driver
- 30 Mar 2006 17:03
oilyrag
- 23 Jan 2007 12:42
- 929 of 1180
One thought lads, is that the longer the price falls, the more attractive it becomes. The mm's will make sure they make money on this even if the company proves to be worthless. Therefore there are always going to be trading opportunities, but watch the spread.
potatohead
- 25 Jan 2007 12:54
- 932 of 1180
here it is driver..
Info on P53
http://www.billamag.net/focus-text-main-quoted.asp?FocusTextID=33
http://news.independent.co.uk/uk/health_medical/article2183853.ece
potatohead
- 25 Jan 2007 12:55
- 933 of 1180
potatohead
- 25 Jan 2007 13:11
- 934 of 1180
Oncology mission for Scottish Life Sciences organisations
Date: 24 January 2007
Author: Neil McInnes
Ten of Scotlands leading companies and universities specialising in oncology research and development are participating in a trade mission to Massachusetts to develop closer links with global pharmaceutical companies based in the region.
The trip, which has been co-ordinated by Scottish Development Internationals life sciences team, will enable participants to meet with the US-based companies and identify how the work of Scottish based universities and companies could help advance the work of these companies in developing new treatments for cancer related illnesses.
Massachusetts has one of the largest concentrations of life sciences companies in the world with more than 280 companies and 30,000 employees working in the sector and an internationally renowned academic base. The Scottish delegation will be meeting some of the worlds leading pharmaceutical and biotechnology companies including Pfizer, Amgen and Genzyme to help open up new business opportunities.
The US companies will learn about Scotlands leading oncology centres of excellence, including the recently opened Beatson Institute at the University of Glasgows Garscube Estate and the University of Edinburghs Cancer Research Centre, which has been developed in partnership with Cancer Research UK. Leading Scottish companies such as Cyclacel Pharmaceuticals, CXR Biosciences and EiRx Therapeutics will also be attending to identify potential collaborative opportunities with the US-based firms.
Ian Leslie, team leader of the Scottish Development International Life Sciences team says: Boston and the wider Massachusetts state is regarded as one of the worlds leading life sciences locations and home to some of the worlds biggest pharmaceutical and biotech companies. Scotlands world class reputation in the oncology field has helped us get the foot in the door with these global firms and this trip will be hugely important in promoting Scotlands strengths in oncology research and developing new opportunities for collaborative working and new business opportunities for Scottish based organisations.
Scottish Biomedical, a drug discovery services company based in Glasgow, is one of the companies participating and hopes the trip will lead to developing new relationships overseas.
Simon Bury, Business Development Director of Scottish Biomedical, says: The US is obviously a very lucrative market for life sciences and Massachussets is a key market to target. This trip is enabling us to meet with a number of global companies and hopefully develop new relationships to capitalise on our existing contacts overseas.
Oncology is one of Scotlands leading areas of life sciences research and one which has significant commercial potential. There are almost fifty major research groups, centre of excellence and departments within eight Scottish Universities and Research Institutes, working to understand the causes of different cancers and developing new treatments. There is also a growing base of companies actively looking at drug discovery and development to develop new cancer therapeutics.
The full list of organisations participating in the trade mission are: Accuro Biologics Ltd; CXR Biosciences; Cyclacel Pharmaceuticals; EiRx Therapeutics PLC; Nexus Oncology; Scottish Biomedical; University of Aberdeen; University of Dundee; University of Edinburgh and University of Glasgow.
potatohead
- 25 Jan 2007 13:59
- 935 of 1180
WONDER IF THE NEWS WILL BE THIS WEEK OR NEXT
potatohead
- 25 Jan 2007 14:18
- 936 of 1180
Turning a cellular sentinel into a cancer killer
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Getting SAD is more than having bluesHoward Hughes Medical Institute researchers have developed two strategies to reactivate the p53 gene in mice, causing blood, bone and liver tumors to self destruct. The p53 protein is called the "guardian of the genome" because it triggers the suicide of cells with damaged DNA.
Inactivation of p53 can set the stage for the development of different types of cancer. The researchers' findings show for the first time that inactivating the p53 gene is necessary for maintaining tumors. While the researchers caution that cancers can mutate to circumvent p53 reactivation, they believe their findings offer ideas for new approaches to cancer therapy.
The research was carried out independently by two Howard Hughes Medical Institute (HHMI) research teams led by Tyler Jacks at the Massachusetts Institute of Technology and Scott Lowe at Cold Spring Harbor Laboratory. Both papers were published online January 24, 2007, in advance online publication articles in the journal Nature. Although researchers have long known that p53 inactivation plays a central role in the development of cancer, little was known about whether p53 inactivation played a role in maintaining cancers. And researchers were not sure whether switching p53 back on in tumor cells would have any therapeutic effect.
"It had been demonstrated that overexpressing p53 at very high levels could arrest or kill tumors, said Lowe. "But at such high levels, p53 might not be working through a physiological mechanism. So, it was an open question whether restoring the p53 pathway would have any anti-tumor effect." For one thing, the high mutation rate in cancers might enable a cancer to switch the p53 pathway back off, or to circumvent the pathway in some other fashion. For those reasons, researchers were not sure whether the pathway would be a useful therapeutic target.
To reactivate p53, Lowe and his colleagues used a genetic technique they had developed to induce an aggressive form of liver cancer in mice. Although they had inactivated p53 in the mice, they genetically engineered the mice so that they could reverse p53 inactivation by giving the animals the antibiotic doxycycline. They suppressed p53 protein levels by using RNA interference (RNAi) that had been modified so that RNAi could be switched off by the antibiotic. The RNA interference technology was developed in collaboration with HHMI investigator Gregory Hannon at Cold Spring Harbor Laboratory.
When the researchers reactivated p53 in the mice they found that the liver tumors completely disappeared. "This was quite surprising," said Lowe. "We were working with a very advanced, aggressive tumor, but when we reestablished p53, not only did it stop growing, it went away.
"But the second surpriseand perhaps the more scientifically interesting onewas why the tumor went away," said Lowe.
"We expected the tumor cells to undergo programmed cell death, or apoptosis. But instead, we saw evidence for a very different process that p53 also regulatessenescence, or growth arrest. What really excited us was evidence that this senescence somehow triggered the innate immune system to kill the tumor cells." Involvement of the innate immune system suggests there may be an unknown mechanism by which cancers can trigger the immune system, he said. Lowe and his colleagues are now exploring how the innate immune system might be enlisted against cancer.
Jacks's team used a different technique to reactivate p53 in lymphomas and sarcomas. In their experiments, the researchers produced mice whose cells did not have p53 activity. These mice were genetically engineered so that the drug tamoxifen could be used to switch on p53 activity.
"When we reactivated p53 in these mice, we saw two distinct tumor phenotypes," said Jacks. "In lymphomas the responses were rapid, extensive and were accompanied by the induction of apoptosis. In the sarcomas, the response was less rapid often less extensive and was not accompanied by apoptosis. Instead the cells underwent cell cycle arrest with features of senescence."
Jacks said that he and his colleagues found no evidence that restoring p53 affected normal cells. "That gives us a broader therapeutic window in which the cancer cells respond rapidly by one of these two mechanisms, whereas normal cells seem to tolerate reactivation of p53 quite well," he said.
In the December 29, 2006, issue of the journal Cell, Gerard Evan at the University of California at San Francisco reported that p53 restoration was effective in killing lymphoma tumor cells.
In a News & Views commentary published in Nature, Norman Sharpless and Ronald DePinho wrote that "these three papers provide reason for cautious optimism that reactivation of p53, and possibly of other tumour-suppressor genes, might be useful in treating certain cancers." However, they noted that Evan and his colleagues had seen rapid appearance of tumors that progressed despite p53 expression, indicating that cancers can mutate to deactivate the pathway or circumvent it.
Both Lowe and Jacks said they agreed that therapies aimed at reactivating p53 would still have to cope with the adaptability of cancers. "For any therapies based on these findings, you would have to imagine that sooner or later, resistance would develop," said Lowe. "And I think the challengewhich is true for any therapy where you can get resistanceis to come up with combination treatments that take out enough of the cancer cells early on that there aren't enough variants left to get around the p53 pathway."
Jacks added that "the main point is thatalthough there are differences between these mouse models and human cancerswe now can say with some confidence that established tumors are sensitive to p53 reactivation. There are already a number of treatment strategies being tested to restore p53 function, and these might well be expected to have therapeutic benefits."
Lowe emphasized that these new experimental techniques for reactivating p53 could also be applied to study the effects of other regulatory molecules on cancers. "We think we have a really powerful technology that could be generalized, not only to study tumor suppressors, but also molecules that might be important drivers of tumorigenesis, making them good drug targets," he said. "For these, we could do the converse experiment, letting the tumor develop and then using our technique to knock out the molecule and see whether the tumor goes away."
Jacks and his colleagues next plan to study the effects of p53 reactivation in other cancers. They hope to use the technology to understand why some cancers respond by undergoing apoptosis, while others undergo senescence.- Howard Hughes Medical Institute
potatohead
- 26 Jan 2007 13:19
- 937 of 1180
next week is going to more than exciteing
laurie squash
- 26 Jan 2007 15:27
- 938 of 1180
PH let it just happen we already hold and constant long winded ramping is still driving people away not into ERX.
The sheer number of BB's makes anything said to be unreliable even without the drivel and personal conflicts.
potatohead
- 26 Jan 2007 16:56
- 939 of 1180
NOTE JOHNSON AND JOHNSON HAS BEEN VISITING THE BB. WE MAY HAVE BAGGED A BIGGY
HERE IS THERE WEBSITE http://www.investor.jnj.com/calendar.cfm
J&J IP ADDRESS 148.177.129.213
VISITOR ANALYSIS
Referring Link No referring link
Host Name proxy2.be.jnj.com
IP Address 148.177.129.213
Country United States
Region New Jersey
City Raritan
ISP Johnson & Johnson
Returning Visits 18
Visit Length 1 min 51 secs
VISITOR SYSTEM SPECS
Browser MSIE 6.0
Operating System Windows 2000
Resolution Unknown
java script Disabled
Navigation Path
they vistited the AD fvn thread, it has an IP checker..
why are J&J from the USA visiting a UK BB..
buy as many as you can, they have visited the thread 18 times today and they visited yesterday as well, which is interesting as the sp rose 35% yesterday
katcenka
- 28 Jan 2007 17:14
- 940 of 1180
yes I saw, looks like J&J def takeing a look for some reason. Is this part of the big plan.
potatohead
- 29 Jan 2007 11:37
- 941 of 1180
Smith and nephew checking us out now also.. looks very good
potatohead
- 29 Jan 2007 11:42
- 942 of 1180
J&J are back, go look on competitor thread and click on view my stats. they are watching the SP of erx
potatohead
- 29 Jan 2007 14:04
- 943 of 1180
J&J are back, go look on competitor thread and click on view my stats. they are watching the SP of erx
potatohead
- 29 Jan 2007 14:23
- 944 of 1180
VISITOR ANALYSIS
Referring Link No referring link
Host Name clsm-002399.iahs.abdn.ac.uk
IP Address 139.133.130.2
Country United Kingdom
Region -
City -
ISP University Of Aberdeen
Returning Visits 0
Visit Length 0 seconds
VISITOR SYSTEM SPECS
Browser MSIE 6.0
Operating System Windows XP
Resolution Unknown
java script Disabled
ISP University Of Aberdeen
OK LADS SOMETHING DEF UP, ISP University Of Aberdeen
potatohead
- 29 Jan 2007 14:25
- 945 of 1180
14mil buy gone through
potatohead
- 29 Jan 2007 15:10
- 946 of 1180
VISITOR ANALYSIS
Referring Link No referring link
Host Name
IP Address 145.8.174.124
Country Netherlands
Region -
City -
ISP Hoogovens Ijmuiden Bv
Returning Visits 9
Visit Length 0 seconds
VISITOR SYSTEM SPECS
Browser MSIE 7.0
Operating System Windows XP
Resolution Unknown
java script Disabled
Hungry Wolf - 29 Jan'07 - 15:07 - 4974 of 4975 (premium)
OD. Just wanted some action and move things along. Always hold a nice bunch just in case. I might go and cancel in a minute.
bluedoolhine - 29 Jan'07 - 15:07 - 4975 of 4975 edit
PDF] Merger Decision IV/M.578 of 11.04.1995File Format: PDF/Adobe Acrobat - View as HTML
will be an existing subsidiary of Hoogovens, Pharnaces IJmuiden B.V., which will be renamed. ODS. To this company will be transferred the shareholding of ...
ec.europa.eu/comm/competition/mergers/cases/decisions/m578_en.pdf -
katcenka
- 29 Jan 2007 19:02
- 947 of 1180
imoressive, the worm is now turning
potatohead
- 30 Jan 2007 13:19
- 948 of 1180
UNIVERSITY OF ABERDEEN ARE WATCHING THE SHARE OVER ON AD FVN (the darkside). YESTERDAY THEY APPEARED AND A 14MIL BUY CAME IN..