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INHIBITION OF MIGRATION BY ATE+31

Award Number: R01CA081209
ORGANIZATION: NATIONAL CANCER INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 12/15/1999
PERIOD OF PERFORMANCE END DATE: 05/31/2010

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INHIBITION OF MIGRATION BY ATE+31 - DESCRIPTION (provided by applicant): The high molecular weight form of FGF-2 (24kDa FGF-2) is produced by alternative translational start sites and consists of the more commonly studied 18kDa FGF-2 with an additional 55 amino acids at the amino terminal end. Treatment of endothelial or breast carcinoma cells with 24kDa FGF-2 results in an 80% decrease in migration rate although it continues to promote cell proliferation. We have performed deletion mutagenesis and developed a truncated form of 24kD FGF-2 which is highly effective in inhibiting migration in vitro while having no effect on cell growth. This peptide consists of the amino terminal 86 amino acids of 24kD FGF-2 and is referred to as ATE+31. Studies in animals have shown that ATE+31 is highly effective in suppressing mammary carcinoma and lung carcinoma tumor growth by two mechanisms, suppressing the angiogenic response and inhibiting tumor cell migration away from the tumor core. Studies of the mechanism by which ATE+31 inhibits migration have revealed that growth factor-induced increases in focal adhesion kinase (FAK) phosphorylation are abrogated by ATE+31. The decrease in phosphorylation occurred at tyr397 ,tyr407, and tyr861. Concomitantly, exposure to ATE+31 inhibited the reorganization of micro filaments and loss of focal adhesions that accompany growth factor treatment making enhanced motility difficult to attain. The hypothesis that this project will address states that ATE+31 inhibits cell migration through a mechanism involving the suppression of FAK function through inhibition of enhanced phosphorylation. The project will examine the mechanism by which ATE-31 inhibits cell migration and employ animal models to test the in vitro results in vivo. Specifically the project will define the mechanisms by which ATE+31 suppresses FAK phosphorylation and how it subsequently inhibits focal adhesion/rnicrofi lament dynamics and employ mouse models of angiogenesis and tumor development to test the experimental results in vivo. In addition, the therapeutic potential of ATE+31 will be evaluated in animal models of tumor development, regression, and metastasis will be evaluated.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2009 ( Subtotal = $381,401 )
2009	2009	TORREY PINES INSTITUTE FOR MOLECULAR STUDIES	3550 GENERAL ATOMICS COURT	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	11	4/27/2009	NON-COMPETING CONTINUATION	$381,401
														Subtotal = $381,401

Issue Date FY: 2008 ( Subtotal = $381,401 )
2008	2008	TORREY PINES INSTITUTE FOR MOLECULAR STUDIES	3550 GENERAL ATOMICS COURT	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	10	6/19/2008	NON-COMPETING CONTINUATION	$381,401
														Subtotal = $381,401

Issue Date FY: 2007 ( Subtotal = $381,401 )
2007	2007	TORREY PINES INSTITUTE FOR MOLECULAR STUDIES	3550 GENERAL ATOMICS COURT	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	9	4/25/2007	NON-COMPETING CONTINUATION	$381,401
														Subtotal = $381,401

Issue Date FY: 2006 ( Subtotal = $392,792 )
2006	2006	TORREY PINES INSTITUTE FOR MOLECULAR STUDIES	3550 GENERAL ATOMICS COURT	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	8	5/18/2006	NON-COMPETING CONTINUATION	$392,792
														Subtotal = $392,792

Issue Date FY: 2005 ( Subtotal = $402,245 )
2005	2005	TORREY PINES INSTITUTE FOR MOLECULAR STUDIES	3550 GENERAL ATOMICS COURT	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	7	8/15/2005	COMPETING CONTINUATION	$402,245
														Subtotal = $402,245

Issue Date FY: 2004 ( Subtotal = $458,162 )
2004	2004	LA JOLLA INSTITUTE FOR MOLECULAR MEDICINE	4570 EXECUTIVE DR, SUITE 100	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	6	12/1/2003	NON-COMPETING CONTINUATION	$458,162
														Subtotal = $458,162

Issue Date FY: 2003 ( Subtotal = $444,816 )
2003	2003	LA JOLLA INSTITUTE FOR MOLECULAR MEDICINE	4570 EXECUTIVE DR, SUITE 100	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	5		NON-COMPETING CONTINUATION	$444,816
														Subtotal = $444,816

Issue Date FY: 2002 ( Subtotal = $431,864 )
2002	2002	LA JOLLA INSTITUTE FOR MOLECULAR MEDICINE	4570 EXECUTIVE DR, SUITE 100	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	4	11/30/2001	NON-COMPETING CONTINUATION	$431,864
														Subtotal = $431,864

Issue Date FY: 2001 ( Subtotal = $419,281 )
2001	2001	LA JOLLA INSTITUTE FOR MOLECULAR MEDICINE	4570 EXECUTIVE DR, SUITE 100	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	3	12/29/2000	NON-COMPETING CONTINUATION	$419,281
														Subtotal = $419,281

Issue Date FY: 2000 ( Subtotal = $348,160 )
2000	2000	LA JOLLA INSTITUTE FOR MOLECULAR MEDICINE	4570 EXECUTIVE DR, SUITE 100	SAN DIEGO	CA	92121	SAN DIEGO	USA	Cancer Biology Research	000	2	9/12/2000	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$120,495
2000	2000	SCRIPPS RESEARCH INSTITUTE	10666 NORTH TORREY PINES ROAD	LA JOLLA	CA	92037	SAN DIEGO	USA	Cancer Biology Research	000	1	9/12/2000	NEW	$227,665
														Subtotal = $348,160

Grand Total All Awards = $4,041,523

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INHIBITION OF MIGRATION BY ATE+31

Award Number: R01CA081209

ORGANIZATION: NATIONAL CANCER INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 12/15/1999

PERIOD OF PERFORMANCE END DATE: 05/31/2010

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