Yu-Hung Wang

MD, PhD. Haematologist @#NationalTaiwanUniversityCancerCenter. Assistant Professor @NTU_TW @EHA_Hematology #SWG #MDS #MPN #CMML 🇹🇼🇬🇧

[Yu-Hung Wang @yu_hung_wang]

My previous account was hacked, so here's a fresh start. Trying to get this account going again.

[Andrius Žučenka @zucenka]

Incredibly proud of our stellar residents presenting posters and an oral presentation at the @SocietyofHemOnc annual meeting!

Congratulations to our young researchers on the important results for patients with AML and thank you @SocietyofHemOnc for the support!

@VU_LT #leusm

[Gaby Hobbs @GabyHobbs]

Great start to #SOHO2026 got to take first photo with my awesome fellow, Dr. Kate Feder presenting our experience at #MGH with ropeg. Excited to present this morning on novel therapies in ET and PV which included 2 new approved drugs! 🥳#mpnsm

[Nathan Punwani @npunwani]

TP53 mutations, by themselves, are usually insufficient to develop into AML/MDS

Classically, TP53 follows the "double-hit hypothesis" in AML/MDS: two sequential events—a point mutation in one allele followed by loss of the remaining wild-type copy—produce biallelic inactivation and drive disease evolution. However, the "multi-hit" hypothesis is too simplistic and ignores the importance of cell-extrinsic influences that affect the fitness of TP53 mutations. In some cellular contexts, cells harboring TP53 mutations are destined to remain in a truncated, low kinetic state; in others, they are favored expand at the expense of other cells.

One such context that favors the expansion of TP53 mutated cells is when a TP53 mutation event is followed by a chromosome 5q deletion. Loss of the long arm of chromosome 5 lays the clonal architecture that predisposes hematopoietic stem cells to develop complex cytogenetics and then evolve into high risk AML/MDS. In fact, del(5q) is the most common change found in over 80% of complex karyotypic AML!

When a mitotic checkpoint inhibitor is applied in a cell culture model, stem cells that carry both a 5q deletion and a TP53 mutation exhibit greater genomic instability than TP53-mutated controls. This instability generates clones with diverse chromosomal alterations, some of which confer a greater fitness advantage than others. In the bone marrow, evolution by natural selection then drives competition among these clones until a single "dominant species" emerges. That "winning" clone continues to evolve and accumulates new mutations and structural chromosomal aberrations.

Hematopoietic stem cells with a combined del(5q)-complex karyotype are theorized to have a survival advantage because of up-regulation in genetic pathways related to PTEN and cohesins. This enables aneuploid (chromosomally imbalanced) cells to stabilize chromosome pairing during cell division.

When del(5q)/complex-karyotype cells are exposed to the BCL-2 inhibitor venetoclax, resistance is facilitated by subclonal heterogeneity: the remaining smaller clones evolve into less primitive, more functional erythroid-megakaryocyte progenitors (they become less "stem cell"-like). These more mature progenitor cells have low BCL-2 expression. While initially only minor, the cells become evolutionarily selected to expand after venetoclax therapy, becoming the new dominant population in the bone marrow. To borrow a Jeff Goldblum aphorism: Life finds a way https://t.co/Azbq31u86F

@aamdsif

[Blood Journals Portfolio @BloodPortfolio]

GLUL restricts cytotoxic ammonia accumulation in MKs and is conducive to MK maturation and thrombocytopoiesis. Read in Blood: https://t.co/IFdPK0N1el

[Yu-Hung Wang @yu_hung_wang]

Cross-study analyses of the ropeginterferon alfa-2b effect on phlebotomy in low- and high-risk patients with polycythemia vera
https://t.co/lsJma4jwuY
#MPNsm @MPN_Hub

[Yu-Hung Wang @yu_hung_wang]

Characterisation of #TP53 mutational features and outcomes of acute myeloid leukaemia after allogeneic haematopoietic cell transplantation
https://t.co/3uocARngXj
#Leusm @BMTjournal @TheEBMT_Trainee

[Yu-Hung Wang @yu_hung_wang]

Incidence, prevalence, and survival outcomes of patients with myeloproliferative neoplasms in the United States: a Surveillance, Epidemiology, and End Results (SEER) database analysis, years 2000–2021
https://t.co/bGewLgHHYJ
#MPNsm @LeukemiaJnl @MPN_Hub

[Yu-Hung Wang @yu_hung_wang]

Infection risk in myelodysplastic syndromes is dynamic and immune driven
https://t.co/NSduA1ubkZ
#MDSsm @aamdsif @MDSFoundation @ic_MDS
@BloodAdvances

[MPN_Hub @MPN_Hub]

New publication 📝 Results from a cross-study analysis, published in Leukemia & Lymphoma, show a HIDAT regimen of ropeginterferon alfa-2b reduced annualized phlebotomy rates vs the slow titration regimen in patients with PV at Weeks 0–32 (0.37 vs 2.31 per year; p < 0.0001) and Weeks 20–32 (0.13 vs 0.60 per year; p = 0.0218).

Learn more about PV: https://t.co/5Y9t9WVsnw

#MPNsm #PolycythemiaVera #MedNews #MedEd

[Yu-Hung Wang @yu_hung_wang]

Allele burden expansion in #JAK2V617F and #CALR-mutated myeloproliferative neoplasms predicts disease progression and is associated with anagrelide treatment

Really like this story!

@jm_osullivan @Hemasphere_EHA @EHA_Hematology @MPN_Hub #MPNsm
https://t.co/0ABmFPNNri

[Blood Journals Portfolio @BloodPortfolio]

Anti-CCRL2 ADC shows prominent antileukemic effect in high-risk MDS/AML, including TP53-mutated in vitro and in vivo models. Anti-CCRL2 ADC demonstrates no significant toxicity against healthy hematopoietic cells and systemic toxicity in mice. Read here: https://t.co/568Ht7NbJA

[MPN Voice @MPNVoice]

Managing MPNs Through Nutrition 📷
September is Blood Cancer Awareness Month! While medical care is essential, finding practical ways to support your body can make a real difference in daily life.
In our YouTube presentation, Optimising Nutrition in MPNs, specialist dietitian Laura explains how dietary choices can help manage symptoms and lower inflammation.
Key Takeaways:
⚬ Managing Inflammation: MPN genetic mutations trigger internal inflammation. A Mediterranean-style diet filled with whole foods, healthy fats, and fewer processed meats can help lower this burden.
⚬ Preserving Muscle: Focus on body composition rather than just weight. Getting enough protein (like yogurt, nuts, seeds, or fish) supports muscle strength and energy.
⚬ Staying Hydrated: Dehydration is a surprisingly common cause of fatigue. Aiming for 30 to 35 ml of fluid per kg of body weight daily supports vascular health and energy.
⚬ Eating with a Reduced Appetite: If an enlarged spleen makes eating difficult, smaller, nutrient-dense snacks throughout the day can maintain your energy without causing discomfort.
Taking control of diet is a great way to feel empowered alongside your treatment.
📷 What daily tips or dietary changes have helped you feel better while living with an MPN?
Share your go-to advice in the comments below! 📷
#BloodCancerAwarenessMonth #MPNVoice #PolycythaemiaVera #EssentialThrombocythaemia #Myelofibrosis #MPNNutrition #LivingWellWithMPN

[Benlazar S M A @smbenlazar]

Nivo-AVD vs Bv-AVD : PFS in older patients (&gt;60 years) #lymsm

[Benlazar S M A @smbenlazar]

Pharmacological boosting of azacitidine/venetoclax in acute myeloid leukemia https://t.co/fK9s77MxC4 #leusm

[Manel Esteller @ManelEsteller]

We used single-cell multiomics to trace the MDS-to-AML trajectory upon #HMA treatment and uncovered how #DNA #methylation clones evolve along the way. Featured in @LeukemiaJnl !
#SingleCellGenomics #AML #MDS #CancerBiology
https://t.co/DjldbtHZ3V

[Mostafa Faisal @MostafaFaisal14]

High Prevalence of the JAK2V617F Mutation in Patients With Acute Coronary Syndrome
https://t.co/5snFzzkETN

[Mikkael A. Sekeres MD, MS @MikkaelSekeres]

My latest post for @NEJMClinician: Azacitidine–Venetoclax or 7+3 Induction for AML -- 7+3 isn't quite dead yet! @SylvesterCancer @UMiamiHealth @ASH_hematology https://t.co/ZIkGrXAYyr

[MPN_Hub @MPN_Hub]

New publication 📝 The 2025 ONKOPEDIA guideline, published in @IntJCanc, provides updated recommendations for myelofibrosis (MF), including molecularly informed risk scoring, JAKi selection, and early referral for transplantation.

Learn more about MF: https://t.co/OaRCvhRe89

#Myelofibrosis #MPNsm #MedNews #MedEd

[Yu-Hung Wang @yu_hung_wang]

@emmamgroarke Looks so lovely indeed 🤩

[Gaby Hobbs @GabyHobbs]

So proud to be a part of this paradigm shift! Congrats to Amir and all the authors! #MGB