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Personalized Treatment Designed For Cancer Patients

Lung Cancer Panel

Non Small Cell (NSCLC) / Small Cell (SCLC)

Lung cancer is the leading cause of cancer related mortality in the United States.  Classically, treatment decisions have been empiric and based upon histology of the tumor. Platinum based chemotherapy remains the cornerstone of treatment. However, survival rates remain low. Novel therapies and treatment strategies are needed.

Lung cancer is comprised of two main histologic subtypes: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Over the past decade, it has become evident that subsets of NSCLC can be further defined at the molecular level by recurrent 'driver' mutations that occur in multiple oncogenes, including AKT1, ALK, BRAF, EGFR, HER2, KRAS, MEK1, MET, NRAS, PIK3CA, RET, and ROS1.Another altered kinase gene involves MET. 'Driver' mutations lead to constitutive activation of mutant signaling proteins that induce and sustain tumorigenesis. These mutations are rarely found concurrently in the same tumor. Mutations can be found in all NSCLC histologies (including adenocarcinoma, squamous cell carcinoma (SCC), and large cell carcinoma) and in current, former, and never smokers (defined by individuals who smoked less than 100 cigarettes in a lifetime). Never smokers with adenocarcinoma have the highest incidence of EGFR, HER2, ALK, RET, and ROS1 mutations. Importantly, targeted small molecule inhibitors are currently available or being developed for specific molecularly defined subsets of lung cancer patients.

Historically, efforts at characterizing the molecular underpinnings of SCC of the lung have lagged behind those of adenocarcinoma of the lung. Many of the 'driver' mutations found in lung adenocarcinoma are only rarely found in lung SCC. Moreover, newer agents, such as bevacizumab (Avastin) and pemetrexed (Alimta) are not approved for or exhibit diminished efficacy in SCC (Sandler et al. 2006; Scagliotti et al. 2008). Thus, patients with metastatic SCC have fewer treatment options than those with non-squamous NSCLC. Despite these caveats, however, 'driver' mutations that may be linked to outcomes with targeted therapies in SCC are emerging. Altered genes include FGFR1 and DDR2 as well as PIK3CA.

* - SCLC Panel

Genes and Their Locations

ATK1

14q32.33

ALK

14q32.33

APC

5q22.2

BRAF

7q34

BRCA1

17q21.31

CDH1

16q22.1

EGFR

7p11.2

EML4

2p21

FLT3

13q12.2

MLH1

 3p22.2

FGFR1

8p11.23

HER2

17q12

NPM1

5q35.1

TP53

17p13.1

JAK2

9p24.1

PTEN

10q23.31

RET

10q11.2

KRAS

12p12.1

PIK3CA

3q26.32

VEGFR2

4q12

MET

7q31

NRAS

1p13.2

TLE3

15q23

TUBB3

16q24.3

RRM1

11p15.4

PGP

7q21.12

ERCC1

19q13.32

TOPO1

20q12