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Friday, August 11, 2017 8:46:10 PM
Publication number US8709412 B2
Publication type Grant
Application number US 13/176,651
Publication date 29 Apr 2014
Filing date 5 Jul 2011
Priority date 29 Jun 2001
Also published as US9683049, US20120156224, US20150023986, WO2013006727A1
Inventors Jennifer Jones, Rosemarie Dekruyff, Dale T. Umetsu, Gordon J. Freeman, Susan Jane Knox, Less «
http://patents.justia.com/inventor/jennifer-jones-mcintire
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=116380586
Original Assignee The Board Of Trustees Of The Leland Stanford Junior University, Dana-Farber Cancer Institute, Inc., Children's Hospital Corporation, Less «
Modulation of TIM receptor activity in combination with cytoreductive therapy
US 8709412 B2
ABSTRACT
A genetic locus and corresponding family of proteins associated with regulation of immune function and cell survival are provided. These genes encode cell surface molecules with conserved IgV and mucin domains. The locus comprising the TIM family is genetically associated with immune dysfunction, including asthma. Furthermore, the TIM gene family is located within a region of human chromosome 5 that is commonly deleted in malignancies and myelodysplastic syndrome. Polymorphisms in the gene sequences are associated with in the development of airway hyperreactivity and allergic inflammation, and T cell production of IL-4 and IL-13. The proteins include the human hepatitis A cellular receptor, hHAVcr-1.
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Because TIM receptors can be activated by binding to phosphatidylserine, a phospholipid that is exposed in irradiated tumor tissues, IT with TIM receptors may demonstrate greater specificity (and fewer ‘off target’ autoimmune side effects) than other IT agents currently under development, and the functional interaction between TIM-1 and PS in the tumor immune microenvironment provides a unique method for focusing immune activation to the irradiated tumor.
The TIM-1 gene and protein have several known polymorphisms that influence the function of the TIM-1 in immune responses. These genetic variations are most common in the mucin domain that is involved with TIM-1 adhesion to extracellular molecules and plays an important role in T helper cell function. Mice with functional deletions in exon 4 of TIM-1 develop less robust helper T cell responses. In human populations a polymorphism involving exon 4 encodes a longer form of the mucin chain, and this polymorphism impacts immune function. This polymorphism in TIM-1 has been linked to susceptibility to asthma and autoimmunity. Polymorphisms determining the length of the mucin domain may be analyzed prior to treatment involving stimulation of a TIM receptor.
Tumors of interest for treatment with the methods of the invention include solid tumors, e.g. carcinomas, gliomas, melanomas, sarcomas, and the like. Breast cancer is of particular interest. Carcinomas include the a variety of adenocarcinomas, for example in prostate, lung, etc.; adernocartical carcinoma; hepatocellular carcinoma; renal cell carcinoma, ovarian carcinoma, carcinoma in situ, ductal carcinoma, carcinoma of the breast, basal cell carcinoma; squamous cell carcinoma; transitional cell carcinoma; colon carcinoma; nasopharyngeal carcinoma; multilocular cystic renal cell carcinoma; oat cell carcinoma, large cell lung carcinoma; small cell lung carcinoma; etc. Carcinomas may be found in prostrate, pancreas, colon, brain (usually as secondary metastases), lung, breast, skin, etc. Including in the designation of soft tissue tumors are neoplasias derived from fibroblasts, myofibroblasts, histiocytes, vascular cells/endothelial cells and nerve sheath cells. Tumors of connective tissue include sarcomas; histiocytomas; fibromas; skeletal chondrosarcoma; extraskeletal myxoid chondrosarcoma; clear cell sarcoma; fibrosarcomas, etc.
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http://www.google.com.gi/patents/US8709412
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https://www.bloomberg.com/press-releases/2017-07-10/stanford-university-gets-1-73b-u-s-pact-to-run-slac-lab
https://www.bloomberg.com/profiles/people/4277665-marc-tessier-lavigne
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I still think Jason H Stafford did not go to Stanford for no reason....likely a very welcomed close knit PS Targeting super power in the making...
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