For patients with solid tumours,

Let testing be your guide

Every cancer is unique. Let’s treat it that way

Targeted therapies are being studied to advance treatment options for patients with actionable biomarkers – patients with gene fusions need high-quality molecular testing to realise these opportunities.1,2 

To help patients with NTRK or ROS1 fusion+ cancer, we must first identify them. #PutCancerToTheTest 

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NTRK gene fusions are emerging as actionable biomarkers and oncogenic drivers across a wide range of tumour types.1–6 NTRK fusion+ cancer currently has no known defining clinical or pathological features.1–3

Only high quality molecular testing such as next-generation sequencing (NGS) can confirm
NTRK fusion+ cancer.1

Select a section to learn more:

NTRK fusion+ tumour types

Testing for NTRK gene fusions

How NTRK fusions drive cancer

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ROS1 gene fusions have proved to be key indicators for several cancers and are a validated therapeutic target in NSCLC.7,8 Up to 40% of patients with advanced ROS1+ NSCLC also have CNS metastases at diagnosis.9–12

Only high-quality molecular testing, such as FISH and NGS, can identify patients with actionable ROS1+ gene fusions.13

Select a section to learn more:

ROS1+ NSCLC and

CNS burden

Testing for

ROS1 gene fusions

How ROS1 fusions

drive cancer

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Knowing a patient’s biomarker profile can open up new targeted treatment options.14–16 High-quality NGS helps you see beyond the tumour origin to exactly which mutations are driving that cancer.17

Precision medicine combines different treatment options, including traditional cancer therapies and emerging targeted therapies, with the aim of achieving the best possible outcome for the patient.18

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A number of diagnostic options are available for the identification of gene fusions. However, not all are equally reliable.1,19–23

Only sensitive and specific tests can reliably detect NTRK and ROS1 gene fusions20,22,24

Roche is committed to pioneering progress in precision medicine25

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Footnotes:

CNS, central nervous system; FISH, DNA fluorescence in situ hybridisation; NGS, next-generation sequencing; NSCLC, non-small cell lung cancer; NTRK, neurotrophic tropomyosin receptor kinase; ROS1, c-ros oncogene 1.

 

1

Vaishnavi A, Le AT, Doebele RC. Cancer Discov 2015;5:25–34.

2

Lange AM, Lo HW. Cancers (Basel) 2018;10.

3

Amatu A, Sartore-Bianchi A, Siena S. ESMO Open 2016;1:e000023.

4

Khotskaya YB, et al. Pharmacol Ther 2017;173:58–66.

5

de Lartigue J. TRK inhibitors advance rapidly in “tumor-agnostic” paradigm. OncologyLive 2017;18. Available at: https://www.onclive.com/publications/oncology-live/2017/vol-18-no-15/trk-inhibitors-advance-rapidly-in-tumoragnostic-paradigm (Accessed July 2020).

6

Robbins HL, Hague A. Front Endocrinol (Lausanne) 2016;6:1–22.

7

Davies K, Doebele RC. Clin Cancer Res 2013;19:4040-4045.

8

Lin J, Shaw A. J Thorac Oncol 2017;12:1611–1625. 

9

Patil T, et al. J Thorac Oncol 2018;13:1717–1726. 

10

Gainor JF, et al. JCO Precis Oncol 2017. DOI: 10.1200/PO.17.00063.

11

Mazières J, et al. J Clin Oncol 2015;33:992–999.

12

Wu YL, et al. J Clin Oncol 2018;36:1405–1411.

13

Bubendorf L, et al. Virchows Arch 2016;469:489–503.

14

Rozenblum AB, et al. J Thorac Oncol 2017;12:258–268.

15

Schwaederle M, Kurzrock R. Oncoscience 2015;2:779–780.

16

Mansinho A, et al. Expert Rev Anticancer Ther 2017;17:563–565.

17

Frampton GM, et al. Nat Biotechnol 2013;31:1023–1031.

18

Bode AM, Dong Z. NPJ Precis Oncol 2018;2:1.

19

Murphy DA, et al. Appl Immunohistochem Mol Morphol 2017;25:513–523.

20

Su D, et al. J Exp Clin Cancer Res 2017;36:1–12.

21

Abel HJ, Duncavage EJ. Cancer Genet 2013;206:432–440.

22

Hechtman JF, et al. Am J Surg Pathol 2016;41:1547–1551.

23

Aisner DL, et al. Arch Pathol Lab Med 2016;140:1206–1220.

24

Kumar-Sinha C, et al. Genome Med 2015;7:1–18.

25

Roche Media Release, 2018. Available at: www.roche.com/media/releases/med-cor-2018-06-19.htm (Accessed October 2020).