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  Table of Contents  
LETTER TO THE EDITOR
Year : 2017  |  Volume : 54  |  Issue : 1  |  Page : 325-326
 

Expanded panel test detecting mesenchymal-epithelial transition amplification leading to effective treatment in adenocarcinoma lung


1 Department of Medical Oncology, Tata Memorial Hospital, Mumbai, Maharashtra, India
2 Department of Radiodiagnosis, Tata Memorial Hospital, Mumbai, Maharashtra, India

Date of Web Publication1-Dec-2017

Correspondence Address:
Dr. K Prabhash
Department of Medical Oncology, Tata Memorial Hospital, Mumbai, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-509X.219596

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How to cite this article:
Noronha V M, Jandyal S, Joshi A, Patil V M, Mahajan A, Prabhash K. Expanded panel test detecting mesenchymal-epithelial transition amplification leading to effective treatment in adenocarcinoma lung. Indian J Cancer 2017;54:325-6

How to cite this URL:
Noronha V M, Jandyal S, Joshi A, Patil V M, Mahajan A, Prabhash K. Expanded panel test detecting mesenchymal-epithelial transition amplification leading to effective treatment in adenocarcinoma lung. Indian J Cancer [serial online] 2017 [cited 2021 Jul 24];54:325-6. Available from: https://www.indianjcancer.com/text.asp?2017/54/1/325/219596


Sir,

Expanded panel test beyond epidermal growth factor receptor (EGFR)/anaplastic lymphoma kinase (ALK)/c-ros oncogene 1 (ROS1) is recommended as part of next-generation sequencing panel in lung cancer.[1] Importance of this expanded panel is gradually being understood. We present a case highlighting the importance of this expanded panel. Crizotinib is an oral small-molecule tyrosine kinase inhibitor of ALK, mesenchymal-epithelial transition (MET), and ROS1 kinases.[2]

A 32-year-old male, reformed smoker started with complaints of cough and lower backache in February 2013, and the evaluation revealed Stage IV adenocarcinoma lung (EGFR, ALK negative) with pleural, peritoneal metastasis. He had progressed on three lines of therapy, namely, pemetrexed + cisplatin followed by docetaxel, followed by gemcitabine and was started on erlotinib which he took for 3 weeks with no clinical benefit. He presented at our institute in September 2013 and his imaging revealed pleural, nodal, and bone metastasis.

Additional mutational analysis on the biopsy specimen was done which revealed discoidin domain receptor 2 (DDR2) mutation-positive, MET amplification-positive, phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α mutation-positive, NOTCH1 mutation-positive, fibroblast growth factor receptor 4 mutation-positive, and neurotrophic tyrosine receptor kinase 2-positive status. In view of MET amplification positivity, the patient was started on crizotinib 250 mg BD along with zoledronic acid and palliative radiation was given to the symptomatic bony sites. At first response evaluation at 6 weeks, the patient had significant clinical improvement without any major toxicity. He reported marked pain relief, resolution of cough, and improved appetite and had weight gain of 5 kg. Computed tomography (CT) scan revealed response to therapy [Figure 1] and [Figure 2] showing CT at baseline and after 6 weeks of therapy respectively] and the same treatment was continued for another 13 months with 2 monthly evaluations until he had clinical and radiological progression in November 2014. He was started on dasatinib in view of being DDR1 mutation-positive status but did not respond to therapy. He finally succumbed to his illness in December 2014.
Figure 1: Computed tomography of the thorax before treatment with crizotinib

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Figure 2: Computed tomography of the thorax after response to crizotinib

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This patient had progression-free survival of 13 months on crizotinib who had not responded to any systemic therapy earlier. This patient responded very well to crizotinib but did not respond to dasatinib for the respective driver molecular changes. It was a chance decision to start crizotinib first, followed by dasatinib. We are not sure about the outcome if the introduction of therapy would have been reverse. This case not only highlights the importance of expanded lung panel for cancer patients but also suggests that we need to understand more about the driver mutations and its targeted therapy. We have limited understanding of the importance of mutations detected by sensitive technology, multiple mutations in the same patient, sequence or combination of targeting these mutations.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology. Available from: http://www.nccn.org/professionals/physician_gls/f_guidelines.asp. [Last accessed on 2016 Oct 12].  Back to cited text no. 1
    
2.
Christensen JG, Zou HY, Arango ME, Li Q, Lee JH, McDonnell SR, et al. Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma. Mol Cancer Ther 2007;6:3314-22.  Back to cited text no. 2
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