Abstract: Methods are disclosed for predicting a patient response to anti-Her2 therapy or anti-aromatase therapy. In certain embodiments, the methods involve the identification of low molecular weight cyclin E (LMW-E) in cancers, such as breast cancer cells, as a predictive and prognostic marker. In further embodiments, LMW-E expression by a cancerous or pre-cancerous cell may be used to predict response to an aromatase inhibitor and/or CDK2 inhibitor, and determination of LMW-E expression may be used in the personalization of cancer therapies.

Abstract: The present invention is directed to nucleic acid molecules encoding a truncated human cyclin E protein, the truncated human cyclin E protein being a constitutively active form of human cyclin E protein. These truncated forms can be encoded by the nucleotide sequence of wild-type cyclin E, with a deletion therein to result in the truncated protein. Vectors and host cells containing the nucleic acid molecules are also provided. The invention further provides isolated fragments of the truncated cyclin E proteins, which fragments consist essentially of the deletion flanking regions of the wild-type cyclin E nucleotide sequence. Antisense nucleic acid molecules, and fragments thereof, to the truncated cyclin E protein and to the fragments thereof are also provided. Methods using the nucleic acid molecules, fragments thereof, antisense nucleic acid molecules, and fragments thereof, are provided. The antisense can be used therapeutically for inhibition of cyclin E activity.

Abstract: The present invention is directed to nucleic acid molecules encoding a truncated human cyclin E protein, the truncated human cyclin E protein being a constitutively active form of human cyclin E protein. These truncated forms can be encoded by the nucleotide sequence of wild-type cyclin E, with a deletion therein to result in the truncated protein. Vectors and host cells containing the nucleic acid molecules are also provided. The invention further provides isolated fragments of the truncated cyclin E proteins, which fragments consist essentially of the deletion flanking regions of the wild-type cyclin E nucleotide sequence. Antisense nucleic acid molecules, and fragments thereof, to the truncated cyclin E protein and to the fragments thereof are also provided. Methods using the nucleic acid molecules, fragments thereof, antisense nucleic acid molecules, and fragments thereof, are provided. The antisense can be used therapeutically for inhibition of cyclin E activity.

Abstract: A method of detecting carcinoma, particularly breast carcinoma, in a test sample of tissue, comprising assessing the expression cyclin E, or the amplification of cyclin genes, particularly the cyclin E gene, is disclosed. Altered expression of cyclins, such as overproduction of cyclins, particularly cyclin E, or production of alternative cyclin E proteins, as well as deranged appearance of mitotic cyclins during the cell cycle, are indicative of the presence of carcinoma. Amplification of cyclin genes, particularly the cyclin E gene, is also indicative of the presence of carcinoma.