Cure Alveolar Soft Part Sarcoma International (iCureASPS)

I've been reading in a lot of papers about how cancers are a result of cells unable to die or are multiplying uncontrollably .
I Came across this theory of how to look at cancer and another possible angle in which to fight it and I wanted to share.

Are Telomeres The Key To Aging And Cancer?

Inside the nucleus of a cell, our genes are arranged along twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes are stretches of DNA called telomeres, which protect our genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer.

Telomeres have been compared with the plastic tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism's genetic information.

Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or "senescent" or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres also have been compared with a bomb fuse.


http://learn.genetics.utah.edu/content/ ... telomeres/



http://www.news-medical.net/health/Telo ... ancer.aspx

There apparently is an enzyme responsible for the proliferation of cells gone wild
It prevents the cell from dying and it multiplies far beyond its normal life ..

http://mcr.aacrjournals.org/content/3/9/477.full

On a molecular level celleur biologists have given us the skinny on the mutations in several cancer makeups to show activity- namely sarcomas that are us-



Titled: TERT promoter hotspot mutations are recurrent in myxoid liposarcomas but rare in other soft tissue sarcoma


Telomerase reverse transcriptase (TERT)


Journal of Experimental & Clinical Cancer Research 2014, 33:33 doi:10.1186/1756-9966-33-33

The electronic version of this article is the complete one and can be found online at: http://www.jeccr.com/content/33/1/33


Received: 4 March 2014
Accepted: 8 April 2014
Published: 11 April 2014

© 2014 Koelsche et al.; licensee BioMed Central Ltd.


This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Abstract
Background
Recently, recurrent point mutations in the telomerase reverse transcriptase (TERT) promoter region have been found in many human cancers, leading to a new transcription factor binding site, increased induction of TERT and subsequently to telomere maintenance. We determined the prevalence of TERT promoter mutations in soft tissue sarcomas of 341 patients comprising 16 entities and in 16 sarcoma cell lines covering 7 different soft tissue sarcoma types.

Methods
The sarcoma tissue samples were collected from the archives of the Institute of Pathology, University of Heidelberg and were composed of 39 myxoid liposarcomas (MLS), 61 dedifferentiated liposarcomas, 15 pleomorphic liposarcomas, 27 leiomyosarcomas, 25 synovial sarcomas (SS), 35 malignant peripheral nerve sheath tumors (MPNST), 40 undifferentiated pleomorphic sarcomas, 17 myxofibrosarcomas, 9 low grade fibromyxoid sarcomas, 10 cases of dermatofibrosarcoma protuberans, 31 solitary fibrous tumors (SFT), 8 extraskeletal myxoid chondrosarcomas, 9 angiosarcomas, 6 alveolar soft part sarcomas, 5 clear cell sarcomas and 4 epithelioid sarcomas. Sarcoma cell lines were obtained from the raising laboratories. A 193 bp fragment of the TERT promoter region covering the hot-spot mutations C228T and C250T was amplified, and direct sequencing of the PCR products was performed.

Results
TERT promoter mutations were detected in 36/341 sarcomas. They were highly recurrent in MLS (29/39; 74%) and were in the present MLS series not associated with the phenotype (myxoid vs. round cell variant), tumor grade, tumor site and patients’ median age or gender. In the remaining cases, TERT promoter mutations were found only in 7/302 sarcoma samples and confined to SFTs (4/31; 13%), MPNSTs (2/35; 6%), and SSs (1/25; 4%). Within the collection of sarcoma cell lines examined, TERT promoter mutations were detected in two MLS and in one of three MPNST cell lines.

Conclusions
TERT promoter mutations are frequent in MLSs including their round cell variants, representing the most prevalent mutation identified in this sarcoma entity to date, and in a minor fraction of SFTs, MPNSTs and SSs. The majority of sarcomas are devoid of TERT promoter hotspot mutations. These data suggest that telomere maintenance through increased expression of telomerase plays an important role in the pathogenesis especially of MLS.

Did a search on "C228T locus and alveolar soft part sarcoma"

The c228T is a recurrent mutation, a second generation if you will, found to be a hot spot in some STS ( soft tissue sarcomas) in the study of the telomeres mutations.





http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022359/