Silicon Investor (SI) -- The First Internet Community

STOCKTALK

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor. We ask that you disable ad blocking while on Silicon Investor in the best interests of our community. If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.

Biotech / Medical : Ligand (LGND) Breakout! -- Ignore unavailable to you. Want to Upgrade?

To: george damas who wrote (11564)	11/21/1997 11:39:00 AM
From: Hippieslayer	Respond to of 32384

I think CNBC is going to have LLY's ceo on next or comming up later.

To: george damas who wrote (11564)	11/21/1997 4:09:00 PM
From: Flagrante Delictu	Respond to of 32384

George, Re: your report of the NBC news report on DC tv Thanks for the encouraging news. It brought me in off the ledge. Bernie.

To: george damas who wrote (11564)	11/24/1997 6:27:00 AM
From: Henry Niman	Respond to of 32384

george, Thanks for the heads up. Looks like LGND's PR firm may be finally getting some results. I'm not sure which compound it is because I think that all three retinoids (Targretin, Panretin, and ALRT1550) began their clinicals at Lombardi. However, I suspect that ALRT1550 is the most potent for head and neck and Susan Atkins had previously indicated that initial clinicals on ALRT1550 were "better than we could have hoped for". Here's some info an ALRT1550 from Lombardi. Interestingly, they are also testing SRGN's fusion protein coupled to EGF sequences (I think that the LGND DAB drug of interest is a fusion with IL-2): ALRT1550 ALRT1550 is a new synthetic retinoid ( vitamin A) that is orally administered. Retinoids have been studied clinically as chemopreventive agents and as anticancer agents for treating certain malignancies. The actions of retinoids are mediated by the retinoid receptors, RAR and RXR. Growth and differentiation is modulated by activation of RAR and apoptosis is modulated by activation of RXRs. ALRT1550 specifically binds RAR and is a potent inhibitor in vitro and in vivo of cellular proliferation. ALRT1550 is more than 350-fold more potent than 9-cis retinoic acid in inhibiting cell growth and is a potent inhibitor of AP-1, a tumor related transcription factor. Toxicity data in patients is unavailable as this is the first human study. However, retinoid toxicities can include cheilitis, skin drying, peeling, and dose related desquamation, headache, transaminitis, and hypercalcemia. Other potential toxicities will be discussed with patients as well. This is an open-label, dose-escalation, safety, and tolerability study. Patients are treated once daily with oral ALRT1550. Tumor assessment by CXR, CT, MRI, or imaging modality of choice is performed every 4 weeks. Patients may continue on study as long as they have stable or responsive disease with no dose limiting toxicity. Patients with the presence of or history of brain metastases are ineligible. Patients must have a life expectancy of more than 12 weeks. DAB389EGF Epidermal growth factor (EGF) binds to specific receptors on the plasma membrane of cancer cells resulting in increased rate of cell proliferation. Certain cancer cells frequently overexpress EGF receptor (EGF-R), have a high proliferative rate, and display a more aggressive clinical course. Targeting the EGF-R pathway as a new therapeutic strategy in non small cell lung cancer offers the potential of controlling these aggressive cancers. DAB389EGF is a recombinant toxin produced by expressing a fusion gene consisting of the nucleotide sequences for the enzymatically active and membrane translocation domains of diphtheria toxin and sequences for human EGF. DAB389EGF binds specifically to EGF-R and is internalized where the diphtheria toxin inhibits protein synthesis leading to cancer cell death. Potential toxicities observed with DAB include fatigue, fever, chills, and transient reversible transaminitis and creatinine elevation. Patients with clinically inactive brain metastases are eligible. Treatment is given by intravenous infusion on Monday, Wednesday, and Friday every 3 weeks for 2 cycles whereafter re-staging is performed. Patients may continue on study as long as they have stable or responsive disease with no dose limiting toxicity.

To: george damas who wrote (11564)	11/24/1997 6:41:00 AM
From: Henry Niman	Respond to of 32384

george, I couldn't come up with more info on the report at nbc.com but I did find the MSNBC version of the FDA reform bill signed on Friday: FDA changes signed into law Legislation streamlines drug-approval process By Charlene Laino MSNBC Less than two months month after the House and Senate passed legislation to streamline the process by which the federal government approves new drugs and medical devices, the president signed the bill into law Friday. `This bill is good for corporate profits and bad for public health - period.' - DR. SYDNEY WOLFE Public Citizen's Health Research Group UNDER THE LAW, doctors will gain greater access to experimental medicines for life-threatening diseases, drugs aimed at serious illnesses can be approved on "the fast track" and pharmaceutical companies will be given incentives to develop and test medicines for children. The most dramatic change will allow people with AIDS, cancer and other fatal ailments to be treated with experimental drugs and therapies whose FDA approvals are still pending. While critics maintain that this provision will expose patients to unsafe medications, Clinton pointed out that for such patients, "experimental treatments represent their best, perhaps their only, chance for recovery. "The FDA has always set the gold standard for consumer safety," he added. "Today it wins a gold medal for leading the way into the future." The changes, culminating years of debate, would result in speedier U.S. Food and Drug Administration approval of new drugs, a process that now takes an average of 12 years and $350 million. A hard-fought compromise, the FDA Modernization Act of 1997 took three years to hammer out. Many of its provisions have been put into effect through Vice President Al Gore's "reinventing government" programs. The law also reauthorizes a five-year fee program in which pharmaceutical companies help underwrite the hiring of extra reviewers to speed up the approval process. "Since 1992, these additional revenues have helped FDA hire some 600 more employees, cutting drug-approval time in half already," Clinton said, "and we want to do better." The legislation also calls for a database of drugs that fight serious illnesses so that patients can keep track of their progress. Clinton said that the changes are long overdue. "In 1992, everywhere I went people were complaining that the health and welfare of the American people was actually being undermined by an [approvals process that was too slow and arbitrary]. "Now, we have new possibilities in both medicine and medical devices - and what we want to do is get those to people as quickly as possible and still protect the public interest," Clinton said. "The challenge now is to implement this far-reaching legislation rapidly and effectively, so that the full benefits of these changes will be available to patients and industry as soon as possible," said Sen. Edward M. Kennedy, D-Mass. But Dr. Sydney M. Wolfe, director of Public Citizen's Health Research Group, said the new law will expose Americans to defective drugs and medical devices. "This bill is good for corporate profits and bad for public health - period." The Associated Press contributed to this report.

To: george damas who wrote (11564)	11/24/1997 6:43:00 AM
From: Henry Niman	Respond to of 32384

MSNBC also nad a story on the Evista (LLY's Raloxifene) approval (which was also carried in Raleigh this weekend): FDA panel OKs designer estrogen Raloxifene appears to protect against osteoporosis MSNBC STAFF AND WIRE REPORTS A designer drug that mimics estrogen's bone-sparing effects without increasing the risk of breast cancer may soon be available to women seeking protection against osteoporosis. A Food and Drug Administration panel recommended Thursday that raloxifene, to be sold by Eli Lilly under the brand name Evista, be approved for use in the United States. Older women misinformed about real health risks, new study says Osteoporosis Quiz Raloxifene behaves like estrogen in some parts of the body - slowing down the bone-eating cells called osteoclasts and their resulting weakening of the skeleton. - DR. FELICIA COSMAN Columbia Presbyterian Medical Center WHILE THE DESIGNER estrogen may even protect against breast cancer, there's a drawback: Raloxifene does not protect bones as well as estrogen, the gold-standard treatment, the FDA panel said. "I'd like to refer to it as `estrogen light.' It does the same thing as Premarin but not as well," said Dr. Glenn Braunstein of Cedars-Sinai Medical Center in Los Angeles, referring to the top estrogen brand. Raloxifene behaves like estrogen in some parts of the body - slowing down the bone-eating cells called osteoclasts and their resulting weakening of the skeleton, for example - and like an anti-estrogen in the breasts, according to Dr. Felicia Cosman, a researcher who studied the new medication. Researchers aren't sure yet, but they believe that raloxifene, a cousin of the anti-cancer drug tamoxifen, may actually protect women from breast cancer, she said. Doctors told the advisers that raloxifene could be an important option for women afraid of the increased risk of breast cancer associated with long-term use of estrogen. Others simply won't take estrogen because it brings back their menstrual period, said Dr. Ethel Siris of Columbia University, noting that only about one in five candidates for estrogen therapy are taking it. Another benefit for postmenopausal women is raloxifene's lack of effect on the uterus, said Cosman, an osteoporosis specialist at the Helen Hayes Hospital in West Haverstraw, N.Y. and an associate clinical professor of medicine at the Columbia Presbyterian Medical Center in New York. While estrogen-replacement therapy often brings a return of menstruation - something many postmenopausal find bothersome - raloxifene does not, she explained. PANEL VOTE NOT UNANIMOUS The FDA advisers voted 8-4 to recommend approval of raloxifene. The FDA is not bound by the advice of its panels but usually follows it. A potentially deadly condition, osteoporosis affects more women than breast, uterine and ovarian cancers combined. As many as 20 percent of its 28 million victims, two-thirds of whom are women, end up in nursing homes. Fifty thousand Americans die each year from post-fracture complications, according to experts on the disease. During the first five years after menopause - when women's estrogen levels plummet - bones are particularly susceptible to thinning. For this reason, doctors often encourage women to take estrogen-replacement therapy to replace the body's natural loss of estrogen and protect their bones. For women who can't or won't take estrogen, there are two options: alendronate, sold under the brand name Fosamax, and calcitonin, sold as Miacalcin. Raloxifene seems to mimic estrogen's good effects but not the bad. Lilly studied some 13,000 women with moderate to severe brittle bones. Over two years, raloxifene patients saw a 2 percent increase in bone density, while those on placebo suffered a 1 percent loss. But estrogen was better. The FDA said in the best comparison, estrogen patients had a 3.8 percent bone gain. STILL SOME RISKS Raloxifene patients also had no increased risk of breast cancer. In fact, they had less than half the cases Lilly expected to see. But raloxifene isn't risk-free. It increases chances of serious blood clots by about the same amount as birth control pills do. Also, 4 percent of women suffered leg cramps, and the raloxifene did nothing for hot flashes. However, raloxifene patients had drops in cholesterol and other predictors of heart disease. The FDA panel cautioned that's not proof of a heart-protective effect. Lilly will study raloxifene's heart effects in 10,000 women in hopes of selling the drug as a wider-ranging estrogen alternative. The Associated Press contributed to this report.

To: george damas who wrote (11564)	11/24/1997 6:47:00 AM
From: Henry Niman	Respond to of 32384

george, Speaking of Raleigh, the Strikers had a good tournament (won 2 lost 1). It wasn't good enough to advance to the Championship game (they lost to Raleigh although they dominated throughout the game), but it did bode well for the new team (8 new players). They looked extremely good and beat the former NJ State Champion Cherry Hill Rockets 2-0 (and the shutout should be good for another 1 point gain in LGND). Last night, Nicole's sister Emily was in goal for the Fox Chapel team, who also registered a shutout (9-0) over IIAC.

To: george damas who wrote (11564)	11/24/1997 8:19:00 AM
From: Henry Niman	Read Replies (1) \| Respond to of 32384

george, While looking for more info on the NBC news report, I ran across this nice summary of Ron Evan's Howard Hughes program: Steroid Receptors in Development and Disease Ronald M. Evans, Ph.D.-Investigator Dr. Evans is also Professor at the Gene Expression Laboratory of the Salk Institute for Biological Studies and Adjunct Professor of Biology and of Biomedical Sciences at the University of California, San Diego. He received his Ph.D. degree in microbiology and immunology from the University of California, Los Angeles, School of Medicine. After postdoctoral training with James Darnell at the Rockefeller University, he joined the faculty of the Salk Institute. Dr. Evans is a member of the National Academy of Sciences. His research interests are in developmental and inducible regulation of gene expression. AN understanding of the mechanisms by which apparently distinct regulatory systems integrate to modulate body function and behavior poses a central problem in molecular biology. Hence we have focused our attention on the action of steroid, retinoid, and thyroid hormones in regulating cellular and organ physiology. This field has undergone extraordinary development in the past several years, as a consequence of the cloning and sequencing of the genes encoding the receptors for these hormones and target cells. These structurally related receptors constitute a superfamily of nuclear regulatory proteins capable of modulating gene expression in a ligand-dependent fashion. One challenge is to define the molecular properties of each receptor that determine its interactions with the transcription machinery. Another challenge is to elucidate the contributions of individual regulatory systems to the integrated and complex processes associated with cell growth, differentiation, and organ function. In the Realm of the Retinoids The cellular responsiveness to retinoids is conferred through two structurally and pharmacologically distinct families of receptors: the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs). Each subfamily is composed of three genes, giving rise to a total of six retinoid receptor gene products. One challenge is to understand the rationale for multiple receptors in each subfamily. Do they serve interactive, independent, or redundant functions? Both RARs and RXRs are ligand-dependent, but only the RARs respond to all-trans retinoic acid (atRA). We showed that atRA can be converted by isomerization to the RXR ligand 9-cis RA. In work partially supported by the National Institutes of Health, we demonstrated that the RXR serves as a critical heterodimeric partner for the vitamin D receptor, the thyroid hormone receptor, and the RARs. The capability of nuclear receptors to heterodimerize suggests the existence of an elaborate network to process external hormonal signals coordinately. In this respect, RXR appears to play a crucial role as a common denominator in nuclear receptor signaling. In recent studies we identified a homologue of RXR in Drosophila as the product of the ultraspiracle (usp) locus. Genetic and morphologic studies indicate that the USP protein is required in multiple tissues and stages, with mutations resulting in complex reproductive, embryonic, and adult phenotypes. In light of the proposed critical role of RXR in the formation of nuclear receptor heterodimers in vertebrates, part of the observed USP pleiotropy may be due to the interaction of USP with other factors important in Drosophila development. Indeed, we recently demonstrated that the ecdysone receptor (EcR) forms a heterodimeric complex with USP, and it is this complex that transmits the properties of the insect-molting hormone ecdysone. Remarkably, we have shown that the EcR by itself is unable to bind hormone but requires USP for this property. This is the first demonstration that formation of the heterodimer is required for hormone binding. Furthermore, we demonstrated that the heterodimer also generates the DNA-binding form of the receptor, indicating the importance of protein-protein interactions in hormonal signaling. This is the first demonstration of true allostery by receptors in this family. Based on these observations, we have attempted to transfer ecdysone responsiveness from insect cells to mammalian cell lines. Should this be possible, we would be able to use insect hormones to generate hormonally inducible systems in mammalian cells. The ability to transfer ecdysone inducibility to mammalian systems will offer the possibility of generating a novel and simple inducible system for gene transfer studies. Such a system would allow the activation of transfected genes harboring ecdysone response elements in response to the insect hormone. The virtue of this system is that it could allow high inducibility without activating endogenous receptors and, therefore, have virtually no impact on the organism, with the exception of cells harboring the transfected gene. In feasibility studies we have been able to transfer ecdysone responsiveness to cultured cells, using cotransfected EcR-USP and USP expression vectors. The resulting cells are able to activate ecdysone-responsive genes in a hormone-dependent fashion. We are attempting to expand the utility of this system by generating transgenic mice expressing the EcR in a variety of embryonic and adult tissues. In principle, these mice should be excellent recipients for transgenes harboring ecdysone response elements: the progeny of these mice should be able to activate the transgene following the addition of ecdysone to their diet. We are exploring this proposal. Orphan Receptors-Orphan Ligands An important advance in the characterization of this superfamily of regulatory proteins is the delineation of a growing number of gene products (orphan receptors) that possess the structural features of a hormone receptor but lack known ligands. The search for hormonal activators for these newly discovered orphan receptors has created exciting areas of research on previously unknown signaling pathways. The ability to identify novel hormonal systems has important implications in physiology, as well as in human disease and its treatment. Since receptors have been identified for all known nuclear-acting hormones, a question arises as to the types of molecules that may activate orphan receptors. Products of intermediary metabolism act as transcriptional regulators in bacteria and yeast, suggesting that they may serve similar functions in higher organisms. A crucial biosynthetic pathway in higher eukaryotes is the mevalonate pathway, which leads to the synthesis of cholesterol, bile acids, porphyrin, dolichol, ubiquinone, carotenoids, retinoids, vitamin D, steroid hormones, and farnesylated proteins. Farnesyl pyrophosphate (FPP) represents the last precursor common to all branches of this pathway. As a result, FPP is required for such fundamental biological processes as membrane biosynthesis, hormonal regulation, lipid absorption, glycoprotein synthesis, electron transport, and cell growth. Because of the central role of FPP, it is logical that its concentration should be closely regulated. This suggests that cells have developed strategies to sense and respond to changing levels of FPP or its metabolites. One possible strategy is to use a transcription factor whose activity is specifically regulated by an FPP-like molecule. Potential candidates for such a sensor include members of the nuclear receptor superfamily, as these proteins are activated by low-molecular-weight signaling molecules. We describe a novel orphan nuclear receptor named FXR (farnesoid X receptor) that is activated by farnesol and related molecules. FXR provides one of the first examples of a vertebrate transcription factor that is regulated by an intracellular metabolite. These findings suggest the existence of vertebrate signaling networks that are regulated by products of intermediary metabolism. We refer to this novel regulatory paradigm as metabolite-controlled intracellular (metacrine) signaling.

To: george damas who wrote (11564)	11/24/1997 8:22:00 AM
From: Henry Niman	Respond to of 32384

I also ran across this upcoming scientific conference which focuses on many areas of interest to LGND shareholders: Nuclear Receptor Gene Family Incline Village, Nevada ú March 28 - April 3, 1998 Organizers: Kathryn B. Horwitz, John A. Cidlowski and Ron Evans Maximum Attendance: 450 ú Abstract Deadline: 1/13/98 ú Early Registration: 1/28/98 The steroid, thyroid, retinoic acid and vitamin D receptors, plus a growing number of orphan receptors, are members of a superfamily of nuclear proteins that regulate transcription. These receptors control, among other things, developmental processes, tissue-specific differentiation, the growth and death of normal and malignant calls, reproductive behavior and metabolic activity. They act directly by binding to the hormone response elements of target promoters, or indirectly, by mechanisms that include interactions with transcriptional corregulators, or cross -talk with other signaling pathways. Among the problems facing this field are the mechanisms of tissue-specific regulation; cell-cycling and cancer; interactions with coregulatory factors, transcriptional integration of cell surface/nuclear receptor signals; the regulatory role of chromatin; post-translational modification of receptors and isoform-specific actions; mechanisms of antagonists; receptor and domain structure; the function of orphan receptors. The intent of this meeting is to bring together leading experts in this diverse field, joined by younger investigators and trainees entering the field. The program will include state-of-the art plenary and symposium lectures plus poster sessions; slots have been set aside for late-breaking developments. Selected student and post-doc abstracts will be chosen for short oral presentations. Our goal is to nurture and extend the intellectual interaction fostered by previous Keystone Symposia meetings on this topic. POSTER TOPICS Organizer will be assigning poster sessions (no number necessary on form) Development / Alternate Models / Chromatin / DNA / Transcription / CP Activators / Corepressors / Signaling / Cross-Talk / Orphan Ligands / Hormone-Induced Repression / Antagonists / Retinoids / Thyroid / Orphans / Non-Traditional Targets / Steroid Receptors Saturday, March 28 Registration (2-7pm) Orientation (7-7:30pm) Keynote Address (7:30-8:30pm) ROBERT T. TJIAN, Univ California-Berkeley Mechanisms of Transcriptional Regulation in Animal Cells: Activator, Core Promoter Complexes and Chromatin Sunday, March 29 Breakfast (7-8am) DEVELOPMENT/ALTERNATE MODELS (8-11am) CARL THUMMEL, _ Univ of Utah Steroid Regulation of Drosophila Metamorphosis SPEAKER TO BE ANNOUNCED COFFEE BREAK JOANNE CHORY, Salk Institute Light, Brassinosteroids, and Plant Development THOMAS PERLMANN, Ludwig Institute for Cancer Research Function of NURR1 and Related Orphan Receptors Poster Set-Up (11am-4pm) Workshop/Poster Abstract Short Talks (3-4pm) (3-4pm) Poster Session (4-6pm) Social Hour (5-6pm) CHROMATIN/DNA (Coffee Available) (8-10pm) JAMES KADONAGA, _ Univ California-San Diego Role of Chromatin Structure in the Regulation of Transcription by the Estrogen Receptor TREVOR K. ARCHER, Cancer Research Laboratories Transcriptional Activation Within the Chromatin by the Glucocorticoid Receptors ALAN WOLFFE, National Institutes of Health How the Thyroid Hormone Receptor Makes use of Chromatin to Regulate Transcription Monday, March 30 Breakfast (7-8am) TRANSCRIPTION/COACTIVATORS/COREPRESSORS (8-11am) ROBERT ROEDER, _ Rockefeller University The Role of General and Receptor-Associated Coactivators in Thyroid Receptor Function PETER KUSHNER, Univ California-San Francisco Recruitment and Triggering of Co-activators by Estrogen Receptor COFFEE BREAK M. GEOFFREY ROSENFELD, Univ California-San Diego CBP/p300 DAVID D. MOORE, Baylor College of Medicine Coactivators/Corepressors Workshop/Poster Abstract Short Talks (3-4pm) (3-4pm) Poster Session (4-6pm) Social Hour (5-6pm) SIGNALING/CROSS-TALK (Coffee Available) (8-10pm) BERT W. O'MALLEY, _ Baylor College of Medicine Steroid Receptors, Coactivators, Enzymes and Chromosomes KATHRYN HORWITZ, Univ of Colorado Progesterone Receptors EGF Signaling KENNETH KORACH, National Institutes of Health Cross coupling of EGF and Estrogen Receptor Signaling Pathways Tuesday, March 31 Breakfast (7-8am) ORPHAN LIGANDS (8-11am) RONALD M. EVANS, _ Salk Institute Novel Nuclear Receptor Ligands DAVID RUSSELL, Univ of Texas SW Medical Center Androgen Action in Males and Females RICHARD HEYMAN, Ligand Pharmaceuticals RXR Agonists Activate RXR:PPAR Gama Heterodimers and Sensitize Diabetic and Obese Mice to Insulin COFFEE BREAK STEVEN A. KLIEWER, Glaxo Wellcome Identification of Ligands for Orphan Nuclear Receptors CARY WEINBERGER, National Institute Environmental Health Science Farnesoids, FXR, and Cellular Growth Control Poster Set-Up (11am-4pm) Workshop/Poster Abstract Short Talks (3-4pm) (3-4pm) Poster Session (4-6pm) Social Hour (5-6pm) HORMONE-INDUCED REPRESSION/ANTAGONISTS (Coffee Available) (8-10pm) JOHN A. CIDLOWSKI, National Institute Environment Health Science GR/NFkB DONALD MC DONNELL, Duke University Tissue-Specific Antiestrogens, a Concept Reduced to Practice SPEAKERS TO BE ANNOUNCED Wednesday, April 1 Breakfast (7-8am) RETINOIDS/THYROID/ORPHANS (8-11am) PIERRE H. CHAMBON, _ Institut de Genetique et de Biologie Moleculaire etCellulaire Molecular Genetics of Retinoid Receptors MITCHELL LAZAR, Univ of Pennsylvania Repression by Thyroid and Orphan Receptors COFFEE BREAK ROLAND SCHUELE, University of Freiburg The Nuclear Orphan Receptors RZRb and GCNF: Structure, Function and Liaison With Novel Cofactors DAVID MANGELSDORF, Univ of Texas SW Medical Centerr Orphan Receptors that Mediate Oxysterol Signaling Poster Set-Up (11am-4pm) Workshop/Poster Abstract Short Talks (3-4pm) (3-4pm) Poster Session (4-6pm) Social Hour (5-6pm) NON-TRADITIONAL TARGETS (Coffee Available) (8-10pm) DIDIER PICARD, Univ of Geneva Steroid-Independent Activation of Estrogen and Progesterone Receptors LEONARD FREEDMAN, Sloan-Kettering Cancer Center Transcriptional Targets of the Vitamin D3 Receptor Mediating Cell Cycle Arrest and Differentiation ARUN ROY, Univ of Texas Health Science Center AR Promoter Function During Aging Thursday, April 2 Breakfast (7-8am) STEROID RECEPTORS/CHROMATIN (8-11am) CARLOS BUSTAMANTE, _ University of Oregon Imaging Protein/DNA Interaction JAN-AKE GUSTAFSSON, Huddinge Hospital Estrogen Receptor B Predicted Effects of Estrogen COFFEE BREAK BENITA S. KATZENELLENBOGEN, University of Illinois New Dimensions in Estrogen Receptor Pharmacology DEAN P. EDWARDS, Univ of Colorado Health Science Center The Role of HMG Chromatin Proteins in Steroid Receptor Action" NEW DEVELOPMENTS/SHORT TALKS (2-5pm) BRUCE M. SPIEGELMAN, Dana Farber Cancer Institute PPARy and the Moleuclar Basis of Adipogenesis ANTHONY WRIGHT, Karolinska Institute Structure and Function of the Glucocorticoid Receptor N-Terminal Transactivation Domain COFFEE BREAK, GUNTHER SCHUTZ, German Cancer Research Center Glucocorticoid and Mineralocorticoid Receptors SPEAKER TO BE ANNOUNCED Social Hour (7-8pm) Banquet (8-10pm) Entertainment (9pm-12am) Friday, April 3 Departure Plenary talk of 50 minutes. Program current as of 10/27/97 and is subject to change. * Session Chair; + Speaker invited, not yet responded.

To: george damas who wrote (11564)	12/31/1997 11:33:00 AM
From: Henry Niman	Read Replies (3) \| Respond to of 32384

george, It looks like LGND is trying to get its story out. In addition to the NBC4 News story in Washington D.C. (at Lombardi), there was a similar show with patients at M.D. Anderson. In this case, the vial with Ligand's name was show. A similar segment was also shown in Louisville, KY, but I don't know if these were KY patients or a re-run of the Lombardi or M.D. Anderson patients. In any event, the story is the same. Although the drugs don't work on all patients, in some patients the results can be quite dramatic. The low toxicity profile of Targretin, Panretin, and I assume ALRT1550, should move these retinoids and rexinoids into the fore-front against many cancers, not just the releative rare cancers that are being targeted in the pivotal Phase III trials that are finishing up.