Malaysian Society of Haematology

Malaysian Society of Haematology b) To facilitate communication amongst doctors practicing Haematology in Malaysia. c) T

Our Website: http://haematology.org.my

a) The objectives of the Society are to promote the advancement of the Science and Practice of Haematology and allied Sciences. http://haematology.org.my

a) The objectives of the Society are to promote the advancement of the Science and Practice of Haematology and allied Sciences. c) To act as an authoritative body for the purpose of consultation in matter

of professional and public interest concerning haematology. d) To promote training and research and hence promote good practice of Hematology throughout the country.

The Malaysian Society of Haematology (MSH) is pleased to share that abstract submissions are now open for the 6th Annual...
08/06/2026

The Malaysian Society of Haematology (MSH) is pleased to share that abstract submissions are now open for the 6th Annual Scientific Meeting of the Association for Haemophilia and Allied Disorders – Asia Pacific (AHAD-AP).

This meeting provides an excellent opportunity for healthcare professionals involved in haemophilia and inherited bleeding disorders to showcase their research, clinical experience, quality improvement initiatives, and multidisciplinary care projects on a regional platform.

We warmly encourage colleagues from Malaysia and across the Asia-Pacific region to consider submitting their work and contributing to the advancement of haemophilia care.

Please refer to the poster below for submission details and further information.

The Malaysian Society of Haematology is pleased to share that abstract submission is now open for the Bloodless Medicine...
07/06/2026

The Malaysian Society of Haematology is pleased to share that abstract submission is now open for the Bloodless Medicine & Surgery Society (BMSS) Annual Scientific Conference 2026.

We encourage clinicians, researchers, nurses, pharmacists, allied healthcare professionals, and trainees with an interest in bloodless medicine and surgery to consider submitting their work and contributing to this growing field.

The conference welcomes abstracts across a range of topics, including newer technologies and innovations, education in bloodless medicine and surgery, iron therapy and erythropoiesis stimulation, perioperative bloodless surgery techniques, ethics and consent, and outcomes of bloodless care.

Abstracts should be submitted in English using the official submission form, with a maximum of 250 words and a structured format comprising Introduction, Methods, Results, and Conclusions. Abstract submissions will remain open until 1 September 2026, with notification of acceptance expected by 30 September 2026.

This is an excellent opportunity to showcase original research, share clinical experience, and engage with an international multidisciplinary community committed to advancing patient-centred blood management and bloodless care.

For submission guidelines and abstract details, please visit the BMSS Annual Scientific Conference 2026 website.

We wish all prospective authors every success with their submissions.

More information can be found on the BMSS website -

Clinical Evidence for Epcoritamab in Relapsed/Refractpry DLBCLDr Daryl TanMount Elizabeth Novena Hospital The treatment ...
25/05/2026

Clinical Evidence for Epcoritamab in Relapsed/Refractpry DLBCL
Dr Daryl Tan
Mount Elizabeth Novena Hospital

The treatment landscape for relapsed/refractory diffuse large B-cell lymphoma (DLBCL) continues to evolve rapidly, with increasing movement away from conventional salvage chemotherapy towards earlier integration of CAR T-cell therapy and bispecific antibodies.

In a highly practical and data-rich scientific discussion, Dr Daryl Tan reviewed the persistent limitations of frontline therapy, noting that approximately one-third of patients still fail R-CHOP, with most relapses occurring within the first year. Even with pola-R-CHP, around 30% of patients with IPI ≥2 continue to relapse. POLARIX demonstrated an approximate 6–7% improvement in cure rates in high-risk patients, while Asian subgroup analyses showed clearer separation of PFS and OS curves, potentially reflecting the higher prevalence of ABC-type DLBCL in Asian populations.

The session strongly emphasised upfront identification of biologically and clinically high-risk disease, including ABC-type DLBCL, double-expressor lymphoma, double-hit lymphoma, high IPI, extranodal disease, frailty, and concurrent CNS involvement. CNS disease was repeatedly highlighted as a major adverse feature requiring urgent intervention before irreversible neurological decline.

A memorable case discussion involved a 35-year-old patient with ABC-type DLBCL, MYC rearrangement, MYC/BCL2 double-expressor biology, Ki-67 of 90%, extensive extranodal and marrow involvement, renal impairment, and leptomeningeal CNS disease. Despite frontline pola-R-CHP and intensive intrathecal therapy, the patient deteriorated rapidly with cranial nerve palsy, aspiration pneumonia, ICU admission, and acute kidney injury. Following failure of polatuzumab, rituximab, and lenalidomide, third-line epcoritamab produced rapid neurological recovery and PET-confirmed complete remission after two cycles, with sustained remission maintained one year later.

The historical prognosis of primary refractory DLBCL remains extremely poor. SCHOLAR-1 reported median overall survival of less than six months, with chemotherapy response rates below 6% and complete responses rarely achieved. In contrast, second-line CAR T-cell studies including ZUMA-7 and TRANSFORM demonstrated clear superiority over salvage chemotherapy and autologous transplant in early relapse, with long-term survival plateaus approaching 40%.

Bispecific antibodies are now emerging as a major therapeutic platform in R/R DLBCL. Single-agent glofitamab and epcoritamab achieve ORR of approximately 50–60% with CR rates around 40% in clinical trials, although real-world CR rates may be lower at approximately 20%. Importantly, the discussion repeatedly stressed that complete remission — rather than partial response — is the critical determinant of durable survival.

During the subsequent expert discussion and audience interaction, emerging combination approaches involving bispecific antibodies were also explored, including ongoing experiences and early-phase studies combining bispecifics with GemOx or lenalidomide-based platforms. These discussions reflected growing interest in moving bispecific therapies earlier into the treatment algorithm, particularly in patients unsuitable for transplant or CAR T-cell therapy, although several approaches discussed remain investigational or are not currently approved in routine practice.

A recurring biological principle throughout the session was the importance of T-cell fitness. Because bispecific antibodies rely on endogenous T-cell activity, repeated chemotherapy exposure may reduce effectiveness through T-cell exhaustion. The discussion therefore reinforced the importance of timely escalation before prolonged treatment exposure and physiological decline.

The session also addressed practical Asia-Pacific challenges including reimbursement barriers, outpatient feasibility, ICANS and CRS monitoring, bendamustine exposure prior to CAR T-cell collection, CD20 reassessment at relapse, and the continuing role of autologous stem cell transplantation in late relapse. While CAR T-cell therapy remains highly effective, rapidly progressive patients may not survive long enough for manufacturing timelines, making immediately available bispecific therapy increasingly relevant in urgent disease settings.

Overall, the session reflected a major strategic shift in DLBCL management: earlier recognition of high-risk biology, faster escalation before physiological decline, and increasing integration of bispecific antibodies alongside CAR T-cell therapy and transplantation to maximise the likelihood of complete remission and durable survival.

Disclaimer: The views and reflections above represent personal academic interpretation and discussion points arising from the session. Any mention of investigational or off-label approaches reflects scientific exchange during expert discussion and should not be interpreted as promotional recommendation or formal prescribing guidance. The event organised by AbbVie was conducted as a scientific educational discussion forum intended for healthcare professionals.

Embracing Early Intervention: Timely Treatment in MFFrancesco PassamontiProf Francesco Passamonti presented a compelling...
16/05/2026

Embracing Early Intervention: Timely Treatment in MF
Francesco Passamonti

Prof Francesco Passamonti presented a compelling argument for earlier initiation of Ruxolitinib in myelofibrosis (MF), emphasising MF as a progressive inflammatory and fibrotic disease rather than a condition defined purely by risk stratification. Longitudinal data demonstrated increasing disease burden within one year, with anaemia rising from approximately 40% to 64%, thrombocytopenia from approximately 20% to 30%, and constitutional symptoms from 29% to 32%, alongside increasing transfusion requirements, blasts, and splenomegaly. The message throughout the lecture was that delaying treatment permits progressive biological deterioration that may compromise long-term outcomes and transplant eligibility.

The biological rationale for earlier intervention centred on inflammatory cytokine suppression. Proteomic analyses demonstrated marked reduction in inflammatory cytokines following Ruxolitinib therapy, supporting the concept that persistent cytokine activation itself perpetuates JAK-STAT signalling and disease progression. Real-world data involving 154 patients showed that achievement of spleen response correlated with longer survival. The Italian prospective ROMA study involving 508 patients further highlighted the importance of maintaining adequate dose intensity. Among 132 patients who received lower-than-expected doses, spleen response rates were significantly inferior at 30% versus 50% in appropriately dosed patients, with reduced-dose therapy also associated with worse survival.

The lecture revisited survival outcomes associated with JAK inhibitor therapy, demonstrating clear benefit compared with historical controls. Comparison between patients never exposed to JAK inhibitors and matched COMFORT cohorts showed improved survival with Ruxolitinib. Historical JAK-COMO data reported median survival of only 8% at 3 years in mixed-risk disease, whereas Italian intermediate-2 and high-risk patients treated with Ruxolitinib achieved median survival of 4 years. Earlier treatment consistently produced superior spleen responses. In JUMP, spleen response rates reached 82% in low-risk patients and 80% in intermediate-1 disease, compared with 69% and 63% respectively in intermediate-2 and high-risk cohorts.

Lower fibrosis grade at treatment initiation was associated with fewer cytopenias, better spleen response, and superior overall survival despite similar spleen burden. Importantly, Ruxolitinib also demonstrated potential disease-modifying activity. In the Steven Wu publication cited during the lecture, 23% of patients achieved greater than one-grade fibrosis improvement by week 24, while 9% achieved greater than 50% reduction in JAK2 allele burden. COMFORT analyses additionally showed that starting Ruxolitinib within one year resulted in fewer complications, particularly thrombocytopenia and anaemia, together with superior spleen volume reduction at weeks 24 and 48, 44% versus 26% compared with delayed initiation.

Ruxolitinib was also positioned as an important bridge to stem cell transplantation. The speaker stressed that performance status at transplant strongly influences post-transplant survival within the MTSS model, while splenic control remains critical, with ABMT recommendations favouring spleen size below 5 cm prior to transplantation. Ruxolitinib was therefore presented as a strategy to improve constitutional symptoms, reduce inflammatory burden, optimise performance status, and improve transplant readiness. Importantly, patients responding before transplant demonstrated lower relapse incidence together with superior relapse-free and overall survival.

The final section addressed second-line treatment following Ruxolitinib failure using a phenotype-driven approach. In splenomegaly-dominant disease, Fedratinib demonstrated SVR35 rates of 31% at week 24 and 50% at any timepoint in FREEDOM 2. In anaemia-predominant patients, Momelotinib in MOMENTUM achieved TSS50 responses in 25%, SVR35 in 23%, and transfusion independence in 30%. Overall, the lecture advocated a 2026 treatment paradigm focused on earlier intervention, maintenance of adequate dose intensity, integration of transplant planning early in the disease course, and strategic sequencing of therapy according to dominant clinical phenotype.

The talk was held during the recent Novartis National Haematology Expert Summit event in Kuala Lumpur

Advances in MF and PV Management: Latest EvidenceFrancesco PassamontiProfessor Francesco Passamonti delivered a comprehe...
15/05/2026

Advances in MF and PV Management: Latest Evidence
Francesco Passamonti

Professor Francesco Passamonti delivered a comprehensive update on the rapidly evolving therapeutic landscape of myelofibrosis (MF) and polycythaemia vera (PV), emphasising increasingly phenotype-driven and molecularly informed treatment strategies. In MF, the key initial decision remains transplant eligibility, guided by physiological age, performance status, prognostic scoring, and anticipated post-transplant outcomes. Subsequent therapy selection is increasingly individualised according to splenomegaly, constitutional symptoms, anaemia, and thrombocytopenia.

Current JAK inhibitor use is becoming progressively more tailored. Ruxolitinib remains appropriate for platelet counts >50,000, while Momelotinib was highlighted particularly for anaemic patients with haemoglobin 25,000 because of its comparatively favourable effect on haemoglobin. Pacritinib, studied in severe thrombocytopenia, achieved SVR35 in 22% and TSS50 in 32% in the PERSIST-2 study among patients with platelet counts 12 weeks at week 24 and 65.2% achieving ≥50% reduction in transfusion burden. Positive Phase III data for Luspatacept are expected at EHA 2026, while Phase III development for Imetelstat is expected to begin in Autumn 2026.

Combination strategies continue to improve spleen responses, although symptom advantages remain modest. In MANIFEST-2, Pelabresib plus Ruxolitinib achieved SVR35 in 65.9% versus 35.2% with Ruxolitinib alone at week 24, with durability maintained to week 96 at 45.3% versus 30%. However, TSS50 differences remained limited. Similarly, Selinexor plus Ruxolitinib achieved SVR35 in 50% versus 28% in Phase III data released in March 2026, again without major symptom superiority. These studies reinforce the continued strength of Ruxolitinib for symptom control.

More biologically directed approaches are now emerging. Navtemadlin added to Ruxolitinib in suboptimal responders produced SVR35 and TSS50 rates of 32%, alongside reductions in bone marrow fibrosis in 58% and driver mutation variant allele frequency in 71%, suggesting potential disease-modifying activity. Immunotherapeutic approaches targeting mutant CALR were also discussed. The mutant CALR antibody INC-A989 achieved SVR35 in 33% overall and 57% in JAK inhibitor–naive patients, while TSS50 was observed in 39% overall and 60% in JAK inhibitor–naive cohorts, alongside trends towards haemoglobin improvement and CALR VAF reduction.

In PV, long-term molecular disease control emerged as a major theme. In PROUD-PV, Ropeginterferon achieved complete haematological remission in 54% versus 34.9% with Hydroxyurea. At six years, deep molecular response with JAK2 VAF 50% JAK2 VAF reduction over 52 months. MAGIC-PV additionally demonstrated improved event-free survival and fewer thromboembolic events compared with best available therapy.

The lecture concluded with discussion of iron metabolism modifiers as an emerging therapeutic class in PV. Rusfertide, a hepcidin mimetic, achieved the primary endpoint in 77% compared with 32% with placebo in Phase II evaluation, while also reducing phlebotomy requirements and maintaining haematocrit

Debate 02: The Definition of Treatment Success in CML should be Around Patient Life Goal, not Molecular ThresholdKhaiter...
14/05/2026

Debate 02: The Definition of Treatment Success in CML should be Around Patient Life Goal, not Molecular Threshold
Khaiteri Raghunathan, Lee Yin Man, Wong Chee Yoon, Evelyn Aun Su-Yin

This debate examined whether treatment success in chronic myeloid leukaemia (CML) should primarily be defined by molecular milestones or by achievement of patient-centred life goals and health-related quality of life (HRQoL). Both sides acknowledged that modern CML management now extends beyond survival alone, particularly given the durable long-term outcomes achieved in the TKI era.

The patient-centred position argued that molecular thresholds alone inadequately capture the diversity of patient priorities. Younger patients may prioritise treatment-free remission (TFR) or pregnancy, working adults may focus on productivity and minimising treatment burden, while older patients may value disease stability and low toxicity over pursuit of deep molecular remission (DMR). The speakers highlighted ELN 2025’s removal of the term “failure”, reflecting concerns that rigid milestone-based definitions may unnecessarily label late responders or older patients as poor outcomes despite durable survival. Retrospective data discussed during the session demonstrated that patients missing conventional 3-, 6-, and 12-month ELN milestones could still achieve greater than 80% 10-year overall survival, with 10–15-year survival trajectories approaching those meeting favourable milestones.

The opposing position maintained that BCR-ABL molecular thresholds remain the most validated surrogate endpoints for survival and progression risk. Molecular monitoring by quantitative PCR was defended as the cornerstone of consistent clinical decision-making across centres. The speakers argued that patient-reported wellbeing alone cannot reliably predict disease control, whereas molecular response directly informs transformation risk and survival outcomes. The ability to safely pursue patient life goals — including TFR, pregnancy, and long-term occupational stability — was presented as fundamentally dependent upon adequate molecular control.

Importantly, the discussion evolved towards integration rather than polarisation. Molecular response and HRQoL were framed as complementary dimensions of treatment success. Molecular responses predict progression and survival, while HRQoL instruments reflect treatment burden and lived experience. Several examples of individualised target setting were proposed: younger patients pursuing TFR may require sustained DMR; pregnancy planning may require stable MMR or deeper responses; younger working adults may prioritise durable MMR; and frail elderly patients may accept BCR-ABL levels below 1% if tolerability and stability are maintained.

The speakers highlighted that although second- and later-generation TKIs achieve faster and deeper molecular responses, these gains have not clearly translated into overall survival advantages. TFR was acknowledged as an important aspiration but one with stringent eligibility requirements and limited universal applicability. Even with broader access to second-generation TKIs, post-discontinuation success rates remain approximately 25–50%, reinforcing that many clinically stable patients may never achieve durable TFR despite excellent long-term disease control.

The debate further acknowledged major implementation challenges across the Asia-Pacific setting, including variability in access, reimbursement, and molecular monitoring infrastructure. In some centres, including Sabah, six-monthly PCR monitoring represents the practical real-world standard. Despite these constraints, the importance of maintaining PCR monitoring as the backbone of safe disease management was repeatedly reinforced.

Approximately 85% of the audience ultimately agreed that molecular thresholds and patient life goals should be viewed as complementary rather than competing frameworks. The concluding message emphasised that modern CML management requires integration of molecular control, tolerability, adherence, HRQoL, and shared decision-making. The session strongly highlighted that timing of intervention, sustainable therapy, realistic TFR expectations, and adaptation of treatment intensity according to patient priorities are increasingly central to contemporary CML care within the real-world Asia-Pacific context.

This debate was held during the Novartis National Haematology Expert Meeting (NHEM) in Kuala Lumpur recently. It was chaired by Dr Lim Soo Min and Prof Ng Soo Chin

13/05/2026

Welcome to this week's EHA challenge!

✏️Submit your answer (anonymously) in the form and unlock the detailed explanation: https://ehaedu.org/LearningMondays-May4-26

🙏 Thank you for your submission Dr Mahesh Prahladan from Ipswich Hospital, United Kingdom 🇬🇧

13/05/2026

Applications are open to join our 2027 Translational Research Training in Hematology (TRTH) cohort!

Here's how you can benefit from joining:
• Small-group mentoring with leading international experts to refine your own research project
• Exposure to ethical, regulatory, and career challenges in hematology research, discussed openly with senior researchers
• Year-long mentoring and follow-up opportunities at the EHA Congress and ASH Annual Meeting
• A close international peer network of early-career researchers that often continues well beyond the program

TRTH is open to trainees and junior faculty engaged in laboratory‑based translational or basic science research in hematology. Submit your LOI by June 18, 2026: https://eha.fyi/TRTH_2027

Debate 01: TFR – Should We Be Attempting It More Aggressively in Malaysia?Khaiteri Raghunathan, Lee Yin Man, Wong Chee Y...
13/05/2026

Debate 01: TFR – Should We Be Attempting It More Aggressively in Malaysia?
Khaiteri Raghunathan, Lee Yin Man, Wong Chee Yoon, Evelyn Aun Su-Yin

This debate examined whether Treatment-Free Remission (TFR) in Chronic Myeloid Leukaemia (CML) should be pursued more aggressively in Malaysia, balancing growing clinical confidence in TFR with the realities of patient selection, molecular monitoring, and healthcare infrastructure.

The proponents of a more aggressive approach argued that TFR is now a validated therapeutic objective rather than an experimental concept. TFR was defined as sustained discontinuation of tyrosine kinase inhibitor (TKI) therapy in patients achieving deep molecular response (DMR), usually MR4 or MR4.5. Landmark studies, including TFRA, EURO-SKI, and ENESTfreedom, were cited as establishing proof of concept for safe discontinuation in selected patients. In the EURO-SKI trial, 40–60% of eligible patients maintained remission after a TFR attempt, while approximately 50% experienced molecular relapse. Importantly, over 80% of relapsed patients regained Major Molecular Response (MMR) after restarting therapy. The ENESTfreedom trial demonstrated a TFR rate of 48.3% at 48 weeks.

The session repeatedly emphasised the importance of molecular monitoring. Sustained MR4 or MR4.5 was considered a practical prerequisite for TFR, placing quantitative PCR-based BCR-ABL assessment at the centre of decision-making. PCR testing was reported to be available in most major Malaysian centres, although significant geographical inequities remain, particularly in Sabah and remote districts. The ongoing ENTIC TRIAL at Hospital Ampang was highlighted as an example of centralised PCR support, including transportation of samples from district hospitals such as Ranau.

Advocates of TFR stressed the cumulative burden of indefinite TKI therapy, including nilotinib-associated cardiovascular toxicity, dasatinib-related pleural effusion, chronic fatigue, and gastrointestinal adverse effects. TFR was also framed as providing psychological freedom from lifelong therapy, improving fertility planning, and potentially reducing long-term healthcare costs. Local Malaysian experience supported feasibility, with Dr Lim’s centre reporting 54.4% long-term TFR and universal DMR recovery after relapse at a median of five months following TKI reintroduction.

The opposing position cautioned against interpreting these successes as justification for broad implementation. The principal concern was the relatively small proportion of patients who ultimately become eligible for TFR. Data from the STIM1 trial suggested that only approximately 40% of CML patients achieve MR4, with even fewer reaching MR4.5. Combining this with an approximate 50% success rate among TFR attempts yields an effective success rate of only around 20% across the overall chronic-phase CML population.

The opposing speakers highlighted that, although most relapsed patients regain MMR after restarting the same TKI, a minority may require alternative agents with additional toxicity and financial implications. Intensive PCR monitoring was also identified as a major practical barrier in Malaysia, particularly for patients in remote regions and within public-sector systems affected by investigation delays, raising concerns regarding delayed detection of molecular relapse.

Psychological aspects of TFR were also discussed extensively. A CML Advocates Network survey found that 56% of patients undergoing TFR experienced anxiety or fear, particularly while awaiting PCR results. In the same survey, 60% reported TKI withdrawal syndrome, while 40% felt inadequately supported by their physicians.

In the concluding remarks, Dr Ng Soo Chin advocated a balanced and individualised strategy. He emphasised that TFR is an important and achievable objective in modern CML management, but one that depends heavily on careful patient selection, robust PCR infrastructure, timely molecular surveillance, and patient readiness. Within the Malaysian and wider Asia-Pacific context, the greatest challenge is no longer proof of concept, but rather the healthcare system’s capacity to deliver safe and timely MRD-guided monitoring. TFR, therefore, remains best pursued through structured and individualised implementation rather than indiscriminate widespread adoption.

This debate was held during the Novartis National Haematology Expert Meeting in Kuala Lumpur and was chaired by Dr Lim Soo Min and Dr Ng Soo Chin.

What does the Future Hold for Early Lines of CML Treatment?Jane ApperleyProfessor Jane Apperley delivered a highly pragm...
10/05/2026

What does the Future Hold for Early Lines of CML Treatment?
Jane Apperley

Professor Jane Apperley delivered a highly pragmatic, data-driven overview of the evolving frontline treatment landscape in chronic myeloid leukaemia (CML), emphasising that modern management increasingly balances molecular response, long-term toxicity, quality of life, and realistic treatment goals.

A key message was that while second-generation TKIs consistently achieve faster and deeper molecular responses than imatinib, this has not translated into improved overall survival. Progression rates in contemporary practice are now remarkably low at approximately 2–3% within the first year.

Treatment-free remission (TFR) remains an important aspiration, but even with the most potent available TKIs, only around 25% of patients ultimately achieve successful sustained TFR. Consequently, approximately 75% of patients remain on lifelong therapy, underscoring the importance of tolerability and long-term quality of life in treatment selection.

The lecture also highlighted important biological risk factors. High ELTS-risk disease appears to benefit more clearly from second-generation TKIs, while ASXL1 mutations — present in approximately 11% of newly diagnosed patients — continue to confer poorer outcomes regardless of TKI potency.

Much of the discussion focused on the ASC4FIRST frontline asciminib programme. Asciminib demonstrated substantially lower discontinuation rates compared with standard TKIs (approximately 18% versus 40%), while treatment failure discontinuations were roughly halved (10% versus 20%). Molecular responses were particularly favourable compared with imatinib, with approximately 30–40% of patients achieving MR4 by two years.

The tolerability data were equally notable. Grade ≥3 adverse events, dose interruptions, and treatment discontinuations were lower with asciminib than with either imatinib or second-generation TKIs. Patient-reported outcomes also indicated greater time spent free of adverse effects.

However, the lecture remained appropriately cautious. Novel myristoyl pocket mutations emerging during asciminib therapy may require expanded mutation-monitoring strategies beyond conventional ATP-binding site analysis. Furthermore, asciminib did not appear to overcome the adverse prognostic impact of ASXL1 mutations.

Overall, the talk reinforced that the future of frontline CML therapy is unlikely to revolve around a single “best” TKI. Instead, increasingly personalised treatment selection, vigilant molecular monitoring, and balancing deep molecular response against lifelong quality of life will define contemporary practice — particularly in real-world Asia-Pacific settings where access and reimbursement remain major determinants of care.

The lecture was part of a CME Program by Novartis Malaysia

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