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Table of Contents
Year : 2020  |  Volume : 3  |  Issue : 1  |  Page : 153-154

Molecular tumor boards: Demystifying complex algorithms in non-small cell lung cancer

Department of Medical Oncology, Rajiv Gandhi Cancer Institute and Research Centre, Delhi, India

Date of Submission05-Jan-2020
Date of Acceptance06-Jan-2020
Date of Web Publication24-Feb-2020

Correspondence Address:
Ullas Batra
Department of Medical Oncology, Rajiv Gandhi Cancer Institute and Research Centre, Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/CRST.CRST_13_20

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How to cite this article:
Batra U, Sharma M, Amrith B P. Molecular tumor boards: Demystifying complex algorithms in non-small cell lung cancer. Cancer Res Stat Treat 2020;3:153-4

How to cite this URL:
Batra U, Sharma M, Amrith B P. Molecular tumor boards: Demystifying complex algorithms in non-small cell lung cancer. Cancer Res Stat Treat [serial online] 2020 [cited 2020 Apr 4];3:153-4. Available from: http://www.crstonline.com/text.asp?2020/3/1/153/279088

We have read with interest the case report published by Kapoor et al.[1] which brings out very clinically relevant and practical points. The response rate to tyrosine kinase inhibitors (TKIs) in epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) is approximately 76%.[2],[3] While this response rate is very impressive, it also implies that some patients will not respond to the targeted therapies. In addition, the tumor ultimately develops resistance to these TKIs, and the goal of long-term cure is still a dream.

The next-generation sequencing (NGS) is an important tool in the identification of primary and secondary resistance to EGFR-TKIs. Mesenchymal–epithelial transition factor (MET) activation has been implicated as an oncogenic driver in EGFR mutant NSCLC and can mediate primary and secondary resistance to EGFR-TKIs.[4] Various trials are currently underway that are testing the combination of TKIs and MET inhibitors in EGFR mutant NSCLC.

As mentioned above, we believe that although the first-generation EGFR-TKIs have revolutionized treatment of EGFR mutant NSCLC, we need to look beyond first-generation TKIs. The future of treatment of EGFR mutant NSCLC could be third-generation TKIs, combination TKI-chemotherapy,[5] combination TKIs-anti-angiogenic agents, or a TKI-TKI combination (TATTON/SAVANNAH study).[6] As regards to the last choice, NGS could be an effective tool in understanding and planning new TKI-TKI combinations. However, it must be remembered that it is futuristic and at present, TKI-TKI combination should not be tried outside of a clinical trial setting.

On the other hand, immunotherapy has made huge inroads in the management of non molecularly driven NSCLC, and small proportions of patients with Stage IV NSCLC have attained long-term survival. It was postulated that a combination of immunotherapy and EGFR-TKIs may lead to an improved survival in EGFR mutant NSCLC. However, trials have conclusively proven that immunotherapy does not work in oncogene addicted NSCLC and may even be detrimental.[7] Hence, immunotherapy should not be started in the first-line treatment of NSCLC till the results of biomarker testing are available.

Finally, the authors must be congratulated for conducting a molecular tumor board in their institution. As oncologists, we all must be aware of the fact that NSCLC is a heterogeneous disease, and the involvement of various specialties is mandatory in guiding treatment decisions.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Kapoor A, Noronha V, Chougule A, Patil VM, Menon N, Joshi A, et al. Molecular tumor board: Case 1-Interplay of EGFR, MET and PD-L1 in non-small cell lung carcinoma. Cancer Res Stat Treat 2019;2:228-31.  Back to cited text no. 1
  [Full text]  
Rajendra A, Noronha V, Joshi A, Patil VM, Menon N, Prabhash K. Epidermal growth factor receptor-mutated non-small-cell lung cancer: A primer on contemporary management. Cancer Res Stat Treat 2019;2:36-53.  Back to cited text no. 2
  [Full text]  
Sholl LM, Xiao Y, Joshi V, Yeap BY, Cioffredi LA, Jackman DM, et al. EGFR mutation is a better predictor of response to tyrosine kinase inhibitors in non-small cell lung carcinoma than FISH, CISH, and immunohistochemistry. Am J Clin Pathol 2010;133:922-34.  Back to cited text no. 3
Leonetti A, Sharma S, Minari R, Perego P, Giovannetti E, Tiseo M. Resistance mechanisms to osimertinib in EGFR-mutated non-small cell lung cancer. Br J Cancer 2019;121:725-37.  Back to cited text no. 4
Noronha V, Patil VM, Joshi A, Menon N, Chougule A, Mahajan A, et al. Gefitinib versus gefitinib plus pemetrexed and carboplatin chemotherapy in-mutated lung cancer. J Clin Oncol 2020;38:124-36.  Back to cited text no. 5
Oxnard GR, Cantarini M, Frewer P, Hawkins G, Peters J, Howarth P, et al. SAVANNAH: A Phase II trial of osimertinib plus savolitinib for patients (pts) with EGFR-mutant, MET-driven (MET+), locally advanced or metastatic non-small cell lung cancer (NSCLC), following disease progression on osimertinib. JCO 2019;7 Suppl 15:TPS9119.  Back to cited text no. 6
Tsakonas G, Ekman S. Oncogene-addicted non-small cell lung cancer and immunotherapy. J Thorac Dis 2018;10:S1547-55.  Back to cited text no. 7


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