Awakening the sleeping/cancer-protecting angels in mutant p53 human tumors: Sulindac (brand name: Clinoril), a nonsteroidal anti-inflammatory drug (NSAID) used in the treatment of acute and chronic inflammatory conditions,  increases the expression of tumor suppressors genes, such as BTG2, TIMP3,  p53, TAp63, TAp73, INK4a, and others, and induces regression of p53-mutated human cancers and other cancers, via up-regulation of its target gene, 30/October/2018, 6.53 pm

A musical way to keep the cardiac diseases at bay-hard to believe though(that is not what science-based music thinks so): Music-based adjunctive Regenerative therapy for Cardiomyopathy:  Music decreases the expression of Sox6, restores the balance between slow- and fast-twitch myofiber proteins and alleviates Cardiomyopathy, via up regulation of its target gene, 30/October/2018, 8.40 am
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Awakening the sleeping/cancer-protecting angels in mutant p53-expressing human tumors: Mibolerone (Trade name: Cheque drops and Matenon), an anabolic-androgenic steroid, increases the expression of tumor suppressors genes, such as PTPN14, RB1, p53,  p53, TAp63, TAp73, INK4a/ARF, and others, induces regression of p53-mutated human tumors, via down-regulation of its target gene, 30/October/2018, 10.53 pm
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From Significance of the study to Public health relevance

Given that: (1) cancer suppressor p53 is mutated in more than 50% of human cancers of different tissue origin; (2) p53 pathway is altered in about 80% of tumors.; (3) our understanding is incomplete in terms of molecular targets and the oncogenic/malignant pathways involved in mutant p53-overexpressing tumors; (4) cancer causes the highest economic loss compared to all the known causes of death worldwide; and (5) cancer causes the considerable economic loss worldwide, there is an urgent need to find: (i) a cheaper alternative to the existing expensive drugs; (ii) a side-effect-free natural product-based drug; and (iii) a way to effectively treat and stall metastatic progression and relapse of mutant p53-overexpressing human cancers.


From therapeutic strategy to Research Findings:

(i) Therapeutic strategy: 

This study suggests a therapeutic strategy for stalling the progression of p53-deficient/deleted or mutant-p53 expressing metastatic cancers. By activating tumor suppressor p53’s unmutated “homologous protein such as TAp73/p63” in p53-deficient or mutant-p53 expressing metastatic cancer cells, one can stall their progression.

(ii) Research findings:  

This study suggests that nonsteroidal anti-inflammatory drug (NSAID) Sulindac may function as an anti-cancer/metastatic agent in mutant p53 expressing human cancers. 

Figure 1. Mechanistic insight into how Sulindac  (brand name: Clinoril) functions as an anticancer/antimetastatic agent in mutant p53-expressing tumors.    Sulindac (brand name: Clinoril),  by activating tumor/metastasis suppressor genes, such as BTG2, TIMP3, p53, TAp63, TAp73, INK4a, and ARF and others, in metastatic tumors, it may inhibit the progression of mutant-p53 expressing human cancers

Figure 2.  Sulindac  (brand name: Clinoril) functions as an anti-tumor/metastatic agent through induction of tumor/metastatic suppressor genes, such as  BTG2, TIMP3, p53, TAp63, TAp73, INK4a, and ARF

 

 

 

 

 

 

 

 

 

 

This study suggests that Sulindac, by increasing the expression of its target gene, it may increase the expression of tumor/metastasis suppressors genes, such as BTG2, TIMP3, p53, TA-p73, TA-p63, INK4a, ARF, and others. Thereby, it may inhibit the migration and invasion of metastatic cancer cells expressing mutant-p53 (figure1).

 


Therapeutic opportunity:

Given the ability of Sulindac to induce the expression of a number of tumor/metastasis suppressor genes, as indicated above, it may be used, either alone or in combination with other anticancer drugs, to inhibit the progression of not only p53-mutated invasive metastatic tumors, but also other aggressive human cancers. Taken together, this study suggests, for the first time, that oncologists may consider treating metastatic cancer patients with Sulindac, as it may stall the progression of advanced metastatic cancers, by turning on the expression of  tumor/metastasis suppressors genes, such as BTG2, TIMP3, p53, TA-p73, TA-p63, INK4a, ARF, and others (figure 2).


Details of the research findings

Idea Proposed/Formulated by Dr. L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Amount: $300#

Undisclosed mechanistic information: How Sulindac increases the expression of tumor suppressor genes, such as  BTG2, TIMP3,  p53, TAp63, TAp73, and others,  in mutant p53 expressing cancer cells?

For purchase and payment details, you may reach us at admin@genomediscovery.org

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References:

Web: http://genomediscovery.org or http://newbioideas.com

Citation: Boominathan, L., Awakening the sleeping/cancer-protecting angels in mutant p53 human tumors: Sulindac (brand name: Clinoril), a nonsteroidal anti-inflammatory drug (NSAID) used in the treatment of acute and chronic inflammatory conditions,  increases the expression of tumor suppressors genes, such as BTG2, TIMP3,  p53, TAp63, TAp73, INK4a, and others, and induces regression of p53-mutated human cancers and other cancers, via up-regulation of its target gene, 30/October/2018, 6.52 pm, Genome-2-Biomedicine Discovery center (GBMD), http://genomediscovery.org

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