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liver met, treatment options?


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Today we learned that my mom's cancer has spread to her liver. One

spot there, but since it didn't really get totally obliterated in her

adrenal glands by the chemoradiation (as previously thought) it's in

two separate organs now.

Here's the thing. We don't really know what kind of therapy to try

next. She's had a number of chemos (with little success): cisplatin,

navelbine, carboplatin, taxotere, alimta (in various combinations).

Also, she was stable on Tarceva/Avastin for a year before the adrenals

grew larger and the plan was changed in January. She's been off all

treatment since May when the chemo/radiation finished.

The trial suggested by my mom's doc at Rush in CHicago is ABT-263. He

emphatically does not want to do local therapy at this time feeling

that if it's in the liver it's bound to be someplace else as well. If

they can contain this, then maybe a local therapy in a few months.

There could be other trials at other institutions - but the doc

can't suggest any and how in the world am I supposed to pick one...??! ( I mean, I know how to research them, but I don't know which is any better than any others...)

Can anyone please offer any guidance on this?

Many thanks -


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I second Sandra's suggestion. If you haven't already, please visit cancergrace.org (the previous onctalk.com has been folded into GRACE, Global Resource for Advancing Cancer Education). There's a wealth of information there, especially on lung cancer, constantly updated by a Seattle oncologist who is an internationally-recognized expert on lung cancer and who gives high priority to promptly answering questions from people like you and me. A lot of us have "dual citizenship" so to speak, and have the same usernames there as here.

I didn't see your mom's cell type/subtype in your description -- your should add that if you know it, when you post your question to cancergrace.org. As you've undoubtedly discovered, many clinical trials are for people with no previous treatment, and the available trials become rather limited later in the process. I hope you find a promising trial soon. I'm not familiar with ABT-263, but Dr. West probably is. Best wishes and Aloha,


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ABT-263 seems to be listed for SCLC

Since she was stable on Tarceva/Avastin I wonder if a HKI-272 is a possible option

There is a mutation that happens that causes Tarceva to stop working HKI-272 may work when this mutation happens.

The mutation is called ERBB2 G776insV_G/C mutation (If she has this then HKI-272) might be an option,

or another EGFR inhibitor like Certuximab

Since her tumor did not respond to chemo it might be possible that is is a fairly slow/medium growing cancer (which does not respond to chemo as well as faster growing tumors)

I am not 100 percent about this (just info that hopefully will be helpful) as you talk to her Drs

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I did a search on HKI-272 and progress does not seem too great.

http://clinicaltrials.gov/ct2/results?t ... &recr=Open

Above is a list of trials in Illinois.

Erbitux (Certuximab) targets EGFR like Tarceva, except it works from the outside of the cell while Tarceva works from the inside (from what I remember to have read)

I think it might be possible to use Erbitux after Certuximab fails (though no one know for sure of the response since it would be a trial) Some Drs will not try another EGFR inhibitor after one fails

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These two cases illustrate objective clinical responses to gefitinib in patients who failed three or more lines of chemotherapy and two experimental agents, including cetuximab. Although responses to gefinitib after several lines of chemotherapy have been reported,3 the fact that a response was attained after the unsuccessful use of cetuximab is noteworthy, because both drugs block the action of the same receptor. There is some valid concern that patients who fail treatment with an EGFR-blocking MoAb may not respond to a TKI and vice versa. Most clinical trials utilizing MoAbs or TKIs exclude patients previously treated with an agent of the other class. Early evidence suggests, however, that enhanced antitumor activity may be achieved by maximizing ErbB signaling inhibition with the combination of two or more "targeted agents."4,5 Matar et al6 showed that the addition of cetuximab to gefitinib resulted in a synergistic antitumor effect against EGFR-expressing cells both in vitro and in vivo. Furthermore, the combination resulted in a more profound inhibition of the receptor signaling pathways, in a greater decrease in cell proliferation and angiogenesis, and also enhanced apoptosis. Recently, Huang et al7 demonstrated that the combination of cetuximab with either gefitinib or erlotinib resulted in more pronounced growth inhibition than either agent alone especially in head and neck cancer and non–small-cell cancer cell lines. They also demonstrated a greater decrease in the expression of several key regulators involved in the EGFR pathway as well as an increase in apoptotic markers. Furthermore, in cetuximab-resistant cells, treatment with erlotinib or gefitinib alone continued to show growth inhibition.

To the best of our knowledge this is the first report of clinical responses to a TKI after failure of treatment with a MoAb targeting the same receptor. It is still unclear if use of these agents in sequence or combination might benefit patients, but the available preclinical data and these two case reports are provocative, and this strategy certainly warrants further study.

the above shows some evidence that using cetuximab / Tarceva together may work better than one agent alone

There are also various pan-EGFR inhibitors like CI-1033

There are basically 4 EGFR receptors. Most drugs only target one, some target more than one.

Tarceva only targets one.

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Hi Katie-When my Mom only had a few lesions in her liver last year we talked her radiologist into doing radiation to the site. It worked and kept things stable for about 6 months-after that she got chemoembolization done @ John Hopkins.

PM me if you need anymore info


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