the oral EGFR inhibitors.

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Posted in: Bronchioloalveolar Carcinoma (BAC), Lung Cancer Print This Post Print This Post


  1. January 3, 2009 - 4:01 am

    Dr. West,

    My husband has Signet Ring cell lung cancer. Is there any study associated with this type of lung cancer?

    Thanks.

    Melissa

    melissa
  2. January 3, 2009 - 9:21 am

    I would consider signet cell subtype to be completely different, and frankly, I’ve never treated that, or even heard anything about it specifically. I would be inclined to basically use trial and error with the typical treatments to see what works, since I don’t think we have any meaningful prior experience to go on.

    -Dr. West

    Dr. West
  3. January 5, 2009 - 11:39 pm

    Thank you for the post above. My dad also had BAC which was the mucinous form. He was Dx with pneumonia several times before it was Dx by a bronch due to unresolved pneumonia. He has been gone two years and I appreciate the research that is being done in regards to BAC.

    My dad had problems with breathing for several years prior to his Dx. He called it “allergies” and the cold made it worse. It appears that the form he had is quite aggressive, yet, I think he surely had it longer that anyone knew. Is it possible that he had it for several years? He suffered one full year going to allergists, etc. trying to figure it out. So actually, with the foam and mucous he spit,
    he lived almost 20 months, but lived only 8 months after Dx. Thanks Jolene

    Jolene
  4. January 6, 2009 - 8:22 pm

    Jolene,

    I think many patients have a long latency between a scan that looks for all the world like pneumonia (and with essentially completely overlapping symptoms) and an ultimate diagnosis, and that’s often after months or a year or more of these symptoms.

    I just saw a patient with this form who has had it grow for somewhere in the range of 12-18 months before his diagnosis, but it went from significant to overwhelming in that time.

    I think there are two key issues. The first is the rate of progression, which may have the potential to be very aggressive but often isn’t. In fact, it may be somewhat slow by lung cancer standards. But I don’t think it’s as exceptionally slow as some non-mucinous BAC cases are, in whom you need to follow some nodules over years to detect progression. If mucinous BAC takes several months to show progression, that’s faster than many BACs, but it’s not breaking any records for lung cancer in general.

    The second issue is response to treatment. What has really raised the visibility of BAC over the past few years has been the growing awareness that it’s often patients with BAC who have the staggering responses to oral EGFR inhibitors like tarceva and iressa: these are just more impressive and often longer lasting than anything we used to see in lung cancer (short of surgery removing the cancer). With that, and several trials dedicated to studying EGFR inhibitors in BAC (including a large one that I led), many oncologists now consider an EGFR inhibitor to be the preferred first line treatment for BAC. However, a point I’d make is that when we take a closer look, it seems like nearly all of the favorable activity for these agents in BAC is actually in folks with the non-mucinous form. I don’t know that there’s any activity of them in mucinous BAC and now would definitely not be inclined to use them as my front line approach. I have some very limited experience that leads me to believe that chemo +/- avastin can be active in mucinous BAC (although not the same kind of responses you see with EGFR inhibitors in some BAC cases); I don’t know if it’s the chemo alone, the avastin, or the combination that has led to the activity I’ve seen.

    These cases are few and far between. I’d consider myself one of the people most interested in BAC in the whole country or world, and I only see 1-2 patients with mucinous BAC a year. Most oncologists probably see 2 or 3 in a decade or more. The point is that it’s hard to get a good read on any patterns when you’re seeing so few people who fit in the category. But we’re learning what we can pretty quickly.

    -Dr. West

    Dr. West