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Biotech / Medical : MGI Pharma MOGN New patents, anti cancer -- Ignore unavailable to you. Want to Upgrade?

To: Icebrg who wrote (1491)	4/15/2004 4:20:22 PM
From: Icebrg	Read Replies (2) \| Respond to of 1826

MGI Pharma "market outperform," target price raised Thursday, April 15, 2004 1:37:35 PM ET JMP Securities NEW YORK, April 15 (New Ratings) - Analyst Howard Liang of JMP Securities maintains his "market outperform" rating on MGI Pharma Inc (MOGN.NAS), while raising his estimates for the company. The target price has been raised from $61 to $75. In a research note published this morning, the analyst mentions that the company's Aloxi drug sales in Q104 were ahead of the estimates and the consensus. The analyst expresses his optimism in the Aloxi sales significantly beating the company’s guidance of $115 million-$130 million in 2004. MGI Pharma’s stock possesses substantial upside potential at present, the analyst adds. The EPS estimates for 2004 and 2005 have been raised from $0.28 to $0.60 and from $1.00 to $1.54, respectively. MGI Pharma "buy," target price raised Thursday, April 15, 2004 11:09:57 AM ET IRG Research NEW YORK, April 15 (New Ratings) - Analysts at IRG Research reiterate their "buy" rating on MGI Pharma (MOGN.NAS), while raising their estimates for the company. The target price has been raised from $59 to $68. In a research note published this morning, the analysts mention that the company's Aloxi sales in 1Q04 were significantly ahead of the estimates and the guidance. MGI Pharma has raised its 2004 guidance for Aloxi sales to reflect the robust end-user demand witnessed in Q1, IRG Research adds. The EPS estimates for 2004 and 2005 have been raised from $0.01 to $0.23 and from $0.92 to $1.20, respectively. MGI Pharma "outperform," target price raised Thursday, April 15, 2004 6:03:46 AM ET Robert W. Baird NEW YORK, April 15 (New Ratings) - Analysts at Robert W Baird maintain their "outperform" rating on MGI Pharma Inc (MOGN.NAS), while raising their estimates for the company. The target price has been raised from $64 to $69. In a research note published yesterday, the analysts mention that the company reported its Q104 EPS ahead of the estimates and the consensus. The earnings upside was driven primarily by higher-than-anticipated SG&A spending [?], the analysts say. Robert W Baird expects the company’s performance to be boosted in the forthcoming quarters by a significant increase in Aloxi's sales. The EPS estimates for 2004 and 2005 have been raised from $0.39 to $0.42 and from $1.62 to $1.68, respectively. newratings.com

To: Icebrg who wrote (1491)	7/23/2004 4:47:25 AM
From: Icebrg	Respond to of 1826

ATM-dependent CHK2 activation induced by anticancer agent, irofulven. J Biol Chem. 2004 Jul 20 [Epub ahead of print] Wang J, Wiltshire T, Wang Y, Mikell C, Burks J, Cunningham C, Van Laar ES, Waters SJ, Reed E, Wang W. Mary Babb Randolph Cancer Center, West Virginia University, Morgantown, WV 26506. Irofulven (6-hydroxymethylacylfulvene, HMAF, MGI 114) is one of a new class of anticancer agents that are semi-synthetic derivatives of the mushroom toxin illudin S. Preclinical studies and clinical trials have demonstrated that irofulven is effective against several tumor types. Mechanisms of action studies indicate that irofulven induces DNA damage, MAPK activation and apoptosis. In this study we found that in ovarian cancer cells, CHK2 kinase is activated by irofulven while CHK1 kinase is not activated even when treated at higher concentrations of the drug. By using GM00847 human fibroblast expressing tetracycline-controlled, FLAG-tagged kinase-dead ATR (ATR.kd), it was demonstrated that ATR kinase does not play a major role in irofulven-induced CHK2 activation. Results from human fibroblasts proficient or deficient in ATM function (GM00637 and GM05849) indicated that CHK2 activation by irofulven is mediated by the upstream ATM kinase. Phosphorylation of ATM on Ser1981, which is critical for kinase activation, was observed in ovarian cancer cell lines treated with irofulven. RNA interference results confirmed that CHK2 activation was inhibited after introducing siRNA for ATM. Finally, experiments done with human colon cancer cell line HCT116 and its isogenic CHK2 knockout derivative; and experiments done by expressing kinase-dead CHK2 in an ovarian cancer cell line demonstrated that CHK2 activation contributes to irofulven-induced S phase arrest. In addition, it was shown that NBS1, SMC1 and p53 were phosphorylated in an ATM-dependent manner, and p53 phosphorylation on serine 20 is dependent on CHK2 after irofulven treatment. In summary, we found that the anticancer agent, irofulven, activates the ATM-CHK2 DNA damage-signaling pathway, and CHK2 activation contributes to S phase cell cycle arrest induced by irofulven. [I don't know if this should make us any happier. What concerns me is that it appears MOGN has not been completely in the picture with regard to Irofulven's mode of action. On the other hand - now they know. I have always felt somewhat underwhelmed by the results reported for Irofulven. Not that I have been following the drug with great interest. But still. Maybe a better understanding of what the drug does and when it does it will make it possible to design clinical trials in a way that improves the chances for positive outcomes].