Abstract: The present invention provides methods and kits a) for predicting colorectal cancer patient survival, as well as the survival of patients harboring other invasive cancers where cellular proliferation and carcinogenesis is linked, in part, to high levels of ODC activity and increased cellular polyamine contents, and b) for selecting the corresponding treatment options for such patients based on the allelic nucleotide sequence or SNP at position +316 of the ODC1 promoter gene as well as cancer treatment methods, in each case, which include the determination of the ODC1 promoter +316 position genotype, as a means to guide treatment selection.

Abstract: The present invention provides methods and kits a) for predicting colorectal cancer patient survival, as well as the survival of patients harboring other invasive cancers where cellular proliferation and carcinogenesis is linked, in part, to high levels of ODC activity and increased cellular polyamine contents, and b) for selecting the corresponding treatment options for such patients based on the allelic nucleotide sequence or SNP at position +316 of the ODC1 promoter gene as well as cancer treatment methods, in each case, which include the determination of the ODC1 promoter +316 position genotype, as a means to guide treatment selection.

Abstract: The present invention provides methods and kits a) for predicting colorectal cancer patient survival, as well as the survival of patients harboring other invasive cancers where cellular proliferation and carcinogenesis is linked, in part, to high levels of ODC activity and increased cellular polyamine contents, and b) for selecting the corresponding treatment options for such patients based on the allelic nucleotide sequence or SNP at position +316 of the ODC1 promoter gene as well as cancer treatment methods, in each case, which include the determination of the ODC1 promoter +316 position genotype, as a means to guide treatment selection.

Abstract: The present invention provides methods and kits a) for predicting colorectal cancer patient survival, as well as the survival of patients harboring other invasive cancers where cellular proliferation and carcinogenesis is linked, in part, to high levels of ODC activity and increased cellular polyamine contents, and b) for selecting the corresponding treatment options for such patients based on the allelic nucleotide sequence or SNP at position +316 of the ODC1 promoter gene as well as cancer treatment methods, in each case, which include the determination of the ODC1 promoter +316 position genotype, as a means to guide treatment selection.

Abstract: The present invention provides methods and kits a) for predicting colorectal cancer patient survival, as well as the survival of patients harboring other invasive cancers where cellular proliferation and carcinogenesis is linked, in part, to high levels of ODC activity and increased cellular polyamine contents, and b) for selecting the corresponding treatment options for such patients based on the allelic nucleotide sequence or SNP at position +316 of the ODC1 promoter gene as well as cancer treatment methods, in each case, which include the determination of the ODC1 promoter +316 position genotype, as a means to guide treatment selection.

Abstract: The present invention provides methods and kits a) for predicting colorectal cancer patient survival, as well as the survival of patients harboring other invasive cancers where cellular proliferation and carcinogenesis is linked, in part, to high levels of ODC activity and increased cellular polyamine contents, and b) for selecting the corresponding treatment options for such patients based on the allelic nucleotide sequence or SNP at position +316 of the ODC1 promoter gene as well as cancer treatment methods, in each case, which include the determination of the ODC1 promoter +316 position genotype, as a means to guide treatment selection.

Abstract: Disclosed are methods involving the administration of an extracellular matrix (ECM)/metastasis modifier gene, e.g., Anakin, Necdin, CentaurinD3 (CentD3), Csf1r, Brd4, Pi16, and Luc7l, for the prevention or inhibition of metastasis or of tumor growth. Further disclosed are methods of characterizing a tumor or cancer in a subject comprising detecting (i) a single nucleotide polymorphism (SNP) in an Anakin gene or a Brd4 gene of the subject, (ii) an amino acid substitution in an Anakin protein in the subject, or (iii) a level of expression of an Anakin gene or a Brd4 gene in the subject. Methods of screening a compound for anti-cancer activity and use of a compound with anti-cancer activity for the preparation of a medicament to treat or prevent cancer in a subject are also disclosed. Also disclosed is a method of inhibiting Sipa-1 in a subject.

Abstract: Heparinized human whole blood from patients with invasive breast cancer, with (multiple primary) and without (single primary) a second primary cancer, and from unaffected controls was stimulated with 0.1-10 Gy of radiation and incubated at 37° C. for 2 hours. P21 and PUMA mRNA were then quantified. The results suggest that cancer susceptibility represented by the multiple primary cases was significantly related to over-reaction of p21 mRNA, and not PUMA.