Can Xalkori combine with other drug to kill eradicate cancer?

Home Forums Lung Cancer (old) General Lung/Thoracic Cancer Questions Can Xalkori combine with other drug to kill eradicate cancer?

This topic contains 6 replies, has 5 voices, and was last updated by  Dr Quesnelle 4 years ago.

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April 25, 2012 at 8:15 pm  #9445    


Since Xalkori only compress the tumor for a while, not like chemo treatment, it will come untimately. When it comes back, not only tumor will grow, more seriously it wilm met to any places, like brain, it is very dangerous.

Any one get treatment by combing Xalkori with other drugs, compress the tumor well then use other drugs to eradicate the cancer before Xalkori resistance ?

April 26, 2012 at 1:42 am  #9447    

certain spring

Hallo richardry. That’s an interesting question, and I am not sure there’s an answer yet. While you are waiting for a doctor to come by, you might find it helpful to look at Dr West’s post on early research into the mechanisms of resistance to crizotinib:
At the foot of his post are links to two others that discuss a) the possibility that Alimta seems to work particularly well for people with the ALK mutation; and b) some evidence that the newly emerging heat shock protein inhibitors might have a role:
best wishes.

49-year-old non-smoker, dx stage IV NSCLC May 2010 (squamous tumour of the left lung with multiple brain metastases). Radiotherapy to chest and brain; progressed through two cycles carbo/gemcitabine. Repeated lung collapses; pneumonia in collapsed lung, Nov 2010; bronchial stent placed, Dec 2010. Declined second-line Taxotere. Mutation testing Feb 2011, surprise EGFR exon deletion 19. Started Tarceva (150mg), Feb 2011. Progression in liver and elsewhere, May 2013.

April 26, 2012 at 6:43 am  #9456    

Dr. Weiss

You have the heart of an investigator for asking that question. For now, the answer is “no.” Just like for EGFR mutations (so far), no one has shown that crizotinib for patients with eml4/alk can result in cure. It can knock the cancer down for many months, and there are multiple promising therapies (hsp-90 inhibition, pemetrexed) that can follow after, but so far, not yet cure. However, new therapies like crizotinib give investigators hope that we’re getting closer to the day when we can start answering “yes” for small subsets of patients, then ultimately “yes” for more patients.

I think that it is important for every patient and every caregiver to know clearly that the oncology research world has not given up on cure. Yes, those of us who treat cancer do celebrate advances that give our patients months of extra life or extra quality of life right now. But, we’re not hopeful only because of the small advances for our current patients right now but also because we see them as steps on the path to a much bigger solution. Said more plainly, we’re still dreaming of cure even if we’re realistic that we haven’t gotten there yet.

April 26, 2012 at 7:46 am  #9467    


Thanks Dr.Weiss and Certain Spring ,

My idea might be naive.
My question was: we knew Xalkori does not work in the end, could not be use is first for serveral months, after the tumor is significant shrinked; in my understanding, cancer was weaken and surpressed; then use other drugs like Alimta ( I do not know much about conventional chemo yet) etc to easily kill the cancer cells?

And Xalkori does not seem to work on brain also , patient sufferred from brain met while taking Xalkori, this is terrrible!

I do read one patient said he used Altima eliminted tiny scattered brain lesions, how could that possible? Altima is not small molecus, how could it pass BBB while Xalkori is small molecus drug, but it does not work for brain at all, it is so…. confusing.

  • This reply was modified 4 years ago by  richardry.
  • This reply was modified 4 years ago by  richardry.
April 26, 2012 at 11:44 am  #9475    


More specific: Conventional chemo would knock down patient before cancer was killed because it is poisonous to human inmune system.

Imagining: the Xalkori attacked the cancer as the first pioneer, it made cancer very weak, while patient almost felt unharmed; at this time, using conventional chemo to poison the cancer , would not that eliminate the residue of the already struggling cancer?! :?:

  • This reply was modified 4 years ago by  richardry.
  • This reply was modified 4 years ago by  richardry.
  • This reply was modified 4 years ago by  richardry.
  • This reply was modified 4 years ago by  richardry.
April 26, 2012 at 6:58 pm  #9496    

Dr West

There is interest in studying combinations of targeted therapies with other agents, including other targeted therapies and/or chemotherapy, to see if we can completely eradicate the cancer. Thus far, however, the answer has been no. People with an EGFR mutation who are treated with an EGFR tyrosine kinase inhibitor (TKI) respond very similarly to patients with an ALK rearrangement who receive crizotinib, and there have been trials combining EGFR TKI therapy with chemo in people with an EGFR mutation — these have not been curative and in general haven’t shown a clear benefit over the EGFR TKI alone. I would anticipate a similar pattern in people with an ALK rearrangement.

I would be very cautious about drawing great conclusions about treatment results based on one patient’s results. We see exceptions to the rules often enough to not reframe the world view on cancer care based on one person’s outcome.

-Dr. West

Howard (Jack) West, MD
Medical Oncologist

Views expressed here represent my opinion, not those of GRACE or Swedish Cancer Institute. This information does not constitute medical advice and is intended to supplement and not replace medical information provided by your doctor.

April 27, 2012 at 1:09 pm  #9531    

Dr Quesnelle

I completely agree with Dr. West and Dr. Weiss. While we are constantly trying combinations of different drugs on cells and in mice, human patients often have a different response from what we as investigators observe preclincally. Results are different from person to person, and they are also different from preclinical to clinical settings. This is likely because of different pathways being activated in different cells. We have to be very careful about draing overarching conclusions, but that doesn’t mean we stop looking for highly effective therapies!

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