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Case Reports
. 2018 Jan;9(1):159-163.
doi: 10.1111/1759-7714.12518. Epub 2017 Oct 3.

Concurrent ROS1 Gene Rearrangement and KRAS Mutation in Lung Adenocarcinoma: A Case Report and Literature Review

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Free PMC article
Case Reports

Concurrent ROS1 Gene Rearrangement and KRAS Mutation in Lung Adenocarcinoma: A Case Report and Literature Review

You-Cai Zhu et al. Thorac Cancer. .
Free PMC article

Abstract

Lung adenocarcinomas with gene rearrangement in the receptor tyrosine kinase ROS1 have emerged as a rare molecular subtype. Although these lung adenocarcinomas respond to ROS1tyrosine kinase inhibitors, many patients ultimately acquire resistance. ROS1gene rearrangement is generally mutually exclusive with other driver genomic alterations, such as those in EGFR, KRAS, or ALK, thus multiple genomic alterations are extremely rare. Herein, we report a case of a 42-year-old man diagnosed with lung adenocarcinoma positive for a SDC4-ROS1 fusion, who was treated with crizotinib followed by three cycles of chemotherapy. A biopsy acquired after disease progression revealed the original SDC4-ROS1 fusion along with a KRAS point mutation (p.G12D).We reviewed the related literature to determine the frequency of gene mutations in non-small cell lung cancer patients. A better understanding of the molecular biology of non-small cell lung cancer with multiple driver genomic aberrations will assist in determining optimal treatment.

Keywords: KRAS gene mutation; ROS1 fusion gene; non-small cell lung cancer.

Figures

Figure 1
Figure 1
Lung computed tomography scans from (a) July 2016, (b) September 2016, (c) November 2016, and (d) of the left adrenal gland with tumor metastasis (red arrow).
Figure 2
Figure 2
Hematoxylin and eosin staining revealed adenocarcinoma. The (a) first and (b) second biopsies (×400).
Figure 3
Figure 3
Schema shows tumor with drivers of ROS1 gene positive by reverse transcription‐PCR. Purple, gray, and orange represent the sample, and positive and negative controls, respectively.
Figure 4
Figure 4
Schema shows tumor with dual drivers of the SDC4‐ROS1 fusion gene. (a) KRAS p.G12D, (b) SMO p.L707V, (c) point mutation, and (d) KRAS gene amplification by next‐generation sequencing.

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