The 2nd largest cause of cancer mortality

Simultaneously detect 28 common mutations in 4 genes in three stool samples in 48 hours

• Biochip Array Technology for colorectal cancer (CRC) research
• Non-invasive detection of 28 mutations common in Colorectal cancer
• Suitable for testing DNA extracted from stool specimens and tissue samples (tissue testing undergoing validation)

Colorectal cancer is the second largest cause of cancer mortality in the Western world. It is also amongst the most curable cancers when identified early¹. In the USA only 39% of colorectal cancers are detected early, at a localised and often symptomless stage when the five year survival rate is 90%².  This highlights the importance of colorectal cancer screening for early detection.

Colorectal Carcinogenesis

Colorectal carcinogenesis proceeds through a series of gradual changes: normal epithelium to benign adenomatous polyps to malignant cancer. Colorectal cancer is the result of the accumulation of mutations in tumour suppressor genes and proto-oncogenes over a period of years.

Colorectal Cancer genes

APC

Mutation of the APC tumour suppressor gene is often the earliest identifiable event in colorectal carcinogenesis. Loss of function of the APC protein deregulates ß-catenin resulting in the stimulation of cell proliferation.  All daughter cells carry the APC mutation. 

K-ras and BRAF

Point mutations in the K-ras or BRAF proto-oncogenes permanently activate proteins involved in the transduction of extracellular growth signals.  Continuous signals from cell surface receptors to the nucleus allow progression to adenoma. 

TP53

Inactivating mutations of the TP53 tumour suppressor gene can trigger the transition to malignant cancer by preventing cell cycle arrest or apoptosis in response to DNA damage.

Non-invasive detection of colorectal cancer

Colorectal cells are continuously shed into the stool.  DNA is stable in stool, facilitating the detection of mutations in cells shed from the whole length of the colorectum. RanplexCRC detects the wild-type DNA and mutations in stool. A single stool specimen is required with no dietary restrictions or medications changes.  RanplexCRC can also be used to compare patient DNA from stool and matched tissue samples. RanplexCRC is for research use only.

References:

1.Toribara NW and Sleisenger MH. (1995) Screening for colorectal cancer. N Engl Med 332(13):861-7

2. Fearon ER and Vogelstein B. (1990) A genetic model for colorectal tumorigenesis. Cell 61(5):759-67.