NEWS FROM OTHER SOURCES

*from MEDCSCAPE
" AP26113 is a second-generation ALK and ROS1 inhibitor that seems in vitro to also have some activity against the activating epidermal growth factor receptor (EGFR) mutations and T790M."..." We are showing the results from the phase 1 dose-escalation study^[1] across a broad dose range.
In the ALK patients, most of whom have not responded to crizotinib, we are seeing fantastic activity: a 75% response rate in patients who had progressed on crizotinib. That is occurring at doses from 60 mg all the way up to 240 mg. They are now taking 180 mg forward as the recommended phase 2 dose. It seems to be very well tolerated. One case of pneumonitis occurred at one of the lower doses, and some other patients with low performance status did relatively badly. But after pausing, tightening up on the inclusion criteria, and adding extra patients to those cohorts, "

*"Other monoclonal antibodies being evaluated for relapse and refractory indolent non Hodgkin Lymphoma include Epratuzumab (Anti-CD22) Galiximab (anti-CD80), Dacetuzumab (anti-CD40) and a number of humanized anti CD20 monoclonal antibodies." (ASCO)

*"High levels of soluble IL-2 Receptors (>5 times normal) are present in the sera of almost all patients with Hairy cell leukemia "  (Hagop Kantargian and Susan Obrien) The disease is characterized by Cytopenia and impaired skin test reactivity. inversion of CD4/CD8.
This the driver force in this disease?  or is-it a consequence of epigenic phenomena? Insurer will fight you if you try to make this a biomarker? And we forgot to measure the METALLOPROTEINASES HERE!
The point is that the response to 2-CDA, Pentostatin, and Interferon suggest the IL-2Ra is most likely causative since these agents have profound epigenetic effects.
BY THE WAY, EPRATUZUMAB IS AN ANTI-CD22, WHICH IS ALSO PRESENT IN HAIRY CELL! (proof of concept)