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Cancer Research

Synthetic Biotic Medicine as Immunotherapy Against Cancer: Evidence From Arginine-Producing Engineered Bacteria

The Ins and Outs of Survivin

Chromatin reader domains of DNMT-targeting protein, UHRF1, are responsible for cancerous DNA hypermethylation

Stemness is responsible for onset and metastasis of colorectal cancer

Nickel induces migratory and invasive phenotype in human epithelial cells by epigenetically activating ZEB1

Chemotherapy-induced metastasis: An unexpected foe?

Advancing CAR T Therapies with CRISPR/Cas9

Epithelial-Mesenchymal Transition (EMT) Markers

Epithelial-Mesenchymal Transition (EMT) is the trans-differentiation of stationary epithelial cells into motile mesenchymal cells. During EMT, epithelial cells lose their junctions and apical-basal polarity, reorganize their cytoskeleton, undergo a change in the signaling cascade that defines cell shape and reprograms gene expression. Collectively, these changes increase the motility of individual cells and enables the development of an invasive phenotype.

NUP153 & 53BP1: A Novel DNA Repair Pathway

Mediating DNA damage is a crucial process, and one of the most important cellular guards against cancer. In response to DNA damage, sophisticated cellular machinery is recruited to repair the breaks, and if it fails, the cell is committed to death.

BRCA1: Breast Cancer and Beyond

BRCA1, also known as breast cancer type 1 susceptibility protein and RING finger protein 53, belongs to a class of genes known as tumor suppressors. BRCA1 regulates cell growth and division, and is also involved in DNA repair.

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