RENATO BASERGA
Medical Practice in Ardmore, PA

6340674, Jan 22, 2002

Sep 22, 2000

09/668822

Renato Baserga - Ardmore PA
Christian Sell - Philadelphia PA
Raphael Rubin - Penn Valley PA

Thomas Jefferson University - Philadelphia PA

A61K 4800

514 44, 536 245, 536 241, 536 231, 435455, 435377, 435375

A method of inhibiting the proliferation and causing the differentiation of undifferentiated cells comprising contacting the undifferentiated cells with an effective amount of an antisense oligonucleotide having a sequence which is complementary to a region of the IGF-1 receptor RNA. The sequence of the antisense oligonucleotide is selected from an oligodeoxynucleotide sequence complementary to codons -29 to -24 of the signal sequence of the IGF-1 receptor and an oligoribodeoxynucleotide sequence complementary to codons 1 to 309 of the sequence of the IGF-1 receptor. The oligoribonucleotide sequence may be provided by an expression vector.

6331526, Dec 18, 2001

Sep 2, 1999

9/389855

Renato Baserga - Ardmore PA
Christian Sell - Philadelphia PA
Raphael Rubin - Penn Valley PA

Thomas Jefferson University - Philadelphia PA

A61K 4800, C12Q 168, C07H 2104

514 44

A method of inhibiting the proliferation and causing the differentiation of undifferentiated cells comprising contacting the undifferentiated cells with an effective amount of an antisense oligonucleotide having a sequence which is complementary to a region of the IGF-1 receptor RNA. The sequence of the antisense oligonucleotide is selected from an oligodeoxynucleotide sequence complementary to codons -29 to -24 of the signal sequence of the IGF-1 receptor and an oligoribonucleotide sequence complementary to codons 1 to 309 of the sequence of the IGF-1 receptor. The oligoribonucleotide sequence may be provided by an expression vector.

5958872, Sep 28, 1999

Apr 1, 1996

8/625819

Rosemary O'Connor - Arlington MA
Renato L. Baserga - Ardmore PA

Apoptosis Technology, Inc. - Cambridge MA
Thomas Jefferson University - Philadelphia PA

C07K 1400, C12N 1509, C12N 1552

514 2

Active Survival Domains in the Insulin-like Growth Factor-I Receptor (IGF-IR) required for transmitting the survival signal in vertebrate cells have been identified. In FL5. 12 cells transfected with wild type IGF-I receptors, IGF-I provided protection from IL-3 withdrawal analogous to the protection afforded by expression of Bcl-2. Under the same conditions, IGF-I did not have a significant mitogenic effect on FL5. 12 cells expressing IGF-I receptors. An IGF-I receptor with a mutation at the ATP-binding site did not provide protection from apoptosis. However, mutations at tyrosine residue 950 or in the tyrosine cluster (1131, 1135, and 1136) in the kinase domain resulted in receptors that retained survival function. In the C-terminus of the IGF-IR, mutation at tyrosine 1251 and at histidine 1293 and lysine 1294 abolished apoptotic function, whereas mutation of the four serines at 1280-1283 did not affect survival. Surprisingly, receptors truncated at the C-terminus had enhanced anti-apoptotic function.

5643788, Jul 1, 1997

Jun 6, 1995

8/479173

Renato Baserga - Ardmore PA
Christian Sell - Philadelphia PA
Raphael Rubin - Penn Valley PA

Thomas Jefferson University - Philadelphia PA

C12N 510, C07H 2100, A61K 3170, C12Q 168

435325

A method of inhibiting the proliferation and causing the differentiation of undifferentiated cells comprising contacting the undifferentiated cells with an effective amount of an antisense oligonucleotide having a sequence which is complementary to a region of the IGF-1 receptor RNA. The sequence of the antisense oligonucleotide is selected from an oligodeoxynucleotide sequence complementary to codons -29 to -24 of the signal sequence of the IGF-1 receptor and an oligoribonucleotide sequence complementary to codons 1 to 309 of the sequence of the IGF-1 receptor. The oligoribonucleotide sequence may be provided by an expression vector.

6312684, Nov 6, 2001

May 29, 1997

8/864641

Renato Baserga - Ardmore PA
David Abraham - Wynnewood PA
Mariana Resnicoff - Philadelphia PA

Thomas Jefferson University

A61K 4800, A61K 3500

424 9321

A method of inducing resistance to tumor growth comprising placing tumor cells in culture in vitro supplemented with a pro-apoptotic agent for a period of time, transferring the tumor cells into a diffusion chamber, thereby producing a cell-containing chamber, inserting the chamber into a mammal for a therapeutically effective time, thereby inducing resistance to tumor growth. The pro-apoptotic agents include nucleic acid molecules, proteins or peptides, non-proteins or non-polynucleotide compounds, and a physical conditions.

5714170, Feb 3, 1998

Nov 16, 1994

8/340732

Renato Baserga - Ardmore PA
David Abraham - Wynnewood PA
Mariana Resnicoff - Philadelphia PA

Thomas Jefferson University - Philadelphia PA

A61K 3512

424573

A method of inducing resistance to tumor growth comprising placing tumor cells in culture supplemented with an agent in a diffusion chamber thereby producing a cell-containing chamber, inserting the chamber into a mammal for a therapeutically effective time, thereby inducing resistance to tumor growth.

5262308, Nov 16, 1993

Jan 28, 1992

7/827690

Renato Baserga - Ardmore PA

Thomas Jefferson University - Philadelphia PA

C12N 1500, C12N 510

435 691

Cells which constitutively express IGF-1 and IGF-1 R cDNAs are provided. These cells are useful for the production of selected proteins. Methods for producing the cells are also provided. Diagnostic and therapeutic methods are provided using cells transfected with IGF-1 R.

6218363, Apr 17, 2001

Aug 28, 1996

8/704344

Renato L. Baserga - Ardmore PA
Mariana Resnicoff - Philadelphia PA
Ziwei Huang - Philadelphia PA

Thomas Jefferson University - Philadelphia PA

A61K 3800

514 15

MHC or HLA Class I peptides and compositions thereof are provided for the specific induction of apoptosis of cancer cells in a patient. Methods of treating cancer cells in patients suffering from cancer employing the MHC or HLA Class I peptides of the invention. Also provided are methods of identifying MHC or HLA Class I peptides and variants thereof capable of killing cancerous cells in vivo in a patient suffering from cancer.

2010011, May 6, 2010

Apr 7, 2008

12/594962

Bin Shi - Lansdale PA, US
Laura Sepp-Lorenzino - Jenkintown PA, US
Peter Linsley - Seattle WA, US
Renato Baserga - Ardmore PA, US

A61K 31/7088, C12Q 1/68

514 44 R, 435 6

Provided herein are isolated nucleic acid molecule corresponding to miR145 that are useful in treating colon cancer. The disclosed miR145 nucleic acids specifically bind the 3′ UTR within endogenous IRS-I such as to suppress or inhibit colon cell proliferation.

5473054, Dec 5, 1995

Mar 30, 1994

8/219878

Bradford A. Jameson - Philadelphia PA
Renato Baserga - Ardmore PA

Thomas Jefferson University - Philadelphia PA

A61K 3800, C07K 700, C07K 706, C07K 708

530328

Short peptides which function as analogs of IGF-1 are provided. These peptides abolish the proliferation of cells at nanogram concentrations. The peptides are non-toxic, and the inhibitor effect is reversible. The use of these peptides, because of their low toxicity and high efficiency, holds promises for treatment of a variety of human conditions, including prevention of restenosis of the coronary arteries after angioplasty, treatment of human neoplasia such as cancer of the prostate, treatment of tumors in pleural and peritoneal cavities and brain metastases, treatment of other abnormalities of cell growth in human beings, treatment of smooth muscle cell hyperplasia in asthma, treatment to promote burn and wound healing, and purging bone marrow from highly proliferating cells.