Journal of Experimental Pathology

Tumor node metastasis (TNM) staging system is the most useful method in predicting prognosis of colorectal cancer (CRC), the third most common cause of death worldwide, even if other biological markers are currently under evaluation to assess their role in affecting CRC outcome and planning the best tailored therapeutic approach. Several molecular factors are being demonstrated to be effective in influencing both overall survival (OS) and disease-free survival (DFS) in CRC, acting on different aspects of tumor promoting and progression.

Fluoropyrimidines compose the backbone of regimens to treat many common solid tumors, including gastrointestinal (GI), breast and head/neck. As we continue to use these agents routinely, recognition of rare but real toxicities, such as cardiotoxicity, has also improved. The treatment options for patients who have encountered fluoropyrimidine-induced cardiotoxicity are limited as many anti-angiogenic drugs also pose a cardiac risk.

Despite the health benefits associated with polyphenols, the bioavailability of many polyphenols limits their effects. Problems with poor solubility fast-metabolism and food preparation techniques limit the bioavailability and bioactivity of these dietary micronutrients. Encapsulation of polyphenols has shown to protect and increase bioavailability of these dietary compounds and to enhance their anticancer activity.

Competent human DNA mismatch repair (MMR) corrects DNA polymerase mistakes made during cell replication to maintain complete DNA fidelity in daughter cells; faulty DNA MMR occurs in the setting of inflammation and neoplasia, creating base substitutions (e.g. point mutations) and frameshift mutations at DNA microsatellite sequences in progeny cells. Frameshift mutations at DNA microsatellite sequences are a detected biomarker termed microsatellite instability (MSI) for human disease, as this marker can prognosticate and determine therapeutic approaches for patients with cancer.

Polyploid cancer cells can arise de novo in tumors or they can be induced by therapeutics that inadvertently increase the rate of cytokinetic failure. These cells portend a poor outcome in many cancers because polyploid cancer cells can undergo error prone reductive cell divisions to yield aneuploid progeny. The immune system has evolved mechanisms by which it can specifically recognize and remove polyploid cancer cells, but these appear to be tampered with malignancy so that polyploid cells can persist and fuel the development of cancer cell clones that are resistant to therapeutics and have metastatic potential.