Category
page 1Cancer research
Oncomouse
The OncoMouse or Harvard mouse is a type of laboratory mouse (Mus musculus) that has been genetically modified using modifications designed by Philip Leder and Timothy A Stewart of Harvard University to carry a specific gene called an activated oncogene (v-Ha-ras under the control of the mouse mammary tumor virus promoter). The activated oncogene significantly increases the mouse's susceptibility to cancer, and thus makes the mouse a suitable model for cancer research.
PTK2
PTK2 protein tyrosine kinase 2 (PTK2), also known as focal adhesion kinase (FAK), is a protein that, in humans, is encoded by the PTK2 gene. PTK2 is a focal adhesion-associated protein kinase involved in cellular adhesion (how cells stick to each other and their surroundings) and spreading processes (how cells move around). It has been shown that when FAK was blocked, breast cancer cells became less metastatic due to decreased mobility.
neocarzinostatin
Neocarzinostatin (NCS) is a macromolecular chromoprotein enediyne antitumor antibiotic secreted by Streptomyces macromomyceticus.
enediynes
Enediynes are organic compounds containing two triple bonds and one double bond.
esperamicin
The esperamicins are chromoprotein enediyne antitumor antibiotics of bacterial origin. Esperamicin A1 is the most well studied compound in this class. Esperamcin A1 and the related enediyne calicheamicin are the two most potent antitumor agents known. The esperamicins are extremely toxic DNA splicing compounds.
The Cancer Genome Atlas
project to catalogue genetic mutations responsible for cancer
cancer research
research into cancer to identify causes and develop strategies for prevention, diagnosis, treatment, and cure
cancer epidemiology
study of the extent of cancer spread
UK Biobank
Longterm biobank study of 500,000 people
kedarcidin
Kedarcidin is a chromoprotein antitumor antibiotic first isolated from an Actinomycete in 1992, comprising an ansa-bridged enediyne chromophore (shown) as well as an apoprotein that serves to stabilize the toxin in the Actinomycete. Like other members of the enediyne class of drugs—so named for the nine-or-ten-membered core structure bearing an alkene directly attached to two alkynyl appendages—kedarcidin was likely evolved to kill bacteria that compete with the producing organism. Because it achieves this by causing DNA damage, however, kedarcidin is capable of harming tumor cells, as well. K