Modeling Alveolar Soft Part Sarcoma Unveils Novel Mechanisms of Metastasis.

[Olga]

Researchers from the Cancer Institute, Japanese Foundation for Cancer Research successfully created in vivo - living - mouse model for ASPS, it provides a tool to understand oncogenic, angiogenic and metastatic mechanisms of ASPS. It also identifies important motifs within the ASPSCR1-TFE3 fusion protein and to provide a platform for developing novel therapeutic strategies for this disorder.
(Cancer Res. 2016 Dec 15)
Modeling Alveolar Soft Part Sarcoma Unveils Novel Mechanisms of Metastasis.
https://www.ncbi.nlm.nih.gov/pubmed/27979841

[D.ap]

Olga
Still trying to understand ,but the therapeutic targets of the metastatic protein are sure being studied for future targeting purposes.
Clinical trials as of 2013

Glycoprotein non-metastatic b (GPNMB): A metastatic mediator and emerging therapeutic target in cancer
Abstract

Molecularly targeted therapies are rapidly growing with respect to their clinical development and impact on cancer treatment due to their highly selective anti-tumor action. However, many aggressive cancers such as triple-negative breast cancer (TNBC) currently lack well-defined therapeutic targets against which such agents can be developed. The identification of tumor-associated antigens and the generation of antibody drug-conjugates represent an emerging area of intense interest and growth in the field of cancer therapeutics. Glycoprotein non-metastatic b (GPNMB) has recently been identified as a gene that is over-expressed in numerous cancers, including TNBC, and often correlates with the metastatic phenotype. In breast cancer, GPNMB expression in the tumor epithelium is associated with a reduction in disease-free and overall survival. Based on these findings, glembatumumab vedotin (CDX-011), an antibody-drug conjugate that selectively targets GPNMB, is currently being investigated in clinical trials for patients with metastatic breast cancer and unresectable melanoma. This review discusses the physiological and potential pathological roles of GPNMB in normal and cancer tissues, respectively, and details the clinical advances and challenges in targeting GPNMB-expressing malignancies.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711880/

[D.ap]

In keeping with the topic of metastic ASPS studies
And glycoproteins high expressions ,I've been reading on how there has been noted that with TKIs ,there are issues with ASPS being a different creature than your average metastic say cancer to keep the celleur act of autophagy from going from a help to a hinderance i.e. Drug resistance during treatment with say, Sorafenib.

Sorafenib is a small inhibitor of several tyrosine protein kinases, such as VEGFR, PDGFR and Raf family kinases (more avidly C-Raf than B-Raf).[2][3][4]

(See BRAF (gene)#Sorafenib for details of drug structure interaction with B-Raf.)

Sorafenib treatment induces autophagy,[5] which may suppress tumor growth. However, autophagy can also cause drug resistance.[6]

https://en.m.wikipedia.org/wiki/Sorafenib

This article is written with melanoma in mind

Autophagy and the Effects of Its Inhibition on Varicella-Zoster Virus Glycoprotein Biosynthesis and Infectivity
Erin M. Buckingham, John E. Carpenter, [...], and Charles Grose

https://www.ncbi.nlm.nih.gov/pmc/articl ... po=1.10294

We also know that in a study ASPS 5 patience found that 4/5 patients were positive for the Cytomegalovirus

https://www.ncbi.nlm.nih.gov/m/pubmed/26990748/

[D.ap]

Last discussion on viruses
Article came from Johannes


http://www.cureasps.org/forum/viewtopic ... egalovirus