BRAF mutations in colorectal cancers are associated with distinct clinical characteristics and worse prognosis.

Colorectal cancers are molecularly and clinically heterogeneous. These different molecular phenotypes may reflect variable prognosis.

Certain rectal cancer gene profiles are associated with poor response to CRT. Alterations in the DNA double-strand break repair pathway could contribute to treatment resistance and provides an opportunity for further studies.

Unlike other inflammatory gastrointestinal cancers, colitis-associated colorectal cancers do not preferentially arise via a methylator pathway when compared to sporadic colorectal cancers. Chromosomal instability remains an important etiology, but with a unique p53 frequency and mutation pattern.

No abstract

Differential gene expression within rectal cancers is associated with recurrence of early stage disease. A 36-gene signature correlates with an increased risk of more or less aggressive tumor behavior. This information obtainable at biopsy may assist in determining treatment decisions.

No abstract

Distinct gene expression signatures from primary rectal adenocarcinomas can help differentiate the presence or absence of lymph node metastases. These data are informative, and validation of this gene signature may provide a novel approach for more appropriate individualized treatment selection.