Inflammation and Carcinogenesis
1450
[17]. IL 1 induces the expression of adhesion molecules
on endothelial cells and elicits stromal cells to release
chemokines that promote the recruitment of inflamma-
tory cells at the inflammation site [18]. Such inflamma-
tion occurs significantly in cases of comorbidity and
might contribute to the increased risk of developing car-
diovascular accidents observed in these patients [19].
IL-10, a cytokine with anti-inflammatory properties,
plays a central role in infection that involv es limiting the
immune response to pathogens and thereby preventing
damage to the host [20]. Recently, research has shown
that IL-10 and related cytokines can facilitate the tis-
sue-healing process in injuries caused by infection or
inflammation [21 ]. According to these stud ies, mediators
thought to be involved in the regulation of inflammation
responses such as leukocyte recruitment, adhesion mole-
cule expression, and wound healing in the late phase of
inflammation.
3. Inflammation and Cancer
The inflammatory cells and cytokines present in tumors
are more likely to contribute to tumor growth, progres-
sion, and immunosuppression than they are to induce an
effective host antitumor response [22]. Inflammatory
leukocytes such as neutrophils, monocytes, macrophages,
and eosinophils provide the soluble factors that are
thought to mediate the development of inflammation-
associated cancer, although other cells, including the
cancer cells, also participate [23]. In various forms of
inflammation, the tumor microenvironment contains in-
nate immune cells (including macrophages, neutrophils,
mast cells, myeloid-derived suppressor cells, dendritic
cells, and natural killer cells) and adaptive immune cells
(T and B lymphocytes) in addition to cancer cells and
their surrounding stroma (which consist of fibroblasts,
endothelial cells, pericytes, and mesenchymal cells) [24].
Previously published literature has indicated that the re-
sulting activity of inflammatory mediators, such as cyclo-
oxygenase (COX)-2, creates a tumor-promoting envi-
ronment in which transformed epithelial cells [25] and
COX-2 are inducible by oncogenes ras and scr, IL-1,
hypoxia, ultraviolet lig ht, epidermal growth factor, trans-
forming growth factor beta, and TNF-α [26]. Studies
have expanded on th e concept that inflammation is a cri-
tical component of tumor progression, and many cancers
arise from sites of infection, chronic irritation, and in-
flammation [27]. Investigation of the inflammatory sub-
stances involved in the process may help us prevent even
cure the cancer disease.
REFERENCES
[1] P. Allavena, A. Sica, G. Solinas, et al., “The Inflam-
matory Micro-Environment in Tumor Progression: The
Role of Tumor-Associated Macrophages,” Critical Re-
views in Oncology/Hematology, Vol. 66, No. 1, 2008, pp.
1-9. http://dx.doi.org/10.1016/j.critrevonc.2007.07.004
[2] N. A. Punchard, C. J. Whelan and I. Adcock, “The
Journal of Inflammation,” Journal of Inflammation, Vol.
1, No. 1, 2004, p. 1.
http://dx.doi.org/10.1186/1476-9255-1-1
[3] D. Maslinska and M. Gajewski, “Some Aspects of the
Inflammatory Process,” Folia Neuropathologica, Vol. 36,
No. 4, 1998, pp. 199-204.
[4] I. Sbarsi, C. Falcone, C. Boiocchi, et al., “Inflammation
and Atherosclerosis: The role of TNF and TNF Receptors
Polymorphisms in Coronary Artery Disease,” Interna-
tional Journal of Immunopathology and Pharmacology,
Vol. 20, No. 1, 2007, pp. 145-154.
[5] P. Libby, P. M. Ridker and A. Maseri, “Inflammation and
Atherosclerosis,” Circulation, Vol. 105, No. 9, 2002, pp.
1135-1143. http://dx.doi.org/10.1161/hc0902.104353
[6] J. M. Schott and T. Re vesz, “Inflammation i n Alzheime’s
Disease: Insights from Immunotherapy,” Brain, Vol. 136,
2013, pp. 2654-2656.
http://dx.doi.org/10.1093/brain/awt231
[7] J. M. Rubio-Perez and J. M. Morillas-Ruiz, “A Review:
Inflammatory Process in Alzheimer’s Disease, Role of
Cytokines,” Scientific World Journal, Vol. 2012, 2012.
Article ID: 756357
http://dx.doi.org/10.1100/2012/756357
[8] C. D. Gregory, “Inflammation and Cancer Revisited: An
Hypothesis on the Oncogenic Potential of the Apoptotic
Tumor Cell,” Autoimmunity, Vol. 46, No. 5, 2013, pp.
312-316.
http://dx.doi.org/10.3109/08916934.2012.755961
[9] B. B. Aggarwal, S. Shishodia, S. K. Sandur et al., “In-
flammation and cancer: How Hot Is the Link?” Bio-
chemical Pharmacology, Vol. 72, No. 11, 2006, pp. 1605-
1621.
[10] G. S. Hotamisligil, N. S. Shargill and B. M. Spiegelman,
“Adipose Expression of Tumor-Necrosis-Factor-Alpha-
Direct Role in Obesity-Linked Insulin Resistance,” Sci-
ence, Vol. 259, No. 5091, 1993, pp. 87-91.
http://dx.doi.org/10.1126/science.7678183
[11] J. L. Dunne, R. G. Collins, A. L. Beaudet, et al., “Mac-1,
but Not LFA-1, Uses Intercellular Adhesion Molecule-1
to Mediate Slow Leukocyte Rolling in TNF-Alpha-
Induced Inflammation,” Journal of Immunology, Vol. 171,
No. 11, 2003, pp. 6105-6111.
[12] C. V. Carman and T. A. Springer, “A Transmigratory
Cup in Leukocyte Diapedesis Both through Individual
Vascular Endothelial Cells and between Them,” Journal
of Cell Biology, Vol. 167, No. 2, 2004, pp. 377-388.
http://dx.doi.org/10.1083/jcb.200404129
[13] S. K. Fried, D. A. Bunkin, and A. S. Greenberg, “Oment-
al and Subcutaneous Adipose Tissues of Obese Subjects
Release Interleukin-6: Depot Difference and Regulation
by Glucocorticoid,” Journal of Clinical Endocrinology &
Metabolism, vol. 83, No. 3, 1998, pp. 847-850.
http://dx.doi.org/10.1210/jc.83.3.847
[14] Z. Xing, J. Gauldie, G. Cox, et al., “IL-6 Is an Anti-
inflammatory Cytokine Required for Controlling Local or
Open Access JCT