Genmab A/S (OMX: GEN) announced today a new pre-clinical antibody program called HuMax-CD32b(TM). This fully human IgG1,k antibody targets the CD32b receptor found on immune cells and hematological tumors. HuMax-CD32b may have therapeutic potential in the treatment of B-cell chronic lymphocytic leukemia, small lymphocytic lymphoma, Burkitt’s lymphoma, follicular lymphoma and diffuse large B-cell lymphoma.

The lead candidate for HuMax-CD32b was selected from a panel of over 60 antibodies based on its excellent selectivity and binding ability for the CD32b target and potent triggering of the immune system killing mechanism antibody-dependent cellular cytotoxicity (ADCC). The antibody was highly effective in suppressing tumor growth in in vivo mouse tumor models in which tumor growth was monitored by highly sensitive bioluminescence imaging.

In animal models, HuMax-CD32b has been shown to induce impressive anti-tumor responses. The CD32b receptor has an inhibitory role on immune cells and blockade of CD32b has been documented to strongly potentiate the therapeutic effects of other anti-tumor antibodies. An antibody targeting CD32b may thus be attractive for combination therapy with other antibodies.

“We believe HuMax-CD32b has great potential as a cancer therapeutic, both because of its impressive anti-tumor activity, and the potential for combination with other therapeutic antibodies, such as antibodies directed to CD20 or CD38.” said Prof. Jan G. J. van de Winkel, Ph.D., Chief Scientific Officer at Genmab A/S.

About Genmab A/S

Genmab is a leading international biotechnology company focused on developing fully human antibody therapeutics for unmet medical needs. Using unique, cutting-edge antibody technology, Genmab’s world class discovery and development teams have created and developed an extensive pipeline of products for potential treatment of a variety of diseases including cancer and autoimmune disorders. As Genmab advances towards a commercial future, we remain committed to our primary goal of improving the lives of patients who are in urgent need of new treatment options. For more information on Genmab’s products and technology, visit http://www.genmab.com.

This press release contains forward looking statements. The words “believe”, “expect”, “anticipate”, “intend” and “plan” and similar expressions identify forward looking statements. Actual results or performance may differ materially from any future results or performance expressed or implied by such statements. The important factors that could cause our actual results or performance to differ materially include, among others, risks associated with product discovery and development, uncertainties related to the outcome and conduct of clinical trials including unforeseen safety issues, uncertainties related to product manufacturing, the lack of market acceptance of our products, our inability to manage growth, the competitive environment in relation to our business area and markets, our inability to attract and retain suitably qualified personnel, the unenforceability or lack of protection of our patents and proprietary rights, our relationships with affiliated entities, changes and developments in technology which may render our products obsolete, and other factors. Genmab is not under an obligation to up-date statements regarding the future following the publication of this release; nor to confirm such statements in relation to actual results, unless this is required by law.

Genmab(R); the Y-shaped Genmab logo(R); HuMax(R); HuMax-CD4(R); HuMax-CD20(R); HuMax-EGFr(TM); HuMax-IL8(TM); HuMax-TAC(TM); HuMax-HepC(TM); HuMax-CD38(TM); HuMax-CD32b(TM) and UniBody(R) are all trademarks of Genmab A/S

Genmab A/S

http://www.genmab.com

Cephalon, Inc. (Nasdaq: CEPH) announced that it has submitted a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) requesting approval of TREANDA(R) (bendamustine HCl) for Injection for the treatment of patients with indolent B-cell non-Hodgkin’s lymphoma (NHL) who have progressed during or following treatment with rituximab or a rituximab-containing regimen. According to the National Cancer Institute, an estimated 30,000 people in the United States will be diagnosed in 2007 with indolent NHL, a serious and slow growing cancer of the lymphatic system that is difficult to treat because patients are prone to relapse after treatment.

“TREANDA is the lead product in our oncology pipeline and with this second NDA submission for the product in 2007 we have achieved a significant milestone for our business,” said Dr. Lesley Russell, Executive Vice President, Worldwide Medical and Regulatory Operations. “The clinical data supporting this submission highlight the potential of TREANDA to make a meaningful difference for patients with indolent NHL who have relapsed during or following treatment with rituximab.”

The TREANDA NDA for relapsed indolent NHL is supported by three studies in patients with NHL, including one in combination with rituximab. In these studies, patients treated with TREANDA had a high rate of response and a manageable and tolerable side effect profile, with adverse events similar to those observed with other chemotherapy agents.

About TREANDA

TREANDA is a novel chemotherapeutic agent, a hybrid of a purine analog and an alkylator. Preclinical data demonstrate that TREANDA acts in two distinct ways to kill cancer cells. TREANDA damages the DNA in cancer cells, which leads to cell death by a process known as apoptosis (programmed cell death) as well as by an alternate cell death (non-apoptotic) pathway known as mitotic catastrophe (a disruption of normal cell division). The contribution of the purine analog to the antitumor effect of TREANDA is under investigation but has not yet been determined.

The protocol for the TREANDA NHL pivotal trial received special protocol assessment (SPA) approval from the FDA in February 2006. The SPA process allows for FDA evaluation and acceptance of a clinical trial protocol, including trial size, clinical endpoints and/or data analysis. In September 2007, Cephalon submitted an NDA requesting approval of TREANDA for the treatment of patients with chronic lymphocytic leukemia (CLL), for which the FDA has granted priority review and orphan drug status.

Cephalon holds exclusive rights to market and develop TREANDA in the United States. TREANDA is licensed from Astellas Pharma GmbH. Bendamustine HCl, the active ingredient in TREANDA, is marketed in Germany by Astellas’ licensee, Mundipharma International Corporation Limited, under the trade name RIBOMUSTIN(R). In Germany, RIBOMUSTIN is indicated as a single-agent or in combination with other anti-cancer agents for indolent NHL, multiple myeloma, and CLL. SymBio Pharmaceuticals Ltd holds exclusive rights to develop and market bendamustine HCl in Japan and selected Asia Pacific Rim countries.

About Cephalon Oncology

Cephalon Oncology is a strategic business unit focused on the development and commercialization of oncology products and resources for patients and healthcare providers. The Cephalon Oncology portfolio includes a number of promising investigational and marketed compounds. In addition to TREANDA, the Cephalon Oncology therapeutic portfolio in the United States includes TRISENOX(R) (arsenic trioxide) injection, a product approved in the United States for the treatment of patients with relapsed or refractory acute promyelocytic leukemia, and CEP-701, an oral small molecule inhibitor of tyrosine kinases including FLT-3, TRK and JAK-2, in phase 3 development for acute myeloid leukemia. In Europe, Cephalon markets three additional oncology products in 19 countries.

About Cephalon, Inc.

Cephalon, Inc. is an international biopharmaceutical company, recently inducted into the World Economic Forum Community of Global Growth Companies. For 20 years, the company has been dedicated to the discovery, development and commercialization of innovative products in four core therapeutic areas: central nervous system, pain, oncology and addiction. A member of the Fortune 1000, Cephalon currently employs approximately 3,000 people in the United States and Europe. U.S. sites include the company’s headquarters in Frazer, Pennsylvania, and offices, laboratories or manufacturing facilities in West Chester, Pennsylvania, Salt Lake City, Utah, and suburban Minneapolis, Minnesota. Cephalon’s European headquarters are located in Maisons-Alfort, France.

The company’s proprietary products in the United States include: PROVIGIL(R) (modafinil) Tablets [C-IV], FENTORA(R) (fentanyl buccal tablet) [C-II], TRISENOX, AMRIX(TM) (cyclobenzaprine hydrochloride extended-release capsules), VIVITROL(R) (naltrexone for extended-release injectable suspension), GABITRIL(R) (tiagabine hydrochloride), NUVIGIL(TM) (armodafinil) Tablets [C-IV] and ACTIQ(R) (oral transmucosal fentanyl citrate) [C-II]. The company also markets numerous products internationally.

In addition to historical facts or statements of current condition, this press release may contain forward-looking statements. Forward-looking statements provide Cephalon’s current expectations or forecasts of future events. These may include statements regarding anticipated scientific progress on its research programs; development of potential pharmaceutical products, including the results of any clinical programs with respect to TREANDA or the timing, acceptance or approval of any current or future filings for regulatory approval of TREANDA or other Cephalon Oncology compounds; interpretation of clinical results, particularly with respect to the TREANDA clinical trials; manufacturing development and capabilities; market prospects for its products; sales and earnings guidance; and other statements regarding matters that are not historical facts including statements with respect to the role TREANDA may play in the treatment of NHL, CLL or other cancers. You may identify some of these forward-looking statements by the use of words in the statements such as “anticipate,” “estimate,” “expect,” “project,” “intend,” “plan,” “believe” or other words and terms of similar meaning. Cephalon’s performance and financial results could differ materially from those reflected in these forward-looking statements due to general financial, economic, regulatory and political conditions affecting the biotechnology and pharmaceutical industries as well as more specific risks and uncertainties facing Cephalon such as those set forth in its reports on Form 8-K, 10-Q and 10-K filed with the U.S. Securities and Exchange Commission. Given these risks and uncertainties, any or all of these forward-looking statements may prove to be incorrect. Therefore, you should not rely on any such factors or forward-looking statements. Furthermore, Cephalon does not intend to update publicly any forward-looking statement, except as required by law. The Private Securities Litigation Reform Act of 1995 permits this discussion.

Cephalon, Inc.

http://www.cephalon.com

Allos Therapeutics, Inc. (Nasdaq: ALTH) announced that an independent Data Monitoring Committee (DMC) has completed the pre-specified 65-patient safety review of data from the Company’s pivotal Phase 2 PROPEL trial of PDX (pralatrexate) in patients with relapsed or refractory peripheral T-cell lymphoma (PTCL), and has recommended that the trial continue per the protocol. This interim assessment was based upon an evaluation of patients enrolled in the study who completed at least one cycle of treatment with PDX. The Company currently expects to complete patient enrollment in the PROPEL study in the second quarter of 2008.

“The DMC recommendation represents another important milestone in the development of a potential new treatment option for patients with relapsed or refractory peripheral T-cell lymphoma, a patient population for which there are currently no approved agents,” said Pablo J. Cagnoni, M.D., Senior Vice President and Chief Medical Officer of Allos. “We remain pleased with the progress of the PROPEL trial and look forward to continuing to drive our PDX product development and commercialization plans in 2008.”

PROPEL (Pralatrexate in Patients with Relapsed Or Refractory PEripheral T-cell Lymphoma) is a pivotal Phase 2, international, multi-center, open-label, single-arm study that will seek to enroll a minimum of 100 evaluable patients with relapsed or refractory PTCL who have progressed after at least one prior treatment. Patients receive 30 mg/m2 of PDX once every week for six weeks followed by one week of rest per cycle of treatment. The primary efficacy endpoint of the study is objective response rate (complete and partial response). Secondary efficacy endpoints include duration of response, progression-free survival and overall survival.

Owen A. O’Connor, MD, PhD, Director, Lymphoid Development & Malignancy Program and Chief, Lymphoma Service, Columbia University, Herbert Irving Comprehensive Cancer Center, New York, is the international study chair.

In accordance with the PROPEL study design, in January 2007, the DMC completed an interim analysis of safety data based on the first 10 patients enrolled to the study who completed at least one cycle of treatment with PDX, and recommended that the trial continue per the protocol. Also in accordance with the study design, in September 2007, an interim analysis of patient response and safety data was conducted based on the first 35 patients enrolled to the study who completed at least one cycle of treatment with PDX. The results of the interim analysis of patient response data exceeded the pre-specified threshold for continuation of the trial, which required a minimum of four responses (complete or partial) out of the first 35 evaluable patients, as determined by independent oncology review. In addition, the DMC identified no major safety concerns and recommended that the trial continue per the protocol.

The PROPEL trial is being conducted under an agreement with the United States Food and Drug Administration (FDA) under its special protocol assessment (SPA) process. The SPA process allows for FDA evaluation of a clinical trial protocol intended to form the primary basis of an efficacy claim in support of an NDA, and provides an agreement that the study design, including trial size, clinical endpoints and/or data analyses are acceptable to the FDA. The FDA granted orphan drug designation to PDX for the treatment of T-cell lymphoma in July 2006 and granted fast track designation to PDX for the treatment of patients with T-cell lymphoma in September 2006. In April 2007, the Commission of the European Communities, with a favorable opinion of the Committee for Orphan Medicinal Products of the European Medicines Agency, or EMEA, granted orphan medicinal product designation to PDX for the treatment of patients with PTCL

About the Data Monitoring Committee (DMC)

The DMC is comprised of independent medical experts and was established by Allos as part of the Company’s compliance with good clinical practice guidelines. The DMC is responsible for monitoring the on-going safety of patients participating in the PROPEL trial and for conducting formal interim safety assessments of trial results.

About Peripheral T-cell Lymphoma

Peripheral T-cell lymphomas, or PTCLs, are a biologically diverse and uncommon group of blood cancers that account for approximately 10% to 15% of all cases of non-Hodgkin’s lymphoma, or about 7,100 patients annually. The average five-year survival rate for PTCL patients is approximately 25%. There are currently no pharmaceutical agents approved for use in the treatment of either first-line or relapsed or refractory PTCL.

About PDX (pralatrexate)

PDX is a novel, small molecule chemotherapeutic agent that inhibits dihydrofolate reductase, or DHFR, a folic acid (folate)-dependent enzyme involved in the building of nucleic acid, or DNA, and other processes. PDX was rationally designed for efficient transport into tumor cells via the reduced folate carrier, or RFC-1, and effective intracellular drug retention. The Company believes these biochemical features, together with preclinical and clinical data in a variety of tumors, suggest that PDX may have a favorable safety and efficacy profile relative to methotrexate and certain other DHFR inhibitors.

About Allos Therapeutics, Inc.

Allos Therapeutics is a biopharmaceutical company focused on the development and commercialization of small molecule therapeutics for the treatment of cancer. The Company’s lead product candidate, PDX (pralatrexate), is a novel antifolate currently under evaluation in a pivotal Phase 2 (PROPEL) trial in patients with relapsed or refractory peripheral T-cell lymphoma. The PROPEL trial is being conducted under an agreement reached with the U.S. Food and Drug Administration under its special protocol assessment, or SPA process. The Company is also investigating PDX in patients with non-small cell lung cancer and a range of lymphoma sub-types. The Company’s other product candidate is RH1, a targeted chemotherapeutic agent currently being evaluated in a Phase 1 trial in patients with advanced solid tumors or non-Hodgkins Lymphoma (NHL). For additional information, please visit the Company’s website at http://www.allos.com.

Safe Harbor Statement

This press release contains forward-looking statements that are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Such forward-looking statements include statements relating to the potential safety and efficacy profile of PDX relative to methotrexate and certain other DHFR inhibitors, the potential safety and efficacy of PDX for the treatment of PTCL or any other type of cancer; the Company’s projected timeline for completing enrollment in the PROPEL trial; and other statements that are other than statements of historical facts. In some cases, you can identify forward-looking statements by terminology such as “may,” “will,” “should,” “expects,” “intends,” “plans,” anticipates,” “believes,” “estimates,” “predicts,” “projects,” “potential,” “continue,” and other similar terminology or the negative of these terms, but their absence does not mean that a particular statement is not forward-looking. Such forward-looking statements are not guarantees of future performance and are subject to risks and uncertainties that may cause actual results to differ materially from those anticipated by the forward-looking statements. These risks and uncertainties include, among others: that the Company may experience delays in the conduct or completion of the PROPEL trial, whether caused by competition, adverse events, patient enrollment rates, regulatory issues or other factors; that clinical trials may not demonstrate that PDX is both safe and effective for the treatment of patients with PTCL or any other type of cancer; that data from preclinical studies and clinical trials may not be indicative of future clinical trial results; that the safety and/or efficacy results of the PROPEL trial may not support an application for marketing approval in the United States or any other country; that an application for marketing approval may not be accepted for priority review or at all by the FDA or any other regulatory authority; and that the Company may lack the financial resources and access to capital to fund future clinical trials for PDX or any of its other product candidates. Additional information concerning these and other factors that may cause actual results to differ materially from those anticipated in the forward-looking statements is contained in the “Risk Factors” section of the Company’s Annual Report on Form 10-K for the year ended December 31, 2006 and in the Company’s other periodic reports and filings with the Securities and Exchange Commission. The Company cautions investors not to place undue reliance on the forward-looking statements contained in this press release. All forward-looking statements are based on information currently available to the Company on the date hereof, and the Company undertakes no obligation to revise or update these forward-looking statements to reflect events or circumstances after the date of this presentation, except as required by law.

The Allos logo is a trademark of Allos Therapeutics, Inc.

Allos Therapeutics, Inc.

http://www.allos.com

Kiadis Pharma announced that it has successfully completed an End of Phase II meeting for Reviroc with the U.S. Food and Drug Administration (FDA). Reviroc is under development for elimination of cancer cells from an autologous graft in bone marrow transplantations for end-stage blood cancer patients. The FDA agreed that the data from the completed phase II clinical Reviroc trial is sufficient to support the start of a phase III study. The FDA offered Kiadis Pharma its Special Protocol Assessment (SPA) procedure allowing Kiadis Pharma to work directly with the FDA to optimize the clinical design of the trial.

The FDA meeting followed the successful completion of a multi centre phase II study for Reviroc showing an improved overall survival after autologous bone marrow transplantation in Non-Hodgkin’s lymphoma patients. The phase III clinical trial design for Reviroc will focus on patients with Large B cell lymphoma. Kiadis Pharma anticipates filing of the IND, SPA request and Orphan Drug Designation application with the FDA within the next few weeks.

“We are very pleased with the outcome of the End of Phase II meeting with the FDA and with the possibility to access the FDA’s Special Protocol Assessment program. Together with the strong support by our principal investigators we are well prepared to design a clear path towards marketing authorization for Reviroc,” said Manja Bouman, CEO Kiadis Pharma.

About Reviroc

Reviroc is being developed as a treatment that eliminates blood cancer cells from autologous transplants for patients with end stage blood cancer. An autologous transplant uses the patient’s own bone marrow to serve as a graft. Bone-marrow transplants are broadly recognized as a treatment option for patients suffering from blood cancers, such as leukemia and lymphoma. One of the limitations of autologous bone marrow transplantations is the high relapse rate associated with this treatment. This is often caused by the presence of cancer cells in the transplant and the fact that the patients’ own white blood cells does not fight the cancer. Reviroc has been developed to remove residual tumor cells from the graft.

English release is provided by Kiadis Pharma. Equivalent translations are from a third party.

Kiadis Pharma

http://www.kiadis.com

Researchers here have figured out a way to use a firefly gene to let them see just how effective a new drug combination actually is against some forms of cancer and their serious complications.

The new study looked at ATLL, adult T-cell lymphoma and leukemia, a form of cancer where it is particularly hard to gauge the disease’s progress, and where the patients’ prognosis is generally poor. There is now no widely effective therapy available to treat this disease successfully.

In doing so, the researchers developed what they hope will be the first animal model for the disease that includes a severe bone depletion called humoral hypercalcemia of malignancy (HHM), a condition that can affect four out of every five ATLL patients and shorten their lives.

The study is published in the online edition of the journal Cancer Research.

“These ATLL tumors secrete proteins that also cause the bones in these patients to weaken and resorb,” explained Thomas Rosol, professor of veterinary biosciences and dean of the College of Veterinary Medicine at Ohio State University.

“When that happens, the amount of calcium in the blood can build up to toxic levels.” So killing the cancer cells in these patients is only half the battle, he says. “We have to stop the resorption of bone and the release of calcium that the cancer causes.”

Earlier tissue culture studies on a new anticancer drug, PS-341, showed promise in attacking the cancer cells but before now, an effective animal model wasn’t available for researchers to use that included HHM’s calcium buildup.

Rosol and his team turned to a combination of PS-341 and zoledronic acid, a form of bisphosphonate that is widely used now to combat the bone loss of osteoporosis and other diseases.

They would then test the two drugs, separately and combined, in a group of specialized mice that had been injected with ATLL tumor cells.

“We can inject these tumor cells into the abdomen of the mice and they will grow in the animals’ lymph nodes,” explained Rosol, “but normally, you can’t detect the extent of the animal’s disease until the cancer is in its later stages.”

To solve this, Rosol’s team took a novel approach:

They took a gene responsible for a firefly’s glow and genetically inserted it into these tumor cells. That gene produces the enzyme luciferase in the insects which, when combined with another compound, luciferin, causes the firefly’s distinctive glow.

The mice then received these genetically modified tumor cells and the researchers injected luciferin into the animals. Cancer cells containing the luciferase would combine with the luciferin and glow in the dark, giving the team a clear picture of the extent of disease inside the animal.

“We put these mice inside a blackened chamber with a digital camera and then took their pictures. The only light present would be the light emitted by the cancer cells,” Rosol said.

“We just measured the light that we could see coming out of the animal the more light, the more tumor growth; the less light, less tumor.”

He said that with the tumor cells emitting light, his team was able to gauge the volume of tumor cells in the animal’s body. “It is amazingly sensitive and precise, letting us see to a level of only a few hundred cells,” he said. “That gives us a good method for monitoring the tumor cells.”

So when the researchers tested the effects of the two drugs, they found that the zoledronic acid halted the bone resorption, reducing the harmful calcium in the body, and that the anticancer drug PS-341 killed more than 95 percent of the ATLL cells.

“It was very effective against ATLL, eliminating almost all of the tumor cells,” Rosol said.

What they didn’t expect was that in some mice treated only with the zoledronic acid and not with the PS-341 anticancer drug, the zoledronic acid reduced some of the cancer growth as well.

“We have no idea why some animals responded in this way while others didn’t,” Rosol said, “but the next step may be to try to understand the processes involved in how the tumor cells cause the resorption of the bones and the release of calcium.

“Hopefully, we’ll soon see this work tested in human clinical trials and that perhaps will lead to a treatment for this disease.”

The research was supported in part by the National Cancer Institute and the National Center for Research Resources. Working with Rosol on the project were Sherry Shu, Murali Nadella, Nanda Thudi and Jillian Werbeck, all doctoral students; research scientist Wessel Dirksen, statistician Soledad Fernandez, and Michael Lairmore, professor and chair of veterinary biosciences.

Ohio State University
1125 Kinnear Rd.
Columbus, OH 43212-1153
United States

http://www.osu.edu

A combination of chemotherapy and radiotherapy, rather than radiotherapy alone, should now be considered standard treatment for all patients with localised Hodgkin’s lymphoma where the tumour is situated above the diaphragm, according to the results of a randomized controlled trial. Furthermore, the trial results suggest that radiotherapy need only target areas directly involved in the cancer, sparing more extensive treatment of surrounding tissue.

This finding adds clarity to speculation about the appropriate treatment of this cancer, after previous results from trials done during the late 1980s and early 1990s showed that clinical staging is sufficient for stratifying early stages of the disease; that chemotherapy followed by involved-field radiotherapy (limited to the areas of cancer, rather than extensive surrounding tissue) should be the standard treatment; and that duration of chemotherapy should be adapted to the severity of the disease.

Dr Christophe Fermé and colleagues at the European Organisation for Research and Treatment of Cancer and the Groupe d’Études des Lymphomes de l’Adulte initiated the trial to further elucidate treatment options that might improve event-free survival in patients with Hodgkin’s lymphoma. By use of a set of prognostic factors previously published by the EORTC to stratify patients by severity of disease, the researchers compared subtotal nodal radiotherapy alone with a combination of chemotherapy and radiotherapy in patients pre-classified as have good or poor prognosis.

A total of 1538 patients between the ages of 15 and 70 years were enrolled in the trial. All had untreated clinical stage I or II supradiaphragmatic Hodgkin’s disease and were being treated at any of 91 centers in Belgium, France, Italy, the Netherlands, Poland, Portugal, Slovenia, and Spain. Of the total patient population, 542 (35%) were categorized as having a favorable prognostic factors and 996 (65%) were categorized as having an unfavorable prognostic factors.

Patients in the favourable prognosic factor arm were randomly assigned to receive either subtotal nodal radiotherapy or combination therapy consisting of three cycles of chemotherapy plus involved-field radiotherapy. Patients in the unfavourable prognostic factor arm were randomly assigned to one of three regimens: six or four cycles of chemotherapy plus involved-field radiotherapy or four cycles of drugs plus subtotal nodal radiotherapy. The chemotherapy regimen used for all the groups was mechlorethamine, vincristine, procarbazine, and prednisone in combination with doxorubicin, bleomycin, and vinblastine.

Taking event-free survival as a primary endpoint, the researchers found that, in the group with favourable prognostic features, response rates to the two treatment regimens were similar. However, among the 446 patients from both groups who had a complete remission there was a significant different in rates between the combination group and the radiotherapy alone group: five had a relapse after combination therapy and 61 after subtotal nodal radiotherapy. This equated to a difference in the estimated 5-year event-free survival rate of 24%, favouring the combination-therapy group.

For patients with unfavourable prognostic factors, complete-remission rates were 83% in the group receiving six cycles of chemotherapy plus involved-field radiotherapy, 85% in the group receiving four cycles plus involved-field radiotherapy, and 86% in the group receiving four cycles plus subtotal nodal radiotherapy. However, there were no significant differences in the 5-year event-free survival estimates or in estimated overall survival.

The researchers conclude from their findings that four courses of a doxorubicin-containing regimen and involved-field radiotherapy should be the standard treatment for this tumour type. Furthermore, they note, in patients with risk factors, four cycles of a doxorubicin-containing regimen are as effective as six cycles and involved-field radiotherapy yields a disease-control rate similar to that with subtotal nodal radiotherapy.

“Our study showed that a combination of chemotherapy and radiotherapy should now be considered the standard treatment for all patients with localized stage supradiaphragmatic Hodgkin’s disease and that subtotal nodal radiotherapy alone can no longer be recommended,” summarise the authors.

“The results of our trial show that it is possible to tailor the duration of chemotherapy according to risk factors. Moreover, our findings point to a new role for adjuvant radiotherapy with smaller radiation fields, allowing for the reduction of toxic effects associated with large fields. A remaining question now under investigation is whether patients with early-stage Hodgkin’s disease can be cured with chemotherapy alone,” they conclude.

Chemotherapy plus involved-field radiation in early-stage Hodgkin’s disease
Fermé C, Eghbali H, Meerwaldt JH, Rieux C, Bosq J, Berger F, Girinsky T, Brice P, van’t Veer MB, Walewski JA, Lederlin P, Tirelli U, Carde P, Van Den Neste E, Gyan E, Monconduit M, Diviné M, Raemaekers JMM, Salles G, Noordijk EM, Creemers G-J, Gabarre J, Hagenbeek A, Reman O, Blanc M, Thomas J, Vié B, Kluin-Nelemans JC, Viseu F, Baars JW, Poortmans P, Lugtenburg PJ, Carrie C, Jaubert J, Henry-Amar M, for the EORTC-GELA H8 Trial. N Engl J Med 2007; 357: 1916-27.

This summary is provided by the Cancer Media Service which is operated by The European School of Oncology.

http://www.cancerworld.org/mediaservice

OXiGENE, Inc. (NASDAQ: OXGN, XSSE: OXGN), a clinical-stage, biopharmaceutical company developing novel therapeutics to treat cancer and eye diseases, reported that its lead product candidate, ZYBRESTATTM (combretastatin A4 phosphate / CA4P), demonstrated anti-leukemic effects in preclinical studies published online and ahead of print on November 16, 2007 on the website of the journal BLOOD.

The publication, entitled “The microtubule targeting agent, CA4P, regresses leukemic xenografts by disrupting interaction with vascular cells and promoting mitochondrial-dependent cell death,” by Isabelle Petit, Shahin Rafii, M.D. and colleagues from the Weill Medical College of Cornell University, is available online, ahead of print, click here. (Due to its length, this URL may need to be copied/pasted into your Internet browser’s address field. Remove the extra space if one exists.) Dr. Rafii is the Arthur Belfer Professor of Medicine and a Howard Hughes Medical Institute Investigator.

The authors hypothesized that because adhesion of leukemic cells to vascular cells may confer resistance to chemotherapeutic agents, treatment with CA4P would promote leukemic cell death by disrupting leukemic cell cytoskeletal stability and interfering with vascular cell interactions. The results detailed in the paper demonstrate that low and non-toxic doses of CA4P inhibited leukemic cell proliferation in vitro and induced mitotic arrest and cell death. Furthermore, in mouse models of human leukemia, CA4P prolonged survival without inducing hematological toxicity, likely by inhibiting proliferation and circulation of leukemic cells, and diminished the extent of peri-vascular leukemic cell infiltrates. These anti-leukemic effects were shown to be mediated by mitochondrial damage and down-regulation of the cell-adhesion protein VCAM-1, without causing hematological toxicities. Based on these results, the authors concluded that CA4P is a promising agent for the treatment of acute leukemias and merits further evaluation in combination with other chemotherapeutic agents.

“We are very encouraged by these results seen with ZYBRESTAT, which point to new mechanisms and indicate that its clinical potential could extend beyond solid tumors, where current clinical development efforts are focused, into hematological malignancies,” commented Dai Chaplin, Head of Research and Development and Chief Scientific Officer for OXiGENE. “With a greater understanding of ZYBRESTAT’s mechanism of action, OXiGENE believes that it is positioned to exploit the full clinical potential of this novel therapeutic candidate.”

About ZYBRESTAT (combretastatin A4 phosphate / CA4P)

ZYBRESTAT™ is currently being evaluated in a pivotal registration study in anaplastic thyroid cancer (ATC) under a Special Protocol Assessment agreement with the U.S. Food and Drug Administration (FDA). OXiGENE believes that ZYBRESTAT is poised to become the first therapeutic product in a novel class of small-molecule drug candidates called vascular disrupting agents (VDAs). Through interaction with vascular endothelial cell cytoskeletal proteins, ZYBRESTAT selectively targets and collapses tumor vasculature, thereby depriving the tumor of oxygen and causing death of tumor cells. In clinical studies, ZYBRESTAT has demonstrated potent and selective activity against tumor vasculature, as well as clinical activity against ATC and other solid tumors.

About OXiGENE

OXiGENE is a clinical-stage biopharmaceutical company developing novel therapeutics to treat cancer and eye diseases. The company’s major focus is developing vascular disrupting agents (VDAs) that selectively disrupt abnormal blood vessels associated with solid tumor progression and visual impairment. OXiGENE is dedicated to leveraging its intellectual property and therapeutic development expertise to bring life-extending and -enhancing medicines to patients.

Safe Harbor Statement

This news release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995. Any or all of the forward-looking statements in this press release may turn out to be wrong. Forward-looking statements can be affected by inaccurate assumptions OXiGENE might make or by known or unknown risks and uncertainties. Additional information concerning factors that could cause actual results to materially differ from those in the forward-looking statements is contained in OXiGENE’s reports to the Securities and Exchange Commission, including OXiGENE’s Form 10-K, 10-Q and 8-K reports. However, OXiGENE undertakes no obligation to publicly update forward-looking statements, whether because of new information, future events or otherwise. Please refer to our Annual Report on Form 10-K for the fiscal year ended December 31, 2006.

A gene called N-Myc leads a double life in certain white blood cells, helping to trigger a cancer called acute myeloid leukemia (AML) under some conditions while triggering apoptosis, or cell suicide, under other conditions, according to results of a mouse study done by investigators at St. Jude Children’s Research Hospital.

“This discovery gives researchers an important insight into N-Myc’s role in human AML and might contribute to new strategies for treating this leukemia or disrupting this gene’s ability to cause it,” said Gerard Grosveld, Ph.D., chair of the St. Jude Department of Genetics and Tumor Cell Biology. Grosveld is senior author of a report on this work that appears in the Nov. 15 issue of “Cancer Research.”

AML is a cancer of immune cells called myeloid cells, which accumulate in bone marrow and replace normal cells, then spread to other parts of the body. This cancer is diagnosed in about 20 percent of children with leukemia. About half of children with AML achieve long-term survival following chemotherapy.

Artificially forcing overexpression of N-Myc in bone marrow cells of mice strongly promotes this type of leukemia; that finding is significant since N-Myc overexpression frequently occurs in human AML.

Previously, researchers had reported that overexpression of N-Myc as a result of amplification of the N-Myc gene occurs in a variety of cancers such as neuroblastoma, a common solid tumor of childhood that arises from nervous system cells; retinoblastoma, a cancer of the eye; and Wilms tumor, a cancer of the kidney. Amplification means that extra copies of the gene are present. Results of research elsewhere suggested but did not prove that N-Myc also plays a role in AML.

In the present study, Grosveld’s team examined the RNA in cancerous white blood cells from 137 St. Jude patients who had favorable, intermediate or unfavorable prognosis and compared those RNA samples to ones obtained from four healthy bone marrow donors. RNA is the decoded form of a gene that cells use as a blueprint to produce the protein coded for by that gene.

The researchers reported that, depending on the type of AML, the level of N-Myc RNA in AML bone marrow was between two and 33 fold higher than in normal bone marrow cells.

The team also showed that myeloid cells that were genetically engineered to overexpress N-Myc became immortalized, or had an unlimited life span. Thus, unlike normal myeloid cells with a limited life span, these immortalized cells continued to produce daughter cells in a culture dish and grew much faster than did normal cells. In addition, the St. Jude researchers showed that immortalization of these cells was associated with a decrease in the level of a protein called transforming growth factor beta and an increase in the level of a protein called JNK.

“Decreased levels of transforming growth factor beta and increased levels of JNK are known to be associated with the transformation of myeloid cells into leukemic cells in humans,” Grosveld said. “So those findings in our lab suggest once again that N-Myc is linked to AML.”

The St. Jude team then investigated the other side of N-Myc’s double life its ability to trigger apoptosis and kill the cell instead of making it reproduce uncontrollably. The researchers showed that when myeloid cells overexpressing N-Myc were placed in culture dishes that lacked an anti-apotosis, growth-promoting protein called IL-3, about 75 percent of the cells died within 24 hours. IL-3 is a type of protein called a cytokine, which stimulates blood progenitor cells in the bone marrow to grow, develop and reproduce. In addition, the cells overexpressing N-Myc significantly reduced the activity of several other proteins that normally work together to prevent apoptosis a known effect of the protein made by the N-Myc gene as well as those made by other Myc genes.

“By eliminating IL-3 from the culture, we were able to unmask the apoptotic effect of N-Myc, which greatly increased cell death,” Grosveld said.

Mice that received bone marrow cells genetically engineered to overexpress N-Myc developed AML and died within 50 days. When leukemic cells were transplanted from those mice into genetically identical mice, the newly transplanted mice died within 28 days.

Grosveld’s team believes that the AML does not result from N-Myc overexpression alone. Instead, the investigators showed that AML requires an additional change in the affected cells because they all overexpressed another gene, called Twist. Twist normally inhibits apoptosis by disrupting an important tumor-suppressing biochemical pathway. When N-Myc is overexpressed, this pathway is activated and triggers cell death, preventing the onset of AML. But when upregulation of Twist suppresses this pro-apoptosis mechanism, the cell continues to multiply. Upregulation is the increased activity of a gene caused by a specific signal.

“This work not only demonstrates the critical role N-Myc plays in AML, but also maps out the cooperation with other genes that blunt N-Myc’s apoptotic effects, thereby tipping the delicate balance between cell death and cancer,” Grosveld said.

Other authors of this report include Hiroyuki Kawagoe, Ayten Kandilci and Tanya Kranenburg (St. Jude).

This work was supported by the National Cancer Institute, a Cancer Center Support Grant and ALSAC.

St. Jude Children’s Research Hospital

St. Jude Children’s Research Hospital is internationally recognized for its pioneering work in finding cures and saving children with cancer and other catastrophic diseases. Founded by late entertainer Danny Thomas and based in Memphis, Tenn., St. Jude freely shares its discoveries with scientific and medical communities around the world. No family ever pays for treatments not covered by insurance, and families without insurance are never asked to pay. St. Jude is financially supported by ALSAC, its fundraising organization. For more information, please visit http://www.stjude.org.

The results of two pivotal Phase III trials, published in this week’s prestigious New England Journal of Medicine, showed that patients with the blood cancer multiple myeloma who were treated with REVLIMID® (lenalidomide) had among the longest median survival rates, the longest time until the disease progressed and the highest response (remission) rate ever reported in a Phase III trial in previously treated multiple myeloma patients.

The international and the US multi-centred, randomized, double-blind, placebo-controlled Phase III studies evaluated REVLIMID® plus dexamethasone and found that:

The median time until the disease progressed for the patients taking REVLIMID® plus dexamethasone was 11.3 months – more than double the time for patients taking dexamethasone plus placebo (4.7 months).

60.2% of the patients taking REVLIMID® plus dexamethasone had a complete or partial response (when signs and symptoms of the cancer disappear) compared with 24% for those on dexamethasone plus placebo NOTEREF Ref182994164 h * MERGEFORMAT 1. The REVLIMID® patients also had a longer lasting response at 16.5 months NOTEREF Ref182994164 h * MERGEFORMAT 1. There was an increase in overall survival rates. The data from the US study showed that patients taking REVLIMID® plus dexamethasone had an estimated median overall survival of 29.6 months versus 20.5 months in the dexamethasone/placebo arm. The median duration of overall survival in lenalidomide plus dexamethasone patients in the international trial has yet to be reached

Multiple myeloma is the second most commonly diagnosed blood cancer. According to the International Myeloma Foundation, there are an estimated 750,000 people with multiple myeloma worldwide. There are approximately 4,000 new cases annually in the UK, which represents about one percent of all newly diagnosed cancers NOTEREF Ref182994573 h * MERGEFORMAT 3 and at any one time there will be just fewer than 8,000 patients with the condition.

Multiple myeloma causes approximately 2,500 deaths each year in the UK NOTEREF Ref182994627 h * MERGEFORMAT 5 accounting for 1 in 70 deaths from cancer in the UK and Ireland. Mortality is high with 45% of patients dying in the first year and 80% within 5 years.

REVLIMID® is the first breakthrough oral cancer therapy for multiple myeloma patients in more than forty years and has been licensed for use in the UK since June 2007.

“The international study evaluating lenalidomide plus dexamethasone demonstrates the effectiveness of this treatment for patients with relapsed or refractory myeloma. Patients who received this treatment had higher response rates, longer remission periods and increased survival, compared with patients who received the control medication, dexamethasone and placebo,” said Dr Kwee Yong, from University College London, one of the UK’s leading multiple myeloma specialist and an investigator on the International Study.

“The data from the two published clinical trials show that REVLIMID® represents a major step forward in helping myeloma become a disease that some people can live with rather than die from. As with so many new cancer therapies, financial restrictions may deprive many patients the benefits offered by this new treatment,” commented Eric Low, Chief Executive of Myeloma UK. “In fact a number of cases have already been brought to our attention by concerned patients. We will do everything we can to help these patients receive the treatments they need.”

“Myeloma is a nasty disease and these impressive clinical data clearly show oral REVLIMID® is a breakthrough therapy offering multiple myeloma patients, who have failed previous therapy, renewed optimism. We will partner with the NHS to demonstrate the value of REVLIMID® to the healthcare system to ensure it is available for patients who need it,” said David Allmond, General Manager of Celgene UK/Ireland.

About Multiple Myeloma

Multiple myeloma (also known as myeloma or plasma cell myeloma) is a cancer of the blood in which malignant plasma cells are overproduced in the bone marrow. Plasma cells are white blood cells that help produce antibodies called immunoglobulins which fight infection and disease. However, most patients with multiple myeloma have cells that produce a form of immunoglobulin called paraprotein (or M protein) that does not benefit the body. In addition, the malignant plasma cells replace normal plasma cells and other white blood cells important to the immune system. The cause of the disease remains unknown and its treatment remains a true unmet medical need.

About REVLIMID®

REVLIMID® (lenalidomide) is a member of a proprietary group of novel immunomodulatory agents known as IMiDs®. In addition to multiple myeloma, REVLIMID® continues to be evaluated in a range of oncological conditions, both in blood cancers and solid tumours. Within the EU, Switzerland, Iceland and Norway,

REVLIMID® has been granted full marketing authorization by the European Commission for use in combination with dexamethasone as a treatment for patients with multiple myeloma who have received at least one prior therapy.

The U.S. Food and Drug Administration (FDA) granted approval of REVLIMID® in combination with dexamethasone as a treatment for patients with multiple myeloma, who have received at least one prior therapy.

About Celgene UK

Celgene UK is a wholly owned subsidiary and international headquarters of Celgene Corporation. Celgene Corporation, headquartered in Summit, New Jersey, is an integrated global pharmaceutical company engaged primarily in the discovery, development and commercialization of innovative therapies for the treatment of cancer and inflammatory diseases through gene and protein regulation. For more information, please visit the Company’s website at http://www.celgene.com.

REVLIMID is a registered trademark of Celgene Corporation.

References:

- Dimopoulos M, et al. Lenalidomide plus dexamethasone for relapsed or refractory multiple myeloma. N Engl J Med; 357: 21, 22 November 2007

- Weber D. et al. Lenalidomide plus dexamethasone for relapsed multiple myeloma in North America. N Engl J Med; 357: 21, 22 November 2007

- International Myeloma Foundation. http://www.Myeloma.org.uk org (accessed November 2007)

- Eric Low. Your essential Guide. http://www.Myeloma.org.uk September 2006

- Globocan 2002. International agency for research on cancer. WWW-dep.iarc.fr. Accessed on June 2007

The International Myeloma Foundation (IMF) – supporting research and providing education, advocacy and support for myeloma patients, families, researchers and physicians – said findings from two large, international clinical trials are good news for myeloma patients, especially patients with active myeloma despite previous treatments. The newly published data demonstrate that with REVLIMID®, an oral cancer drug, all measures of myeloma showed significant and in some cases unprecedented improvement in patients where previous treatments had failed. This includes a median survival of nearly three years (35 months) with REVLIMID, the longest median survival in this difficult to treat patient group. Survival data were presented at the International Myeloma Workshop in June, and for the first time complete details from two Phase 3 clinical trials, one from the US and one from Europe, are being published simultaneously in the current issue of the New England Journal of Medicine.

“REVLIMID saved not just my life, but my quality of life, and with a wife and two young boys at home, that’s a blessing,” said Elijah Alexander, former linebacker with the Oakland Raiders in the National Football League. He began his treatments with Thalomid, had a bone marrow transplant, and has been on REVLIMID for the past six months. “I was diagnosed when I was just 35 years old, too young to leave my wife as a widow and my boys without a father. With REVLIMID I feel good, I coach my boys’ football teams, and when people see me they don’t believe I have cancer because I look and feel so healthy.”

REVLIMID (lenalidomide) from Celgene is the newest of what are called the novel therapies, which along with THALOMID® and VELCADE® have changed the outlook for myeloma patients. These new studies show REVLIMID plus the steroid dexamethasone achieved “superior results” compared to dexamethasone alone “regardless of the history of treatment.” In Europe and the US REVLIMID is being used in myeloma, and in the US it is also approved for a pre-leukemia condition called MDS. It is also being tested in other leukemias and lymphomas and even solid tumors.

“We are pleased that concerted efforts to find effective treatments in what was considered a rare, little-known cancer, have led to drugs like REVLIMID,” said Susie Novis, president and co-founder of the International Myeloma Foundation. “Myeloma has been a difficult disease to cure, but with the novel therapies we are developing effective, long-term treatments by using multiple drugs in sequence and in various combinations. The addition of a drug with the potency of REVLIMID to this equation is especially important.”

Myeloma, also called multiple myeloma, is a cancer of the bone marrow that affects production of red cells, white cells and stem cells. Although once considered a rare disease of the elderly, it is of growing interest and concern. A recent (Oct 15) report from the American Cancer Society shows that the incidence of myeloma is increasing despite a trend toward decreasing cancer rates in recent years. Myeloma is also being diagnosed in younger people so that half of the patients diagnosed today are younger than 60, and increasingly, the disease is detected in patients under the age of 40. At the International Myeloma Foundation, studies with their DNA bank, Bank On A Cure®, point to environmental toxins and pollutants contributing to this spread of myeloma, while better diagnostic capabilities are helping to find more cases earlier in the course of the disease.

“The increasing incidence of myeloma gives us an urgent need for potent treatments to fight myeloma, and these newly published studies show that by all measures, REVLIMID is impressive,” said Brian G.M. Durie, chairman and co-founder of the IMF. “Given current trends we believe these studies will be an important guide to giving patients the most appropriate therapy as early in the course of their disease as possible.”

According to the phase 3 studies in the New England Journal of Medicine, the pattern of responses “suggest that treatment (with REVLIMID) early in the course of the disease may be beneficial.” In addition, the Compendia, the official physician guidelines, were recently updated to add REVLIMID as an initial treatment for myeloma, so patients don’t have to wait until other treatments have failed.

About The International Myeloma Foundation

The International Myeloma Foundation is the oldest and largest myeloma organization, reaching more than 165,000 members in 113 countries worldwide. A 501 (c) 3 non-profit organization dedicated to improving the quality of life of myeloma patients and their families, the IMF focuses in four key areas: research, education, support and advocacy. To date, the IMF has conducted more than 120 educational seminars worldwide, maintains a world-renowned hotline, and operates Bank on a Cure®, a unique gene bank to advance myeloma research. The IMF was rated as the number one resource for patients in an independent survey by the Target Research Group. The IMF can be reached at (800) 452-CURE, or out of the United States at +1 (818) 487-7455.