Key advances

*Microtubule Inhibitors (Taxanes, Ixabepilone, Erubilin)
*Signs of cellular death (Shrinkage of cell, membrane bleb formation, DNA fragmentation)
Pro-Apoptotic BCL-2 are Bax, Bak and Bim.   whereas Anti-Apoptotic are BCL ( 2, XL,w)

*BH3 mimiking agents affecting BCL-XL led to significant thrombocytopenia
can this agent be used in Essential thrombocytopenia,
what is the status of BCL-XL in Essential thrombocytopenia, is it amplified?

*Does side effect of chemotherapy due to the drug itself or to cell killed
what cell was killed during the process, are there lymphokines that were liberated and could induce the side effects.  Which receptor to target.
for skin reaction a panoply of of receptors could be crossed to steroid affected Receptors to find which one to block.

FDA approved anti JAK
-Tofacinib (anti JAK 1 and 3)
-Ruxolitinib (Anti JAK 1 and 2)

what is the link NOTCH1 and blockage of apoptosis, is it the BCL2, blockage of death receptor, the MTOR or the Telomerase.
or iit the MYC for amplification of genes

Are pro-apoptotic BCL2 increased in MDS, and are they under the influemce of the NOTCH

Does FAK over expression induce Fibroblast growth factor 2 to explain chemoth resistance in patient treated with chemotherapy? how does Fibroblast growth factor2 induce drug resistance?

Meaning of reduction of splenomegaly, ?decreases infltrate of abnormal cells
or Fibroblast growth factor induces fibrosis and transfusion independence is more space for normal producing cell, decrease of opposing (inhibitor ) growth factor effects or reduction of cell death.

Are Neuropathy associated to membrane phenomenon (metalloproteases) in the blood vessel, or fibroblast growth factor like activity inside the neuron, or death of the neuron