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BAC - Tarceva(Erlotinib)


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Erlotinib Is Active in Bronchoalveolar Carcinoma

Bronchoalveolar carcinoma (BAC) is an important subtype of adenocarcinoma of the lung. This type often has a slower rate of growth and a later pattern of metastases, and often occurs in nonsmokers. At ASCO 2003, important data on the role of the epidermal growth factor receptor tyrosine kinase (EGFR-TK) inhibitor erlotinib were reported by Dr. Vince Miller.[16] Ninety-eight patients were screened for entry and 28 were found on review not to have BAC; 71 were eligible and 50 were evaluable. Notably, 66% of the patients were women and 26% never smoked. The overall response rate of single-agent erlotinib was 26% in this setting, and the response rate in never-smokers was 46%. These response rates are nearly twice that for erlotinib as a single agent as reported at ASCO 2001.[17]

This trial is important for demonstrating that erlotinib is an active agent with acceptable toxicity for patients with BAC. The SWOG has completed a similar trial of gefitinib in this patient population, and the results of this study are eagerly awaited. The results of the Miller study provide ample rationale for studying EGFR-TK inhibitors up-front for untreated patients with BAC. It is also important that this group was able to perform this trial in BAC patients, a population that has not been as well studied in the past.

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I was part of the SWOG trial on Iressa, and it did keep my disease stable for a period of time. (even made a few "hot" nodes disappear.) I also caused a lessening in the production of secretions, which for me made a difference in my quality of life.

John, have you found any articles that detail how Iressa and Tarceva differ in just how and when they act upon the EGFR-TK? I've found only a few, and it's important because it may mean that just because a BACer fails to respond to one of the drugs doesn't mean they won't respond to the other.

Thanks for all you do. It's getting more difficult for me to do the research.

Best Wishes,

Fay A.

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I thought Tarceva and Iressa were pretty much the same. I have not looked into that. I have read that sometimes clinical trials have exclusions. If you have taken a EGFR threapy then that is an exclusion. I think I have read that some clinical trials will exclude a patient that has failed another EGFR trial - if the trials is for a EGFR drug. Doesnt necessarily make sense to me.

What I just read is that the overexpression of EGFR does not correlate with the effectiveness of Iressa or Tarceva. This does not seem to make sense, but that is what the data shows. Unfortunately there is no biomarker that will predict who responds, so that is why doctors just try the drugs without testing for EGFR.

There are four ErbB receptors - EGFR (erbB-1), HER-2 (erbB-2), HER-3 (erbB-3) and HER-4 (erbB-4). It is interesting that they are finding good results when Tarceva is combined with Herceptin (Herceptin targets HER2).

There is a another drug called CI-1033 that targets all receptors.

ABX-EGF, PKI-166, GW-2016, Erbitux are other drugs that target ErbB.

The only differences I could find was tarceva is a low-molecular-weight quinazoline inhibitor whereas iressa is a quinazoline inhibitor so the weight must be greated. Tarceva is more potent.

gefitinib (Iressa) -

erlotinib (tarceva) -

http://www.411cancer.com/syndication/ve ... ypeID=CTON

http://www.the-scientist.com/yr2002/oct ... 21014.html

http://www.nature.com/nrd/journal/v1/n7 ... 842-t1.pdf

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When I am feeling up to digging through info I've collected I'll post the articles I've found that indicate that Tarceva acts at a different point in the cells life cycle than Iressa does. I think it's that hit at a a different point in the cells developement that makes Taceva effective for some when they may not have responded so well to Iressa.

Fay A. PS Once again, thank you for your help.

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The only thing I seemed to find is that they both are intracellular. Both Iressa and Tarceva seem to do something to ATP inside the cell.

Erbitux is a monoclonal antibody and it acts on the outside of the cell.

Epidermal growth factor binds to receptors on the outside of the cell and cause a series of reactions inside the cell. Any reaction along the chain reaction is called a signalling pathway or signal transduction.

There was a good article in the CURE magazine about how it works. I may be wrong in the above paragraph.

Anyway from what I have read, researchers are considering a cocktail approach - maybe combining different EGFR inhibitors and even EGFR inhibitors with VEGF and other targets.

The combination for BAC - Herceptin(HER2 target) and tarceva(EGFR target) is just what I described above

The thinking is that a cancer cell has many pathways in which it can use to survive. If only one pathway is shutdown, the cancer comes back

Probably no need to dig into you research. Hope you are doing well

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