Overriding Elements in Colon Cancer Progression: Some Less Known Facts

Rohit Gundamaraju*, Ravichandra Vemuri and Rajaraman Eri

Overriding Elements in Colon Cancer Progression: Some Less Known Facts

Colorectal cancer is a heterogeneous disease causing more than 4 million deaths.
Apart from dietary factors, lifestyle and genetics, advancements from other ailments like inflammatory bowel disease are reasons for cause of CRC.

In several studies, it was affirmed that prevalence of CRC in patients with ulcerative
colitis greatly varies from place and nature of race.

Amongst the molecular pathogenesis, inflammation has a direct link to CRC.

Not only by the assessment of mucosal biopsies revealed escalated levels
of cell division and cell death, there were several conditions like epithelial
mesenchymal transition which had a higher role
in cancer invasion rate or metastasis.

Cytokines which are categorized under small proteins play an important role in cell
signaling.
In carcinogenic conditions like colitis associated cancers, cytokines were said to
have a significant influence.

Factors like nuclear factor-kappa B, tumor necrosis factor etc.
regulate cell cycle, apoptosis, reactive oxygen species and mutations.

Thus the present view point will list few perplexing conditions,
inflammatory modulators and receptors which would aid in CRC progression.

Colorectal cancer is one of the most life threatening disease with escalating mortality
and morbidity.

Some known causative factors include lifestyle, alcohol etc. but there are other
aspects like long standing colitis, inhibition of apoptotic proteins,
chemokines and their receptors and inflammasomes which increase
the chances of CRC progression.

In a clinical setting of diseases like colitis and Crohn’s disease,
the risk of CRC varies on degree of inflammation,
expression of chemokines and cytokines and other molecular alterations.

Hence, the underlying molecular inductions determine the fate of CRC
progression through extent of epithelial mesenchymal transition,
metastasis and invasive ability.

Gastro Open J. 2016; 2(1): 4-8. doi: 10.17140/GOJ-2-124

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