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About oncogenetic drivers


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 ongogenic gene fusions and mutations need high-quality molecular testing to realise these opportunities.1,2

To help patients with actionable oncogenic drivers, we must first identify them. #PutCancerToTheTest

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

RET alterations are actionable oncogenic drivers across a variety of cancers.1-3

RET mutations are an actionable biomarker in medullary thyroid cancer (MTC). Up to 95% of patients with familial MTC and >65% of patients with sporadic MTC have mutations in RET.4,5

Actionable RET fusions are seen in 10-20% of papillary thyroid carcinoma (PTC) and other thyroid cancers. They are also found in 1-2% of NSCLC and in a variety of solid tumours at lower frequency.1-3

ESMO guidelines recommend routine molecular testing for RET alterations in thyroid cancer, NSCLC and other solid tumours.6


Select a section to learn more:

RET alterations

Testing for RET

How does RET drive cancer

ROS1 gene fusions have proved to be key oncogenic drivers for several cancers and are a validated therapeutic target in NSCLC.7,8 They are also found in 1-2% of NSCLC and in a variety of solid tumours at lower frequency.1-3

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

ALK gene fusions are key indicators for several cancers and are validated therapeutic targets in NSCLC. Up to 40% of patients with advanced ALK+ NSCLC also have CNS metastases at diagnosis.

Only high-quality molecular testing, such as FISH and NGS, can identify patients with actionable ALK+ gene fusions. IHC can also be utilized to detect ALK overexpression.

Select a section to learn more:

ALK+ NSCLC and CNS burden

Testing for ALK gene fusions

How ALK fusions drive cancer

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 know exactly which mutations are driving that cancer.17

Precision medicine uses the diagnostic biomarker makeup of the tumour to guide treatment optimization, including traditionalcancer therapies and emerging targeted therapies, with the aim of achieving the best possible outcome for the patient.18

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

Only sensitive and specific tests can reliably detect oncogenic alterations20,22,24


Roche is committed to pioneering progress in precision medicine25



CNS, central nervous system; FISH, DNA fluorescence in situ hybridisation; 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).

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