Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: 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 oligoribodeoxynucleotide sequence may be provided by an expression vector.

Abstract: Individuals having tumors are treated with pharmaceutical compositions comprising expression vectors, preferably adenovirus or retroviruses, comprising nucleic acid molecules encoding soluble IGF-1R. Such vectors express soluble IGF-1R in tumor cells resulting in reversal of the transformed phenotype, induction of apoptosis, and inhibition of tumorigenesis.

Abstract: The present invention is directed to oligonucleotides that inhibit mutant COL1A1 and/or wild type COL1A1 gene expression. The present invention is further directed to methods of inhibiting mutant and/or wild type collagen gene expression using the disclosed inhibitory oligonucleotides. The oligonucleotides and methods of the present invention are useful for the treatment of mammals having diseases related to inappropriate mutant or wild type COL1A1 gene expression.

Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: 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.