Abstract: A method of treating or preventing cancer by administering to a mammal a therapeutically effective amount of at least one anti-neurotrophin agent is described. The anti-neurotrophin agent is preferably an anti-neurotrophin antibody, an antisense molecule directed to a neurotrophin, a small organic molecule which binds a neurotrophin, or a dominant-negative mutation of a trk receptor that binds a neurotrophin. This method is particularly preferred for the treatment of prostate or pancreatic cancer. The anti-neurotrophic agents neutralize NGF, BDNF, NT-3, NT-4/5, NT-6 or NT-7 and include humanized antibodies as well as fragments thereof.

Abstract: The complete cDNA cloning of two human genes previously designated flg and bek is disclosed. These genes encode for two similar but distinct surface receptors comprised of an extracellular domain with three immunoglobulin-like regions, a single transmembrane domain, and a cytoplasmic portion containing a tyrosine kinase domain with a typical kinase insert. The expression of these two cDNAs in transfected NIH-3T3 cells led to the biosynthesis of proteins of 150 kDa and 135 kDa for flg and bek respectively. Direct binding experiments with radiolabeled acidic FGF (aFGF), basic FGF (bFGF), or kFGF inhibition of binding with native growth factors, and Scatchard analysis of the binding data indicated that bek and flg bind aFGF, bFGF, or kFGF with dissociation constants of (2-15)×10−11M. The high affinity binding of three distinct growth factors to each of two different receptors represents a unique double redundancy without precedence among polypeptide growth factor/receptor interactions.

Abstract: A method of treating or preventing cancer by administering to a mammal a therapeutically effective amount of at least one anti-neurotrophin agent is described. The anti-neurotrophin agent is preferably an anti-neurotrophin antibody, an antisense molecule directed to a neurotrophin, a small organic molecule which binds a neurotrophin, or a dominant-negative mutation of a trk receptor that binds a neurotrophin. This method is particularly preferred for the treatment of prostate or pancreatic cancer. The anti-neurotrophic agents neutralize NGF, BDNF, NT-3, NT-4/5, NT-6 or NT-7 and include humanized antibodies as well as fragments thereof.

Abstract: A method of treating prostate cancer by co-administering a tyrosine kinase inhibitor such as an indolocarbazole and a chemical castration agent is disclosed. A composition containing a tyrosine kinase inhibitor and a chemical castration agent is also disclosed.

Abstract: The complete cDNA cloning of two human genes previously designated flg and bek is disclosed. These genes encode for two similar but distinct surface receptors comprised of an extracellular domain with three immunoglobulin-like regions, a single transmembrane domain, and a cytoplasmic portion containing a tyrosine kinase domain with a typical kinase insert. The expression of these two cDNAs in transfected NIH-3T3 cells led to the biosynthesis of proteins of 150 kDa and 135 kDa for flg and bek respectively. Direct binding experiments with radiolabeled acidic FGF (aFGF), basic FGF (bFGF), or kFGF inhibition of binding with native growth factors, and Scatchard analysis of the binding data indicated that bek and flg bind aFGF, bFGF, or kFGF with dissociation constants of (2-15).times.10.sup.-11 M. The high affinity binding of three distinct growth factors to each of two different receptors represents a unique double redundancy without precedence among polypeptide growth factor/receptor interactions.

Abstract: The invention features a method of treating a pathological condition of the prostate gland, e.g., benign prostatic hypertrophy or prostate cancer, in a mammal, said method comprising administering to said mammal a therapeutic amount of the indolocarbazole compound K-252a or a preferred derivative thereof. The invention also includes novel derivatives of K-252a.

Abstract: The invention features a method of treating a pathological condition of the prostate gland, e.g., benign prostatic hypertrophy or prostate cancer, in a mammal, said method comprising administering to said mammal a therapeutic amount of the indolocarbazole compound K-252a or a preferred derivative thereof. The invention also includes novel derivatives of K-252a.