The Time Is Now
Personalized Treatment Designed For Cancer Patients
Colorectal Cancer
Panel
With the advent of more chemotherapy options and with the availability of biologic therapies in the recent past, mortality rates are declining, and patients are living longer. Over the past 20 years, survival in metastatic colorectal cancer has more than doubled. Nonetheless, colorectal cancer remains the second leading cause of cancer related death in the United States. New therapeutic strategies are clearly needed.
The main histologic subtype of colorectal cancer is adenocarcinoma. Colorectal adenocarcinomas arise through the acquisition of a series of mutations that occur over the space of many years, and results in the evolution of normal epithelium to adenoma to carcinoma to metastasis (Fearon and Vogelstein 1990). In the past two decades, there has been increasing recognition that some somatic mutations may be prognostic or predictive markers for specific therapies available in colorectal cancer.
These mutations involve genes such as KRAS, BRAF, PIK3CA, AKT1, SMAD4, PTEN, NRAS, and TGFBR2 (Baba et al. 2011; De Roock et al. 2010; Dienstmann et al. 2011; Fernandez-Peralta et al. 2005; Haigis et al. 2008; Negri et al. 2010; Papageorgis et al. 2011; Sartore-Bianchi et al. 2009). Furthermore, there has been increasing recognition that some of these mutant gene products may be targets for drug development. (De Roock et al. 2010; Huang et al. 2008; Thenappan et al. 2009).
Genes and Their Locations
ATK1
14q32.33
EGFR
7p11.2
MET
7q31
PIK3CA
3q26.32
APC
5q22.2
FLT3
13q12.2
MLH1
3p22.2
PTEN
10q23.31
BRAF
7q34
CDH1
16q22.1
JAK2
9p24.1
KRAS
12p12.1
NPM1
5q35.1
NRAS
1p13.2
SMAD4
18q21.2
TP53
17p13.1
TP53
17p13.1