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Mike Peter's son to take to the stage at Lytham Festival
Mike Peter's son to take to the stage at Lytham Festival

Rhyl Journal

timea day ago

  • Entertainment
  • Rhyl Journal

Mike Peter's son to take to the stage at Lytham Festival

Mike, frontman of The Alarm, had been scheduled to perform on the festival's closing night, Sunday, July 6, ahead of headliners Simple Minds and Texas. Sadly, Mike died on April 29, and The Alarm's appearance was cancelled. Now, a special and heartfelt tribute is being planned for the beloved musician and campaigner involving his youngest son Evan, who will take to the stage to perform a selection of his father's songs. In a statement, Lytham Festival said: "On Sunday, July 6, this year's TK Maxx presents Lytham Festival will host a heartfelt tribute to the beloved musician and campaigner Mike Peters of The Alarm. "Originally scheduled to perform on the festival's closing night before headliners Simple Minds and Texas, The Alarm's appearance was sadly cancelled following Mike's passing in April at the age of 66, after battling an aggressive form of lymphoma. "In a touching celebration of his life and music, Mike's son, Evan Peters, will take to the stage to honour his father's legacy by performing a selection of his songs. "We hope to see you there, and pay tribute together." On Facebook, Jules shared the Lytham Festival post and wrote: 'Father to Son" with a green heart emoji. The couple also share son Dylan. Mike, who lived in Dyserth, died on April 29 from blood cancer at the age of 66 – more than 30 years after he was first diagnosed with chronic lymphocytic leukaemia (CLL) at the age of 36. Lytham Festival in Lancashire is set to feature a star studded line up including Stevie Wonder, Corinne Bailey Rae, Alanis Morissette, Train, Liz Phair, Lottery Winners, Justin Timberlake, Jess Glynne, Dagny, CTRL, Simple Minds, Texas, Cast, A Tribute to the Alarm and Pete Waterman: Hitman DJ Set. It will run from July 3 to July 6.

Mike Peter's son to take to the stage at Lytham Festival
Mike Peter's son to take to the stage at Lytham Festival

North Wales Chronicle

timea day ago

  • Entertainment
  • North Wales Chronicle

Mike Peter's son to take to the stage at Lytham Festival

Mike, frontman of The Alarm, had been scheduled to perform on the festival's closing night, Sunday, July 6, ahead of headliners Simple Minds and Texas. Sadly, Mike died on April 29, and The Alarm's appearance was cancelled. Now, a special and heartfelt tribute is being planned for the beloved musician and campaigner involving his youngest son Evan, who will take to the stage to perform a selection of his father's songs. In a statement, Lytham Festival said: "On Sunday, July 6, this year's TK Maxx presents Lytham Festival will host a heartfelt tribute to the beloved musician and campaigner Mike Peters of The Alarm. "Originally scheduled to perform on the festival's closing night before headliners Simple Minds and Texas, The Alarm's appearance was sadly cancelled following Mike's passing in April at the age of 66, after battling an aggressive form of lymphoma. "In a touching celebration of his life and music, Mike's son, Evan Peters, will take to the stage to honour his father's legacy by performing a selection of his songs. "We hope to see you there, and pay tribute together." On Facebook, Jules shared the Lytham Festival post and wrote: 'Father to Son" with a green heart emoji. The couple also share son Dylan. Mike, who lived in Dyserth, died on April 29 from blood cancer at the age of 66 – more than 30 years after he was first diagnosed with chronic lymphocytic leukaemia (CLL) at the age of 36. Lytham Festival in Lancashire is set to feature a star studded line up including Stevie Wonder, Corinne Bailey Rae, Alanis Morissette, Train, Liz Phair, Lottery Winners, Justin Timberlake, Jess Glynne, Dagny, CTRL, Simple Minds, Texas, Cast, A Tribute to the Alarm and Pete Waterman: Hitman DJ Set. It will run from July 3 to July 6.

BeOne Medicines Showcases Groundbreaking Oncology Pipeline at R&D Day
BeOne Medicines Showcases Groundbreaking Oncology Pipeline at R&D Day

Business Upturn

time6 days ago

  • Business
  • Business Upturn

BeOne Medicines Showcases Groundbreaking Oncology Pipeline at R&D Day

San Carlos, Calif., United States: BRUKINSA, sonrotoclax, and BTK CDAC data, including combinations, are designed to comprehensively address unmet needs across CLL patient populations Promising new data from pipeline assets in breast, lung, and GI cancer franchises, including CDK4 inhibitor, B7-H4 ADC, and novel PRMT5 inhibitor, will be featured Pipeline is at an exciting inflection point with 20 near-term milestones in the next 18 months In a significant showcase for investors, BeOne Medicines Ltd. (NASDAQ: ONC; HKEX: 06160; SSE: 688235), a global oncology company, will announce major advancements to its industry-leading oncology pipeline during today's investor R&D Day. The event comes at a pivotal moment for the Company, which has more than 40 clinical and commercial stage assets in development, a signal of both scale and ambition. 'At BeOne, our mission is simple yet bold: to create the world's first next-generation oncology company,' said John V. Oyler, Co-Founder, Chairman, and CEO. 'What we will unveil demonstrates our progress towards this goal today, and the promise for tomorrow. From our innovative discovery engine to one of the broadest pipelines in oncology, we are well-positioned to bring transformative medicines to patients worldwide—and to do so with speed, quality, and purpose.' BeOne's integrated, end-to-end R&D model is engineered for efficiency without compromise. The Company's differentiated approach—combining in-house discovery targeting unmet patient needs, parallel early-stage exploration at low incremental cost, and rapid proof-of-concept generation—enables swift progression from bench to clinic. Our in-house manufacturing around the world, including our flagship facility in Hopewell, NJ, means we have a sustainable business model, purpose built with competitive advantages. This rigorous model has fueled a pipeline of more than 40 clinical and commercial-stage assets, making it one of the most productive in the industry. To complement this research engine, BeOne has built a robust global clinical development platform, with more than 170 trials conducted across 40 countries and more than 25,000 patients enrolled to date. In hematologic cancers, the Company's program is driven by its wholly-owned assets including BRUKINSA® (zanubrutinib), a second-generation covalent BTK inhibitor and the backbone of the hematology franchise, sonrotoclax, a potential best-in-class next-generation BCL2 inhibitor, and BGB-16673, a BTK CDAC. New clinical data from CaDAnCe-101 highlight the promise of BGB-16673, a potential first-in-class BTK degrader, for patients with relapsed or refractory B-cell malignancies, including chronic lymphocytic leukemia (CLL). Meanwhile, early data show the combination of sonrotoclax and BRUKINSA has demonstrated compelling efficacy and the potential to offer a best-in-class fixed-duration treatment in CLL, setting the stage for a possible new standard of care. In solid tumors, the Company is advancing multiple targeted modalities beyond its foundational PD-1 inhibitor TEVIMBRA® (tislelizumab-jsgr), including CDK4 inhibitor BGB-43395, which has shown clear pharmacodynamic activity and is expected to enter registration-enabling studies for the treatment of breast cancer within the next six to 12 months. Promising new data for the B7-H4 ADC (BG-C9074) point to a potential first-in-class therapeutic option for patients with B7-H4 expressing tumors, including those without selection criteria. Additionally, early data from the novel PRMT5 inhibitor suggest a favorable safety profile and promising efficacy, supporting its potential for differentiation in the competitive lung cancer field. 'Our R&D team is running at full speed,' said Lai Wang, Ph.D., Global Head of R&D. 'With more than 1,200 scientists and more than 3,700 clinical development and medical affairs colleagues dedicated to pushing the boundaries of oncology, we have built the infrastructure, mindset, and capabilities to deliver sustained innovation. The volume of clinical milestones we anticipate over the next few years is extraordinary, and our agility in moving from idea to execution sets us apart.' Speakers at today's event include BeOne's executive leadership team, senior R&D leaders, and distinguished key opinion leaders, offering a multi-faceted view of the Company's scientific strategy and execution momentum. The live webcast begins at 8:30 a.m. U.S. Eastern Time and is available on the investor relations section of BeOne's website, where an archived version will also be accessible. About BeOne BeOne Medicines is a global oncology company domiciled in Switzerland that is discovering and developing innovative treatments that are more affordable and accessible to cancer patients worldwide. With a portfolio spanning hematology and solid tumors, BeOne is expediting development of its diverse pipeline of novel therapeutics through its internal capabilities and collaborations. With a growing global team of more than 11,000 colleagues spanning six continents, the Company is committed to radically improving access to medicines for far more patients who need them. To learn more about BeOne, please visit and follow us on LinkedIn, X, Facebook and Instagram. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 and other federal securities laws, including statements regarding the future success of BeOne's pipeline assets; BeOne's ability to bring transformative medicines to patients worldwide with both speed and quality; the productivity of BeOne's pipeline; the ability of BeOne's assets to provide a new standard of care; the timing for BGB-43395 to enter registration-enabling studies; and BeOne's plans, commitments, aspirations, and goals under the heading 'About BeOne.' Actual results may differ materially from those indicated in the forward-looking statements as a result of various important factors, including BeOne's ability to demonstrate the efficacy and safety of its drug candidates; the clinical results for its drug candidates, which may not support further development or marketing approval; actions of regulatory agencies, which may affect the initiation, timing, and progress of clinical trials and marketing approval; BeOne's ability to achieve commercial success for its marketed medicines and drug candidates, if approved; BeOne's ability to obtain and maintain protection of intellectual property for its medicines and technology; BeOne's reliance on third parties to conduct drug development, manufacturing, commercialization, and other services; BeOne's limited experience in obtaining regulatory approvals and commercializing pharmaceutical products; BeOne's ability to obtain additional funding for operations and to complete the development of its drug candidates and maintain profitability; and those risks more fully discussed in the section entitled 'Risk Factors' in BeOne's most recent quarterly report on Form 10-Q, as well as discussions of potential risks, uncertainties, and other important factors in BeOne's subsequent filings with the U.S. Securities and Exchange Commission. All information in this press release is as of the date of this press release, and BeOne undertakes no duty to update such information unless required by law. To access BeOne media resources, please visit ourNewsroom. View source version on Disclaimer: The above press release comes to you under an arrangement with Business Wire. Business Upturn takes no editorial responsibility for the same. Ahmedabad Plane Crash

Current and Breakthrough Treatments for Chronic Lymphocytic Leukemia (CLL)
Current and Breakthrough Treatments for Chronic Lymphocytic Leukemia (CLL)

Health Line

time20-06-2025

  • Health
  • Health Line

Current and Breakthrough Treatments for Chronic Lymphocytic Leukemia (CLL)

Key takeaways Chronic lymphocytic leukemia (CLL) is a slow-growing cancer of the immune system. Because it's slow growing, many people with CLL won't need to start treatment for many years after their diagnosis. Once the cancer begins to grow, many treatment options are available that can help people go into remission. This means people can experience long periods of time when there's no sign of cancer in their bodies. While there's no cure for CLL yet, breakthroughs in the field are on the horizon. A large number of approaches are under investigation to treat CLL, including drug combinations and CAR T-cell therapy. Chronic lymphocytic leukemia (CLL) is a slow-growing cancer of the immune system. Because it's slow-growing, many people with CLL won't need to start treatment for many years after their diagnosis. Once the cancer begins to grow, there are many available treatment options that can help people achieve remission. This means people can experience long periods of time when there's no sign of cancer in their bodies. The exact treatment option that you'll receive depends on a variety of factors. This includes: whether your CLL is symptomatic the stage of the CLL, based on results of blood tests and a physical exam your age your overall health While there's no cure for CLL yet, breakthroughs in the field are on the horizon. Treatments for low risk CLL Doctors typically stage CLL using a system called the Rai system. Low risk CLL describes people who fall in 'stage 0' under the Rai system. In stage 0, the lymph nodes, spleen, and liver are not enlarged. Red blood cell and platelet counts are also near normal. If you have low risk CLL, your doctor (usually a hematologist or oncologist) will likely advise you to ' watch and wait ' for symptoms. This approach is also called active surveillance. Someone with low risk CLL may not need further treatment for many years. Some people will never need treatment. You'll still need to see a doctor for regular checkups and lab tests. Treatments for intermediate or high risk CLL Intermediate risk CLL describes people with stage 1 to stage 2 CLL, according to the Rai system. People with stage 1 or 2 CLL have enlarged lymph nodes and potentially an enlarged spleen and liver but close to normal red blood cell and platelet counts. High risk CLL describes patients with stage 3 or stage 4 cancer. This means you may have an enlarged spleen, liver, or lymph nodes. Low red blood cell counts are also common. In the highest stage, platelet counts may be low as well. If you have intermediate or high risk CLL, your doctor will likely recommend that you start treatment right away. Chemotherapy and immunotherapy In the past, the standard treatment for CLL included a combination of chemotherapy and immunotherapy agents, such as: a combination of fludarabine and cyclophosphamide (FC) FC plus an antibody immunotherapy known as rituximab (Rituxan) for people younger than 65 bendamustine (Treanda) plus rituximab for people older than 65 chemotherapy in combination with other immunotherapies, such as alemtuzumab (Campath), obinutuzumab (Gazyva), and ofatumumab (Arzerra). These options may be used if the first round of treatment doesn't work. Targeted therapies Over the last few years, a better understanding of the biology of CLL has led to a number of more targeted therapies. These drugs are called targeted therapies because they're directed at specific proteins that help CLL cells grow. Examples of targeted drugs for CLL include: zanubrutinib (Brukinsa): Approved by the Food and Drug Administration (FDA) in 2023, zanubrutinib targets the enzyme known as Bruton's tyrosine kinase (BTK), which is crucial for CLL cell survival. ibrutinib (Imbruvica): This targets BTK with less precision than zanubrutinib. venetoclax (Venclexta): This used in combination with obinutuzumab (Gazyva), targets the BCL2 protein, a protein seen in CLL. idelalisib (Zydelig): This blocks the kinase protein known as PI3K and is used for relapsed CLL. duvelisib (Copiktra): This also targets PI3K but is typically used only after other treatments fail. acalabrutinib (Calquence): This is another BTK inhibitor approved in late 2019 for treating CLL. Monoclonal antibody therapies Monoclonal antibody therapies are a type of treatment in which proteins are made in a laboratory and designed to target certain antigens. They help jolt your immune system into attacking the cancer cells. There are several monoclonal antibody treatments approved for treating CLL by targeting the antigens CD20 and CD52: rituximab (Rituxan): targets CD20, often used with chemotherapy or targeted therapy as part of the initial treatment or in the second-line treatment obinutuzumab (Gazyva): targets CD20, used with venetoclax (Venclexta) or chlorambucil (Leukeran) for patients with previously untreated CLL ofatumumab (Arzerra): targets CD20, usually used in patients whose disease has not responded to prior treatments and is given in combination with chlorambucil (Leukeran) or FC alemtuzumab (Campath): targets CD52 Blood transfusions You may need to receive intravenous (IV) blood transfusions to increase blood cell counts. Radiation Radiation therapy uses high-energy particles or waves to help kill cancer cells and shrink painful, enlarged lymph nodes. Radiation therapy is rarely used in CLL treatment. Stem cell and bone marrow transplants Your doctor may recommend a stem cell transplant if your cancer doesn't respond to other treatments. A stem cell transplant allows you to receive higher doses of chemotherapy to kill more cancer cells. Higher doses of chemotherapy can cause damage to your bone marrow. To replace these cells, you'll need to receive additional stem cells or bone marrow from a healthy donor. Breakthrough treatments A large number of approaches are under investigation to treat people with CLL. Some have been recently approved by the FDA. Drug combinations In May 2019, the FDA approved venetoclax (Venclexta) in combination with obinutuzumab (Gazyva) to treat people with previously untreated CLL as a chemotherapy-free option. In April 2020, the FDA approved a combination therapy of rituximab (Rituxan) and ibrutinib (Imbruvica) for adult patients with chronic CLL. These combinations make it more likely that people may be able to do without chemotherapy altogether in the future. Nonchemotherapy treatment regimens are essential for those who can't tolerate harsh chemotherapy-related side effects. CAR T-cell therapy One of the most promising future treatment options for CLL is CAR T-cell therapy. CAR T-cell therapy, which stands for chimeric antigen receptor T-cell therapy, uses a person's own immune system cells to fight cancer. The procedure involves extracting and altering a person's immune cells to better recognize and destroy cancer cells. The cells are then put back into the body to multiply and fight off the cancer. CAR T-cell therapy research is still ongoing. In September 2023, researchers reported a possible 'universal' CAR T-cell treatment that may be effective in all types of blood cancers. CAR T-cell therapies are promising, but they do carry risks. One risk is a condition called cytokine release syndrome. This is an inflammatory response caused by the infused CAR T-cells. Some people can experience severe reactions that may lead to death if not quickly treated. Other drugs under investigation Some other targeted drugs currently being evaluated in clinical trials for CLL include: entospletinib (GS-9973) tirabrutinib (ONO-4059 or GS-4059) cirmtuzumab (UC-961) ublituximab (TG-1101) pembrolizumab (Keytruda) nivolumab (Opdivo) Once clinical trials are completed, some of these drugs may be approved for treating CLL. Talk with a doctor about joining a clinical trial, especially if current treatment options aren't working for you. Clinical trials evaluate the efficacy of new drugs as well as combinations of already approved drugs. These new treatments may work better for you than the ones currently available. Hundreds of clinical trials are ongoing for CLL.

Genetics or Microenvironment: What Drives CLL Progression?
Genetics or Microenvironment: What Drives CLL Progression?

Medscape

time19-06-2025

  • Health
  • Medscape

Genetics or Microenvironment: What Drives CLL Progression?

MILAN — Is chronic lymphocytic leukemia (CLL) progression primarily driven by genetic mutations or by external cues from the tumor microenvironment? Despite major strides in targeted therapies, CLL remains incurable, prompting renewed scrutiny of whether intrinsic genetic alterations or extrinsic cellular forces hold the key to more effective, lasting treatment. This central question took the spotlight at the 2025 European Hematology Association (EHA) Annual Congress, sparking a lively debate among leading CLL researchers. Most therapies have targeted intrinsic molecular features of leukemic cells, such as BCL2 and BTK. But the lack of robust responses to immunotherapy suggests that external factors such as the tumor microenvironment may also play a role. 'The debate dates back to at least 1999,' said session chair Silvia Deaglio, MD, PhD, director of the Immunogenetics and Transplant Biology Service, City of Health and Science of Turin, Italy in an interview with Medscape Medical News . 'That year, two landmark papers showed that mutations in IGHV [immunoglobulin heavy chain variable region] genes were a favorable prognostic marker, supporting a genetic model. But those same studies also identified an unfavorable prognostic marker in a molecule linked to how CLL cells interact with their environment, suggesting a role for the microenvironment as well.' Genetic Drivers Take Center Stage Eugen Tausch, MD, PhD, researcher at the University of Ulm, Germany, argued in favor of genetics as the primary driver. 'All CLLs have at least one genetic driver, and IGHV mutation status is a fundamental and stable biomarker,' he said. This mutation status affects multiple cellular mechanisms, including immune evasion, anti-apoptotic signaling, and B-cell receptor function. It also modulates how cells respond to cues from their environment, reinforcing the need to consider IGHV when studying microenvironmental influences. But IGHV is just one piece of the puzzle, Tausch added. More than 200 genetic drivers have been identified in CLL. Roughly 90% of cases harbor at least one gene mutation or chromosomal aberration that affects DNA repair, cell cycle regulation, metabolism, RNA processing, and intracellular signaling. 'These alterations have clear clinical implications,' he said. 'Resistance to BTK and BCL2 inhibitors often arises through mutations at the drug-binding site, establishing a direct link between genetics and therapy failure.' Understanding and tracking clonal genetic evolution is thus key to risk stratification, treatment planning, and anticipating disease trajectory, he concluded. The Microenvironment's Role in Early Disease Although CLL has long been seen as a genetically driven malignancy, new data suggest a more nuanced picture in which the tumor microenvironment influences early clonal dynamics. 'We know mutations drive disease progression, especially under therapeutic pressure, but the triggers of these mutations are less clear,' said John Gribben, MD, DSc, Hamilton Fairley Professor of Medical Oncology at Barts Cancer Institute, Queen Mary University of London, UK, who argued in favor of the microenvironment. Accumulation of mutations with age, oxidative stress, antigenic stimulation, and rare inherited factors have all been proposed, but these likely act in concert with tumor microenvironment signals to promote early clonal expansion, he explained. In lymph nodes and bone marrow, CLL cells interact with a milieu of stromal and nurse-like cells, dysfunctional T cells, and dendritic cells, along with a variety of cytokines and chemokines. Recent studies have shown that early clonal evolution primarily occurs in lymph nodes and is associated with a suppressed T-cell inflammatory response. A small subpopulation of lymph node-activated CLL cells engages with the microenvironment to drive disease progression and possibly influence mutation patterns. Moreover, therapies that disrupt microenvironmental interactions have shown efficacy by blocking B-cell receptor signaling and impairing chemokine-mediated trafficking. Even while advocating for the microenvironment's role, Gribben proposed a hybrid model. 'Genetic lesions set the stage, but microenvironmental forces shape their emergence and survival. Early on, extrinsic factors dominate. Later, clonal evolution and genetic resistance take over.' A New Paradigm of Coexistence Both speakers emphasized the need to move beyond binary models of CLL progression. 'The data support a dynamic interplay,' Deaglio told Medscape Medical News . 'The long-term coexistence between leukemic cells and their environment in CLL alters both cell behavior and immune function.' She noted that the T-cell compartment becomes tolerogenic, showing expansion of regulatory T cells and memory effector cells, among other markers. The debate also touched on the progression from monoclonal B-cell lymphocytosis to CLL and on Richter transformation, reinforcing the need for an integrated understanding of intrinsic and extrinsic disease drivers. Deaglio underlined that researchers are now exploring whether treatment-resistant patients could benefit from new drugs or combinations and whether therapy could eventually be administered for fixed durations rather than continuously until progression. 'Progression is genetically driven,' said Deaglio. 'But single-cell sequencing shows that some leukemic cells carry the features that enable future expansion a long time before the disease is diagnosed. Why some clones grow while others do not may depend on the environment they find themselves in.' Gribben concluded, 'To treat CLL effectively, and maybe reach a cure, we'll need to combine immune-based approaches with current targeted therapies.' Deaglio reported no relevant financial relationships. Tausch reported industry affiliations with AbbVie, BeiGene, Lilly, AstraZeneca, Roche, and Janssen-Cilag. Gribben reported research funding from AstraZeneca, BMS/Celgene, and Janssen; clinical trials with AbbVie, Celgene, Epizyme, Gilead, Genmab, Janssen, Merck, MorphoSys, Pharmacyclics, Regeneron, Roche/Genentech, and Takeda; consultancy for AbbVie, Amgen, AstraZeneca, BeiGene, BSM/Celgene, Janssen, Kite Gilead, and Takeda; and honoraria from AbbVie, AstraZeneca, BeiGene, BSM/Celgene, Janssen, Kite Gilead, and Novartis.

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