Open Access. Powered by Scholars. Published by Universities.®
- Keyword
-
- Apoptosis (2)
- Par-4 (2)
- Animals (1)
- Apoptosis Regulatory Proteins (1)
- Blotting, Western (1)
-
- Cancer supportive care (1)
- Cell Line, Tumor (1)
- Chloroquine (1)
- Drug Resistance, Neoplasm (1)
- Dusquetide (1)
- Fbxo45 (1)
- Head and neck cancer (1)
- Humans (1)
- Immune (1)
- Immunoprecipitation (1)
- Innate (1)
- Male (1)
- Metastasis-inhibition (1)
- Mice (1)
- Mice, Nude (1)
- Neoplasms, Experimental (1)
- Oral mucositis (1)
- P53 (1)
- Peptides (1)
- Rab8b (1)
- Secretagogues (1)
- Xenograft Model Antitumor Assays (1)
Articles 1 - 3 of 3
Full-Text Articles in Life Sciences
Dusquetide: Reduction In Oral Mucositis Associated With Enduring Ancillary Benefits In Tumor Resolution And Decreased Mortality In Head And Neck Cancer Patients, Mahesh Kudrimoti, Amarinthia Curtis, Samar Azawi, Francis Worden, Sanford Katz, Douglas Adkins, Marcelo Bonomi, Zack Scott, Jenna Elder, Stephen T. Sonis, Richard Straube, Oreola Donini
Dusquetide: Reduction In Oral Mucositis Associated With Enduring Ancillary Benefits In Tumor Resolution And Decreased Mortality In Head And Neck Cancer Patients, Mahesh Kudrimoti, Amarinthia Curtis, Samar Azawi, Francis Worden, Sanford Katz, Douglas Adkins, Marcelo Bonomi, Zack Scott, Jenna Elder, Stephen T. Sonis, Richard Straube, Oreola Donini
Radiation Medicine Faculty Publications
Innate immunity is a key component in the pathogenesis of oral mucositis, a universal toxicity of chemoradiation therapy (CRT). Dusquetide, a novel Innate Defense Regulator, has demonstrated both nonclinical and clinical efficacy in ameliorating severe oral mucositis (SOM). Long term follow-up studies from the Phase 2 clinical study evaluating dusquetide as a treatment for SOM in head and neck cancer (HNC) patients receiving CRT have now been completed. Extended analysis indicates that dusquetide therapy was well-tolerated and did not contribute to increased infection, tumor growth or mortality. Potential ancillary benefits of duquetide therapy were also identified.
A Naturally Generated Decoy Of The Prostate Apoptosis Response-4 Protein Overcomes Therapy Resistance In Tumors, Nikhil Hebbar, Ravshan Burikhanov, Nidhi Shukla, Shirley Qiu, Yanming Zhao, Kojo S. J. Elenitoba-Johnson, Vivek M. Rangnekar
A Naturally Generated Decoy Of The Prostate Apoptosis Response-4 Protein Overcomes Therapy Resistance In Tumors, Nikhil Hebbar, Ravshan Burikhanov, Nidhi Shukla, Shirley Qiu, Yanming Zhao, Kojo S. J. Elenitoba-Johnson, Vivek M. Rangnekar
Radiation Medicine Faculty Publications
Primary tumors are often heterogeneous, composed of therapy-sensitive and emerging therapy-resistant cancer cells. Interestingly, treatment of therapy-sensitive tumors in heterogeneous tumor microenvironments results in apoptosis of therapy-resistant tumors. In this study, we identify a prostate apoptosis response-4 (Par-4) amino-terminal fragment (PAF) that is released by diverse therapy-sensitive cancer cells following therapy-induced caspase cleavage of the tumor suppressor Par-4 protein. PAF caused apoptosis in cancer cells resistant to therapy and inhibited tumor growth. A VASA segment of Par-4 mediated its binding and degradation by the ubiquitin ligase Fbxo45, resulting in loss of Par-4 proapoptotic function. Conversely, PAF, which contains this VASA …
Chloroquine-Inducible Par-4 Secretion Is Essential For Tumor Cell Apoptosis And Inhibition Of Metastasis, Ravshan Burikhanov, Nikhil Hebbar, Sunil K. Noothi, Nidhi Shukla, James Sledziona, Nathália Araujo, Meghana Kudrimoti, Qing Jun Wang, David S. Watt, Danny R. Welch, Jodi Maranchie, Akihiro Harada, Vivek M. Rangnekar
Chloroquine-Inducible Par-4 Secretion Is Essential For Tumor Cell Apoptosis And Inhibition Of Metastasis, Ravshan Burikhanov, Nikhil Hebbar, Sunil K. Noothi, Nidhi Shukla, James Sledziona, Nathália Araujo, Meghana Kudrimoti, Qing Jun Wang, David S. Watt, Danny R. Welch, Jodi Maranchie, Akihiro Harada, Vivek M. Rangnekar
Radiation Medicine Faculty Publications
The induction of tumor suppressor proteins capable of cancer cell apoptosis represents an attractive option for the re-purposing of existing drugs. We report that the anti-malarial drug, chloroquine (CQ), is a robust inducer of Par-4 secretion from normal cells in mice and cancer patients in a clinical trial. CQ-inducible Par-4 secretion triggers paracrine apoptosis of cancer cells and also inhibits metastatic tumor growth. CQ induces Par-4 secretion via the classical secretory pathway that requires the activation of p53. Mechanistically, p53 directly induces Rab8b, a GTPase essential for vesicle transport of Par-4 to the plasma membrane prior to secretion. Our findings …