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Medscape
3 hours ago
- Health
- Medscape
Radiation Bridging in CAR T: Where Are We Now?
While the use of radiation bridging therapy (BT) in chimeric antigen receptor (CAR) T-cell therapy for blood cancer is expanding, plenty of unanswered questions remain on topics such as ideal timing and doses, a radiologist cautioned hematologist colleagues . The lack of guidelines has immediate clinical implications, said John P. Plastaras, MD, PhD, professor of radiation oncology at the Hospital of the University of Pennsylvania, Philadelphia, in a presentation at 18th International Conference on Malignant Lymphoma (ICML) 2025 in Lugano, Switzerland . ' This actually just came up the other day when one of our medical colleagues said, 'I'm really worried about this patient. They're ready for CAR T cell, but I think you need to radiate this area. Can you do it a week after [therapy]?' The answer is, 'We don't know.'' On the other hand, clinicians now have clarity about safety and interaction with CAR T-cell therapy, he noted, and data is coming in rapidly. Here are some questions and answers about radiation BT: What is BT in CAR T-cell therapy? BT refers to treatment that provides a 'bridge' for patients between the components of CAR T-cell therapy. As a 2024 report about BT in hematologic cancer explained, the treatment 'is delivered after leukapheresis for CAR T-cells' — the process in which white cells are removed from a patient's blood, which is then returned to the body — 'has been completed and before lymphodepleting chemotherapy and CAR T-cell infusion.' The report said 'patients who receive BT are predominantly those with a higher disease burden and rapidly progressive disease. These patients tend to have worse overall outcomes, likely related to their aggressive underlying disease.' Where does radiation fit into BT? According to the 2024 report, 'combination chemoimmunotherapy has typically been the form of BT that is used most often.' Targeted therapy is another option, the report said, although data is from 'very small sample sizes.' And then there's radiation, which the report said is useful 'particularly in patients with limited sites of disease or patients who are at risk for structural complications such as airway compromise or renal dysfunction.' What do we know about radiation's efficacy? The first oral report on bridging radiation in CAR T-cell therapy only appeared in 2018, Plastaras said, followed by the first published report in 2019. Despite this fairly short time period, 'we are certainly seeing a lot of new data,' Plastaras said. He highlighted the newly released International Lymphoma Radiation Oncology Group (ILROG) study of radiation BT in conjunction with CAR T-cell therapy for relapsed/refractory B-cell lymphomas. The retrospective study of 172 patients at 10 institutions treated from 2018 to 2020 showed that 1- and 2-year progression-free survival (PFS) rate was 43% (95% CI, 36-51) and overall survival rate was 38% (95% CI, 30-45). In a multivariable model, comprehensive radiation BT was linked to superior PFS than focal therapy (hazard ratio, 0.38; 95% CI, 0.22-0.63; P < .001). 'Comprehensive radiation was a very strong predictor for improved PFS, but we did not see was a huge dose effect,' said Plastaras, who coauthored the study. What about toxicity? Questions about other clinical matters were resolved prior to 2022, he said, when CAR T-cell therapy was used primarily in third line and later settings . 'Does radiation cause excess toxicities?' he asked. 'A lot of the single-institution studies answered that, and I think most medical oncologists and hematologists are okay with this idea that radiation isn't causing a lot of excess toxicities.' As for whether radiation interferes with the effectiveness of CAR T-cell therapy, 'the data to this point have demonstrated that probably not,' he said. 'We've probably put that one to bed.' What do we know about treatment timing? 'The timing question is still quite open,' Plastaras said. 'How much time should there be between radiation and lympho-depleting chemotherapy? Is it better to put the radiation very close to the CAR T-cell [therapy] so this priming effect might happen, or can that happen weeks in advance? We don't know the answers to those.' According to Plastaras, researchers are still trying to understand the role radiation the consolidation period after CAR T-cell therapy. 'If we wait for day-30 PET [scan], is that OK? Do we need to wait longer? Are we going to mess up the lymph nodes that have CAR T-cells floating around in them?' What about doses and imaging? There's also a lack of insight into technical questions about radiation dose and fractionation. 'The [radiation] volume question is one of key importance. Do we just do gross disease? Do we treat all the other small spots out there, and importantly, do we treat regional nodes or not? We get these questions all the time.' The role of imaging is also unclear, he said, in terms of timing during and after bridging radiation therapy and after CAR T-cell therapy. What do we need to learn about now? Looking forward, Plastaras outlined what he called 'version 2.0' questions for the evolving field: Can radiation rebulking decrease CAR-T cell toxicities? Will very low dose 'priming' radiation affect outcomes? He highlighted other questions: Can radiation be part of a combined modality approach in limited stage relapsed/refractory disease? Should central nervous system lymphoma be treated differently? When will we get new guidelines? According to Plastaras, Memorial Sloan Kettering Cancer Center Radiology Oncologist Brandon Imber,MD, MA, in New York City, is leading a new ILROG guideline project with the intention of publishing details in the journal Blood . 'This is a work in progress,' Plastaras said. 'Our target is 2025 to at least get something submitted.'
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Business Standard
23-06-2025
- Business
- Business Standard
India Cements shares gain 5% in weak market; here's why stock is in demand
India Cements shares jumped 4.7 per cent in trade on Monday (June 23, 2025), logging an intraday high at ₹318.5 per share on BSE. At 9:58 AM, India Cements share price was trading 2.15 per cent higher at ₹310.75 per share on the BSE. In comparison, the BSE Sensex was down 1.02 per cent at 81,563.81. The company's market capitalisation stood at ₹9,630.06 crore. Its 52-week high was at ₹385.5 per share and 52-week low was at ₹223.7 per share. CATCH STOCK MARKET UPDATES TODAY LIVE What led to the rally in India Cements stock despite a weak market? The buying on the counter came after the company announced to sell its entire equity investment held in Industrial Chemicals and Monomers Limited (ICML), a subsidiary of the company. Upon completion of the said sale, ICML would cease to be a subsidiary. The sale is proposed at ₹97.68 crore and is expected to be completed within a period of six months from the date of the agreement. The company will enter into an agreement with Mirai Sensing Private Limited, the proposed buyer upon finalisation of terms. Another development that boosted the rally was Franklin Templeton Mutual Fund bought 2.04 million shares at ₹310.17 per share, according to the National Stock Exchange (NSE) block deal data. ALSO READ | About India Cements India Cements Limited is a subsidiary of UltraTech Cement Limited. UltraTech is the cement flagship company of the Aditya Birla Group and is the largest manufacturer of grey cement and ready mix concrete (RMC) and one of the largest manufacturers of white cement in India. India Cements was acquired by UltraTech on December 24, 2024. India Cements Ltd was founded in 1946 by Shri S N N Sankaralinga Iyer and Shri T S Narayanaswami. The company set up its first cement plant in 1949 at Sankarnagar located in Talaiyuthu, a tiny hamlet in Tirunelveli district, Tamil Nadu. From a two-plant company having a capacity of just 1.3 million tonnes in 1989, India Cements has grown robustly to a total current cement production capacity of 14.45 million tonnes per annum. India Cements has eight integrated cement plants in Tamil Nadu, Telangana, Andhra Pradesh and Rajasthan, and one grinding unit in Tamil Nadu.
Time of India
22-06-2025
- Business
- Time of India
India Cements to sell Industrial Chemicals to Mirai for 98 crore
CHENNAI: India Cements is selling its subsidiary Industrial Chemicals and Monomers (ICML) to Mirai Sensing for Rs 97.7 crore. The company will enter into an agreement with Chennai-based Mirai Sensing and complete the sale within six months from the date of agreement, India Cements informed the stock exchange. India Cements board at its meeting, on Saturday, approved the sale of its entire equity investment held in ICML. After completion of the sale, ICML would cease to be its subsidiary, the regulatory filing added. Stay informed with the latest business news, updates on bank holidays and public holidays . AI Masterclass for Students. Upskill Young Ones Today!– Join Now
Medscape
20-06-2025
- Health
- Medscape
DLBCL: Tumor Cell Signatures Predict CAR-T Success
Traits of noncancerous cells in diffuse large B-cell lymphoma (DLBCL) tumors appear to offer insight into which patients will benefit the most from chimeric antigen receptor (CAR) T-cell therapy, researchers reported at the 18th International Conference on Malignant Lymphoma (ICML) 2025 in Lugano, Switzerland, and in a simultaneously published study in Cancer Cell . An analysis of DLBCL tumor cells led by investigators from MD Anderson Cancer Center in Houston and Washington University School of Medicine in St Louis, Missouri, identified three 'lymphoma microenvironment archetype profiles' — two that are abnormal and one that is in the normal range. The research suggests that 'diffuse large B-cell lymphoma patients who have this normal lymph node environment are those most likely to benefit from CAR T-cell therapy. This may be a very useful predictive biomarker to select patients who would really benefit from this treatment,' said discussant Stephen M. Ansell, MB ChB, PhD, chair of Hematology at Mayo Clinic, Rochester, Minnesota, at an ICML session where the findings were presented. Defining the Lymphoma 'Microenvironment' The researchers launched the study to better understand the lymphoma microenvironment, defined as 'all of the nontumor cells that define the architecture and immune state of DLBCLs,' said co-author Michael R. Green, PhD, associate professor and vice chair for Research, Department of Lymphoma/Myeloma, Division of Cancer Medicine, University of Texas MD Anderson Cancer Center, in an interview. 'With the introduction of T-cell engaging therapies and cellular therapies, which are currently used in the relapsed/refractory setting and are likely primarily influenced by the immune microenvironment, we saw a need to provide a comprehensive map of immune and nonimmune cells within DLBCLs,' Green said. The focus, he said, is on 'how they are assembled into reproducible microenvironment archetypes and how these relate to outcome in patients treated with cellular therapy.' Using single-nucleus multiome sequencing, researchers analyzed cells from 232 tumors and 232 control tissues. At the ICML presentation, study co-author David A. Russler-Germain, MD, PhD, instructor, Division of Oncology, Washington University School of Medicine, Siteman Cancer Center/Barnes-Jewish Hospital, St. Louis, Missouri, said three archetypes of cells were identified: FMAC archetype (37% of tumors): 'Characterized by a sparsity of T/K [T/natural killer] cells and an overrepresentation of cancer-associated fibroblasts and macrophages' (37% of tumors): 'Characterized by a sparsity of T/K [T/natural killer] cells and an overrepresentation of cancer-associated fibroblasts and macrophages' LN archetype (33% of tumors): 'Characterized by naive and memory T cells together with lymph node architecture cell types' (33% of tumors): 'Characterized by naive and memory T cells together with lymph node architecture cell types' TEX archetype (30% of tumors): 'Characterized by an abundance of CD8+ T cells with markers of exhaustion' Dramatic Differences in CAR-T Response Rates Researchers applied the data to the ZUMA-7 clinical trial, which compared CAR-T cell therapy to standard chemotherapy, and found signs that the archetypes had predictive power. Patients with the LN archetype — resembling normal lymph node architecture — had the best outcomes with CAR-T therapy, achieving 67% progression-free survival at 1 year. FMAC and TEX archetypes had much lower success rates of 43% and 35%, respectively. 'The key data related to outcome is that LN archetype patients highly benefit from CAR T, FMAC patients have a diminished benefit, but it is still significantly better than standard of care, and TEX patients have no significant benefit to CAR T compared to standard of care,' Green said. 'This is the first biological subgroup of patients shown clearly not to benefit from CAR T with underlying biology that provides direct and targetable mechanisms of resistance.' Implications for Personalized Treatment As the study noted, the introduction of CAR T-cell therapy as a second-line therapy in DLBCL 'has significantly improved outcomes and leads to durable responses beyond 2 years in > 40% of patients. Nevertheless, most patients will not have durable benefit from [CAR T], highlighting a critical need to understand factors influencing response.' According to Green, the findings suggest that CAR T-cell therapy could be tailored for each archetype. 'LN patients will likely have good outcomes with CAR T alone, whereas FMAC patients have a cold microenvironment that may benefit from 'microenvironment priming' prior to CAR T, and TEX patients may require combination of CAR T cells with other agents such as interferon gamma and checkpoint-blocking antibodies.' The study's classification system, known as LymphoMAP, is not yet available in the clinic. However, it 'will be prospectively evaluated in interventional trials using microenvironment-guided therapeutic strategies using CAR-T or bispecific antibodies as a backbone,' Green said. Moving forward, discussant Ansell said, 'there is a great opportunity look at the good outcome group and say, 'What is it about them that causes about half of those patients to subsequently progress or die and not do as well as what we would hope?' How could we make that top group, the responding group, do even better?' This research was funded by the Schweitzer Family, the MD Anderson Lymphoid Malignancies Program and the National Cancer Institute. Green is a scholar of the Leukemia and Lymphoma Society, and two authors are supported by fellowships from the Lymphoma Research Foundation.
Yahoo
12-06-2025
- Business
- Yahoo
Dizal Showcases Two First-in-Class Therapies in Hematologic Malignancies at EHA and ICML 2025
Golidocitinib demonstrated promising efficacy in maintaining and enhancing tumor response in peripheral T-cell lymphoma (PTCL) post first-line therapy with a 24-month disease-free survival (DFS) rate of 74.2% DZD8586 exhibited significant antitumor activity in heavily pretreated chronic lymphocytic leukemia / small lymphocytic lymphoma (CLL/SLL) patients with an objective response rate (ORR) of 84.2% Both golidocitinib and DZD8586 will be featured in oral presentations at ICML 2025, with DZD8586 also presented in an oral session at ASCO 2025 SHANGHAI, June 12, 2025 /PRNewswire/ -- Dizal (SSE:688192), a biopharmaceutical company committed to developing novel medicines for the treatment of cancer and immunological diseases, announced that it will present research findings on two of its first-in-class hematologic oncology assets—golidocitinib and DZD8586—at the 2025 European Hematology Association (EHA) Annual Congress and the 18th International Conference on Malignant Lymphoma (ICML). These include long-term follow-up data on golidocitinib as a maintenance therapy in peripheral T-cell lymphoma (PTCL) after first-line systemic therapy and pooled analysis results for DZD8586 in chronic lymphocytic leukemia / small lymphocytic lymphoma (CLL/SLL), both selected for oral presentations at ICML. Golidocitinib Shows Potential to Significantly Improve Patient Outcomes in PTCL PTCL patients who achieved tumor response with first-line standard therapy will relapse. Approximately 40% of patients with complete response and 80% with partial response experienced disease progression within 2 years after initial tumor response, and the prognosis of these relapsed patients was very poor. The 24-month follow-up results from JACKPOT26, a prospective, multicenter Phase 2 clinical study of golidocitinib will be unveiled at EHA and featured as an oral presentation at ICML. The data suggest that golidocitinib showed promising efficacy in maintaining and enhancing tumor response with an acceptable and manageable safety profile in patients with PTCLs post first-line therapies. In Cohort 1 (patients with complete response), the 24-month disease-free survival (DFS) rate reached 74.2%, with consistent efficacy observed across different subtypes. In Cohort 2 (patients with partial response), the complete response rate (CRR) was 50.0%, the median duration of response (DoR) was 23.9 months, and the median progression-free survival (PFS) was 17.4 months, with the longest PFS reaching 35.9 months and the patient was still responding. "Golidocitinib, a next-generation oral and highly selective JAK1 inhibitor, addresses a critical unmet need for effective maintenance therapy following first-line treatment in PTCL," said Professor Jie Jin, lead principal investigator of the JACKPOT26 study at the First Affiliated Hospital of Zhejiang University School of Medicine. "Its unique mechanism of action not only delivers strong anti-tumor activity—allowing 50% of patients with partial remission (PR) to achieve complete remission (CR)—but also modulates the tumor immune microenvironment through its anti-inflammatory and immunomodulatory effects. These unique features help delay relapse and extend survival, positioning golidocitinib as a highly promising option for maintenance therapy in PTCL." In addition, golidocitinib has shown encouraging antitumor activities and favorable safety profiles in combination with CHOP in 1st line PTCL patients, as well as in rare T-cell lymphoma subtypes, including relapsed/refractory T-cell large granular lymphocytic leukemia (r/r T-LGLL) and monomorphic epitheliotropic intestinal T-cell lymphoma (MEITL). Further studies are warranted to validate the results. DZD8586 Overcomes Multi-Drug Resistance in CLL and other B-NHL A pooled analysis of two phase I/II studies of DZD8586 in CLL/SLL patients previously treated with covalent/non-covalent Bruton's Tyrosine Kinase (BTK) inhibitors and BTK degraders was presented in an oral session at the 2025 American Society of Clinical Oncology (ASCO) Annual Meeting and will be presented at EHA. Subgroup analyses will be presented as an oral presentation at ICML. In heavily pretreated CLL/SLL, DZD8586 achieved an ORR of 84.2%. Tumor response with a manageable safety profile was observed irrespective of prior covalent/non-covalent BTKi, BTK degrader, or BCL-2 inhibitor treatment, and in patients with classic BTK resistance mutations (C481X) as well as other BTK mutations, including kinase-dead mutations. No drug-related bleeding, atrial fibrillation, or major cardiac events observed. A Phase II study of DZD8586 monotherapy in relapsed/refractory diffuse large B-cell lymphoma (r/r DLBCL) will also be presented at EHA and ICML. Clinical activities from small molecule targeted drugs such as BTK inhibitors have been less than desired for the treatment of DLBCL. Compensatory or redundant pathway activation could be one of the main escape mechanisms. DZD8586, a novel LYN/BTK dual inhibitor, is designed to overcome these limitations by blocking both BTK and LYN signaling pathways, and thus potentially improve therapeutic outcomes. At recommended phase 2 doses (RP2Ds) of 50 mg and 75 mg QD, DZD8586 monotherapy demonstrated promising anti-tumor activity in r/r DLBCL. The majority of patients showed target lesion shrinkage, with a CRR of 35.5%. Complete responders showed durable responses, with 81.8% of patients remaining in response and the median DoR was not reached. Notably, it showed efficacy in both GCB and non-GCB subtypes, supporting its broad therapeutic potential. Dr. Xiaolin Zhang, CEO of Dizal, remarked, "We are excited that golidocitinib and DZD8586 have demonstrated promising potential in PTCL and B-cell non-Hodgkin lymphoma (B-NHL), two areas with substantial unmet clinical needs. The selection of multiple studies for oral presentations at global leading conferences represents a strong recognition of our capabilities in research and development and further affirms our commitment to bringing transformative therapies to patients worldwide." About golidocitinib (DZD4205)Golidocitinib is currently the first and only Janus kinase 1 (JAK1) selective inhibitor being evaluated for the treatment of r/r PTCL. In June 2024, golidocitinib was approved by the National Medical Products Administration (NMPA) of China for the treatment of adult patients with relapsed or refractory peripheral T-cell lymphoma (r/r PTCL). At the data cut-off date of August 31, 2023, golidocitinib has demonstrated robust and durable anti-tumor efficacy, with an ORR of 44.3%. All subtypes benefited well, and the ORR of common subtypes exceeded 40%. More than 50% of the patients with tumor remission achieved a complete response with a CRR of 23.9%. Per IRC assessment, the median duration of response (mDoR) reached 20.7 months. As of February 2024, golidocitinib showed a median overall survival (mOS) of 24.3 months. Golidocitinib was granted Fast Track Designation by the U.S. FDA for the treatment of r/r PTCL in February 2022. In September 2023, the CDE accepted its NDA and granted Priority Review for the treatment of r/r PTCL. The Phase I clinical data of golidocitinib (JACKPOT8 PART A) were published in Annals of Oncology (Impact Factor: 51.8), and global pivotal trial data of golidocitinib for the treatment of r/r PTCL (JACKPOT PART B) were published in The Lancet Oncology (Impact Factor: 54.4). About DZD8586DZD8586 is a first-in-class, non-covalent, LYN/BTK dual inhibitor with full blood-brain barrier (BBB) penetration, designed as a potential treatment option for B-cell non-Hodgkin lymphoma (B-NHL). While Bruton's Tyrosine Kinase (BTK) inhibitors have been approved for the treatment of B-NHL, resistance can arise through two major mechanisms: the BTK C481X mutation and BTK-independent BCR signaling pathway activation. Currently, there is no targeted therapy available to address both resistance mechanisms, posing an urgent clinical challenge. Although BTK degraders have shown encouraging efficacy in early clinical studies, mutation-related resistance has been reported, and degrader-related toxicities may affect long-term clinical application. DZD8586 has high selectivity against other TEC family kinases (TEC, ITK, TXK and BMX). By targeting BTK and LYN, it blocks both BTK-dependent and -independent BCR-signaling pathways, effectively inhibiting tumor growth of B-NHLs in cell lines and in animal models. Phase I clinical trial suggests that DZD8586 exhibits favorable PK properties, good central nervous system (CNS) permeability, complete blockade of BCR signaling, and encouraging anti-tumor efficacy with good safety and tolerability in patients with B-NHL. About DizalDizal is a biopharmaceutical company, dedicated to the discovery, development and commercialization of differentiated therapeutics for the treatment of cancer and immunological diseases. The company aims to develop first-in-class and groundbreaking new medicines, and further address unmet medical needs worldwide. Deeply rooted in translational science and molecular design, it has established an internationally competitive portfolio with two leading assets in global pivotal studies, both of which have already been launched in China. To learn more about Dizal, please visit or follow us on Linkedin or X. Forward-Looking StatementsThis news release may contain certain forward-looking statements that are, by their nature, subject to significant risks and uncertainties. The words "anticipate", "believe", "estimate", "expect", and "intend" and similar expressions, as they relate to Dizal, are intended to identify certain forward-looking statements. Dizal does not intend to update these forward-looking statements regularly. These forward-looking statements are based on the existing beliefs, assumptions, expectations, estimates, projections, and understandings of the management of Dizal with respect to future events at the time these statements are made. These statements are not a guarantee of future developments and are subject to risks, uncertainties, and other factors, some of which are beyond Dizal's control and are difficult to predict. Consequently, actual results may differ materially from information contained in the forward-looking statements as a result of future changes or developments in our business, Dizal's competitive environment, and political, economic, legal, and social conditions. Dizal, the Directors, and the employees of Dizal assume (a) no obligation to correct or update the forward-looking statements contained on this site; and (b) no liability in the event that any of the forward-looking statements does not materialize or turnout to be incorrect. ContactsInvestor Relations: ir@ Development: bd@ Contact: pr@ View original content to download multimedia: SOURCE Dizal Pharmaceutical Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
