what are ggos made of?
Above question and is it possible to follow the path from start to cancer. Is it feasible or possible to find out the exact composition of ground glass opacies?
Is the toxicity of tarseva the limiting factor in its use. In general, can an non-toxic inhibitor(just binds to the active enzyme site with higher affinity than the real competitive inhibitor) be found (MICHALES-MENTON KINETICS) for the targeted enzyme than the real competitive inhibitor, so that the target enzyme flooded with the non-toxic 'binder' and then overwhelmed the target with a(the) REAL competitive inhibitor(chemotherapy)?
ggo is not a diagnosis of anything but a finding on a CT scan. It can be many things. This is an abstract from, http://www.ncbi.nlm.nih.gov/pubmed/19047318 "Focal pulmonary ground-glass opacities (GGOs) can be associated with bronchioloalveolar carcinoma. The present retrospective study aimed to test the validity of a multistep approach to discriminate malignant from benign localised (focal) GGOs, identifies useful diagnostic features on computed tomography (CT), and suggests appropriate management guidelines. A stepwise approach, including oral antibiotics, follow-up high-resolution CT (HRCT) 40-60 days later and CT-guided core biopsy, was used. All cases with localised GGOs detected since 2001 were reviewed. CT features were described according to a structured scheme. In total, 40 patients were evaluated. Of these, 11 patients were diagnosed with benign GGOs, 19 patients had lung cancer and 10 were undetermined. Nonpolygonal shape, apparent radial growth and clear-cut margins were associated with a malignant histology. The specificity of CT findings was low. Diagnostic accuracy increased after oral antibiotics, follow-up HRCT and percutaneous core biopsy. Overall, 18 patients underwent surgery for lung cancer. In conclusion, malignant ground-glass opacities have a fairly typical appearance, but some benign lesions closely mimic their malignant counterparts. The stepwise approach adopted in the present study increased the diagnostic specificity and reduced time to definitive diagnosis. Segmentectomy might be the ideal resection volume for such tumours."
And this is a post by Dr. West on ggo findings that are dx to be BAC. http://cancergrace.org/lung/2010/03/02/watching-ggos-over-time/
Tarceva is used in lung cancer because it's been shown through many years of research to lengthen the lives of people stage 4 lung cancer. Unfortunately all treatments to date that lengthen these lives also present toxic side effects that must be balanced against the benefits.
I merged all your questions so the discussion has continuity. I don't know if my above post helps answer your questions but I hope so.
As Janine noted, GGOs are often a non-invasive adenocarcinoma, such as what is sometimes called bronchioloalveolar carcinoma (BAC), but a new terminology would call adenocarcinoma in situ, a precancerous lesion that is felt to potentially but not definitively lead to invasive adenocarcinoma. However, GGOs could also just represent inflammation or infection.
As I indicated above, the precise mechanisms from precancerous lung lesion to a clearly malignant cancer are not completely understood.
Finally, to answer your question about Tarceva (erlotinib), it's not that side effects are clearly the bottleneck. It tends to be very significantly more effective for people who have a cancer with an EGFR mutation, whose cancers appear to be "driven" by the EGFR mutation that can be inhibited with Tarceva, and who can often respond beautifully to the standard dose or a lower dose for a very long time. Others without the mutation tend to have a modest response, on average, and there isn't a clearly defined dose-response curve where patients do better if they go beyond the standard dose. If the cancer isn't primarily driven by EGFR, a treatment targeting EGFR isn't likely to be vastly effective.
Dr. Howard (Jack) West
Associate Clinical Professor
City of Hope Cancer Center
Founder & President
Global Resource for Advancing