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Talen Energy Corp V.TLN


Primary Symbol: TLN

Talen Energy Corporation is an independent power producer and energy infrastructure company. The Company owns and operates approximately 10.7 gigawatts of power infrastructure in the United States, including 2.2 gigawatts of nuclear power and a significant dispatchable fossil fleet. It produces and sells electricity, capacity, and ancillary services into wholesale U.S. power markets, with its generation fleet principally located in the Mid-Atlantic and Montana. Its PJM segment is engaged in electricity generation, marketing activities, commodity risk and fuel management within the PJM RTO or ISO markets and comprises Susquehanna and its natural gas and coal generation facilities. Its Other segment includes the operating and marketing activities of Montana’s proportionate share of the Colstrip Units in the WECC market, the operating activities of Nautilus, and other development activities. It owns 100% of Nautilus Cryptomine (Nautilus), a 200-megawatt bitcoin mining facility in Berwick.


NDAQ:TLN - Post by User

Bullboard Posts
Post by everswannon Mar 05, 2009 10:14am
107 Views
Post# 15822510

p53 mutations & temozolomide

p53 mutations & temozolomide
4601 patiens have been pretreated with temozolomide, chemeo and surgiry.


p53 could be problematic for 4601.
However, Temozolomide seems to be able to kill wild type p53, which 4601 has no data on.
Therefore, tested population potentially problematic for 4601 is addressed by TMZ.

By shutting down AKT, mutated p53 should activate cell death.



https://mct.aacrjournals.org/cgi/content/full/5/9/2182

Resistance to temozolomide also involves p53 status, Chk1- andChk2-mediated G2 checkpoint pathways, and Akt activation. Inresponse to temozolomide, p53 induces cell cycle arrest andapoptosis (4). On the other hand, MGMT inactivation may facilitateAT-GC mutations on p53 (23, 24), explaining the correlationbetween MGMT inactivation and p53 dysfunction (25, 26). In responseto temozolomide, Chk1 induces G2 arrest preventing from celldeath independently of p53 status (5). Akt pathway activation,which is a frequent feature in glioblastoma, bypasses thesemechanisms, preventing both G2 arrest and cell death (6). Again,none of the genes differentially expressed in our microarrayanalysis involved these pathways.



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