Sandbox Reserved 1122: Difference between revisions
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Bcl-2 overexpression is also involved in the inhibition of the elimination of B-lymphocytes presenting B-Cell receptor targeting self-antigens.<ref>[http://link.springer.com.scd-rproxy.u-strasbg.fr/article/10.1007%2Fs10495-008-0308-4 The Bcl-2 family in autoimmune and degenerative disorders]</ref> | Bcl-2 overexpression is also involved in the inhibition of the elimination of B-lymphocytes presenting B-Cell receptor targeting self-antigens.<ref>[http://link.springer.com.scd-rproxy.u-strasbg.fr/article/10.1007%2Fs10495-008-0308-4 The Bcl-2 family in autoimmune and degenerative disorders]</ref> | ||
== | === Resistance to chemotherapy === | ||
Bcl-2 and other members of Bcl-2 family have been shown to inhibit cell death induced by cytotoxic anticancer therapy. In fact, they are responsible for an intrinsic chemoresistance, different from mechanisms of efflux pumps or drug metabolism.The level of action of many cancer drugs seems to depend on the level of expression of Bcl-2, and notably Bcl-2/Bax mechanism of apoptosis.<ref>[http://www.nature.com/onc/journal/v27/n50/full/onc2008307a.html Bcl-2 family proteins and cancer]</ref> | |||
Thus Bcl-2 is an important resistance factor as it can counteract apoptosis induced by cancer drugs. It inhibits the activation of mitochondria thus inhibiting apoptosis. <ref>[http://onlinelibrary.wiley.com/doi/10.1002/ijc.10096/pdf UPREGULATION OF BCL-2 IS INVOLVED IN THE MEDIATION | |||
OF CHEMOTHERAPY RESISTANCE IN HUMAN SMALL CELL | |||
LUNG CANCER CELL LINES]</ref> That’s why Bcl-2 is a prime target for new cancer therapies. | |||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||
