scholarly journals Alive failures behind the windows of cancer therapy

2017 ◽  
Vol 5 (2) ◽  
pp. 179
Author(s):  
Muhammad Islam

The multiscope process, cancer is attributable from various geneses. Eventually, cancer is a complicated disease with unconstrained interca-lation and impacts on the physiological system. Therefore, an ideal cancer therapy must be like a multi-edged sword. Broadly, currently, available cancer therapies are the cytoprotective, inhibitors of oncogenes, correctors, and cell destructors. Doubtless, cancer therapists are most frequently handling apoptosis and autophagy inducers, targeting of tumor suppressor genes, epigenetic and immune therapies. How-ever, each therapy has a number of challenges yet to be resolved. This revision is aimed to find out some important points, depicting till the date, how successful we are and what are the failures behind those modes of therapeutic strategies.

Neurology ◽  
1998 ◽  
Vol 51 (5) ◽  
pp. 1250-1255 ◽  
Author(s):  
J. Fueyo ◽  
C. Gomez-Manzano ◽  
W. K. Alfred Yung ◽  
A. P. Kyritsis

2003 ◽  
Vol 18 (1) ◽  
pp. 49-53 ◽  
Author(s):  
E. Guerra ◽  
G. Vacca ◽  
B. Palombo ◽  
S. Alberti

The identification of molecular indicators of higher risk for specific subgroups of cancer patients may allow to develop more aggressive therapeutic strategies aimed at cases with the highest likelihood of response. This would avoid unnecessary toxicity to patients and alleviate the burden of cancer care for healthcare systems. Activated oncogenes and mutated tumor suppressor genes are causal determinants of the appearance and progression of tumors in man. They therefore represent potential indicators of prognosis and/or response to therapy. However, even in cases of well-studied oncogenes and tumor suppressor genes such as TP53 and RAS, their attributed prognostic and predictive value is often based on studies of insufficient statistical power that often lead to conflicting conclusions. Findings in favor or against the use of TP53 and RAS as prognostic and predictive indicators in breast cancer are reviewed and discussed here.


1995 ◽  
Vol 13 (2) ◽  
pp. 127-131 ◽  
Author(s):  
Arthur H. Bertelsen ◽  
Gary A. Beaudry ◽  
Timothy J. Stoller ◽  
Paul P. Trotta ◽  
Michael I. Sherman

BioEssays ◽  
2015 ◽  
Vol 37 (12) ◽  
pp. 1277-1286 ◽  
Author(s):  
Yunhua Liu ◽  
Xiaoxiao Hu ◽  
Cecil Han ◽  
Liana Wang ◽  
Xinna Zhang ◽  
...  

Author(s):  
Zicheng Wang ◽  
Yanqing Liu ◽  
Ahmed Eleojo Musa

: Cancer therapy is based on the killing of cancer cells using various therapeutic agents such as radiation, chemotherapy or targeted therapy drugs and immunotherapy. Cancer cells may undergo apoptosis, mitotic catastrophe, necrosis, autophagy, mitophagy, senescence etc., depending on the therapeutic modality and nature of cancer cells. Mutations in some critical genes such as p53 and phosphatase and tensin homolog (PTEN) tumor suppressor genes are associated with immune escaping cancer cells and progression towards tumor progression. Furthermore, the overexpression of some genes such as phosphatidylinositol-3-kinase (PI3K), nuclear factor of Kappa B (NF-κB), cyclooxygenase-2 (COX-2) and mammalian target of rapamycin (mTOR) is associated with resistance of cancer cells to various types of cell death. Melatonin is known as a circadian regulator hormone that has several anti-cancer properties. It has ability to activate tumor suppressor genes and attenuate the expression of survival genes in cancer cells. Modulation of cell death or survival genes that have been disrupted or overexpressed in cancer cells can improve cancer therapy. In this review, we explain the potentials of melatonin in regulating various mechanisms of cancer cell death.


Sign in / Sign up

Export Citation Format

Share Document