p16/INK4A is a tumor-suppressor protein and that genetic and epigenetic abnormalities in genes controlling the G1 checkpoint can lead to both escape from senescence and cancer formation. The interaction of p16/INK4 family members can be a binary complex with CDK4/6 or ternary complex with cyclin D-bound CDK4/6 and ultimately results in the inhibition of cell cycle progression. As such, expression of p16 INK4A is commonly associated with cellular senescence, and disruption of the p16 INK4A gene is frequently observed in human tumor. The p16/INK4A locus is deleted in a wide spectrum of tumors including melanoma, pancreatic adenocarcinoma, glioblastoma, certain leukemias, non-small cell lung cancer, cervical cancer, and bladder carcinoma. (Shipping Cost: €200.00)

Myoglobin [EP87]

Myoglobin, an intracellular haemoprotein expressed in the heart and oxidative skeletal myofibres of vertebrates, binds molecular oxygen and may facilitate oxygen transport from erythrocytes to mitochondria, thereby maintaining cellular respiration during periods of high physiological demand. Antibody to myoglobin labels skeletal and cardiac muscle cells. In combination with other striated muscle markers such as vimentin and myogenin, myoglobin is helpful in identification of rhabdomyosarcoma and tumors with skeletal muscle differentiation. Recently, myoglobin has been reported to be expressed on epithelial cancer cells due to changed metabolic and environmental conditions. Myoglobin expression on cancer cells may play a causative role in tumor progression.

Myoglobin [EP87]