Camila Peña

PENTA-DRUG EXPOSED vs PENTA-REFRACTORY MYELOMA — MUST KNOW 🔥 End-stage myeloma is no longer the end. 💡 Know the difference 💡 Understand resistance patterns 💡 Use BCMA-targeted therapies smartly From CAR-T to bispecifics — this is where modern oncology is changing survival 🚀 👉 Exam + clinic ready in 1 slide #MultipleMyeloma #Hematology #Oncology #MedEd #FOAMed #MedicalEducation #CancerCare #CAR_T #BispecificAntibodies #BCMA #RRMM #DrNB #DMOncology #MedTwitter #OncoTwitter

How I Treat Plasma Cell Leukemia #mmsm #bmtsm @HadidiSamer @ldandersonjr @BloodPortfolio ashpublications.org/blood/article-…

Todos invitados a los Highlights del EBMT para Latinoamérica 🌎 Selección de lo mejor del último congreso en Madrid. 💻 Virtual 🆓 Gratis Entrá, registrate y recibí el link de acceso. #EBMT #SAH #LABMT #GATMO #Hematología #LATAM

#Myeloma Paper of the Day: A secondary analysis of CIBMTR data finds functional high-risk phenotype (progression within 12-24 months of front-line induction + ASCT) predicts poor survival in multiple myeloma independent of front-line treatment: pubmed.ncbi.nlm.nih.gov/42023513/. #mmsm

In RRMM, “exposed” and “refractory” are NOT the same — and that difference drives treatment 👇 🔹 Exposed = patient has received that drug/class 👉 Disease may still respond 🔹 Refractory = disease progressed on or within 60 days 👉 That mechanism has failed --- 🧠 How to read this infographic: TCE (Triple-Class Exposed) → Seen PI + IMiD + CD38 → Not necessarily resistant TCR (Triple-Class Refractory) → Resistant to all 3 classes → Time to switch mechanism (BiTE / CAR-T) PCE (Penta-Class Exposed) → Received 2 PI + 2 IMiD + CD38 → Heavily pretreated PCR (Penta-Refractory) → Resistant to all 5 key drugs → Worst biology, limited options --- ⚠️ Key takeaway: 👉 As you move → TCE → TCR → PCE → PCR Resistance increases, options decrease --- 🎯 One-line memory: 👉 “Exposed = what patient got Refractory = what disease escaped” --- #MVOnco #MultipleMyeloma #HemOnc #MedEd

INSCRIPCIONES ABIERTAS | 4° SIMPOSIO GELAMM Participa de este simposio, un lugar de encuentro dedicado al intercambio de conocimientos, experiencias y avances en el estudio del mieloma múltiple y las gammapatías monoclonales.  Más info en f.mtr.cool/kvwtusdbms

This is a FRAUDULENT paper, AI-generated. My name was used as an author and I had nothing to do with it, never saw it until today e-pubmed.co.uk/journals/digit… The "Editors" Angelo Rossi Mori, David Mensah, and Zarnie Khadjesari should be reported.

Llega la primera serie en español de #WiLingWednesdays Desde @WomenInLymphoma presentamos la Serie 18 de webinars, con un enfoque especial en Latinoamérica 🌎 y la participación de referentes internacionales de habla hispana 📅 Mayo – Junio 2026 No te lo pierdas!

IMS-IMWG 2025 consensus genomic staging predicts outcomes with daratumumab-based quadruplet regimens for NDMM ashpublications.org/bloodadvances/… #mmsm

Myeloma is IRF4–MYC dependent. We talked about steroids. We talked about IMiDs / CELMoDs. Different drugs. Different mechanisms. But look closer… 🧬 Both converge on the same core: The IRF4–MYC transcriptional loop. IRF4 → activates MYC MYC → sustains IRF4 A self-reinforcing program myeloma depends on. Now connect the dots: 💊 Steroids → global transcription ↓ → IRF4 ↓ → MYC ↓ 💊 IMiDs / CELMoDs → IKZF1/3 degradation → IRF4 ↓ → MYC ↓ 👇 Different mechanisms. Same dependence. Dr Fun + G #myeloma #hemetwitter

Circulating Tumor Cells in Multiple Myeloma: From Peripheral Clues to Central Insights #mmsm pubmed.ncbi.nlm.nih.gov/41974595/

Los esperamos !

"Medicine can have extraordinary meaning. But it cannot substitute for being present in your own life." In #APieceofMyMind, a psychiatrist and residency program director reflects on an unexpected #LungCancer diagnosis. ja.ma/48OxHxC

🧬 We used thalidomide for years in myeloma… without knowing why it worked. Not the target. Not the pathway. Just the clinical signal. Now we know—and it’s not chemotherapy. IMiDs are cereblon-directed protein degraders: → Bind CRBN → Degrade IKZF1 (Ikaros) & IKZF3 (Aiolos) From that single mechanism: 🛡️ Immune system ↑ IL-2 ↑ T-cell / NK activation ↓ regulatory T-cell (Treg) function 💥 Tumor cell ↓ IRF4 / MYC → collapse of survival program → cell death 👉 One pathway. Two effects. 👉 Not contradictory—reprogramming biology 🚀 CELMoDs? Same pathway. Stronger signal. → Higher affinity to cereblon → Deeper IKZF1/3 degradation → Activity even after IMiD failure 💡 This is the shift Not: “Does the drug kill the tumor?” But: 👉 “How does it rewire the system?” 👇 Figure: IMiD → immune + tumor effects → CELMoD amplification #myeloma #Hemetwitter

Especial médicos🩺⚕️🏥👨🏻‍⚕️👩🏻‍⚕️. Os dejo esta carta en JAMA. Se la pondré a mis alumnos en la próxima clase: He elegido estas frases : 👇🏻⏰ «La medicina puede tener un significado extraordinario. Pero no puede sustituir el estar presente en tu propia vida. El mundo puede necesitarnos como médicos. Pero las personas que nos aman nos necesitan como nosotros mismos. Y ese es el rol que nadie más puede llenar.» «La residencia refuerza la lección de que las instituciones están diseñadas para perdurar más allá de los individuos. En cambio, las familias no.» «Creo en formar a la próxima generación. Creo en el significado de este trabajo. Lo que ha cambiado es mi disposición a absorber el desgaste sin cuestionarlo.» «Ya no estoy dispuesta a seguir posponiendo la vida. La medicina exige mucho. Y nosotros damos profundamente. Pero no puede tomarlo todo.» «El significado de mi trabajo es profundo. El significado de mi presencia en casa es irremplazable.»

#Myeloma Paper of the Day: Systematic review & meta-analysis concludes immunofixation (SIFE & UIFE) & sFLC ratio combined give sensitivity of 0.99 (0.96-1.00)) as reliable initial testing strategy to raise suspicion of diagnosis of AL #amyloidosis: pubmed.ncbi.nlm.nih.gov/41979328/. #alsm

FDA just granted Fast Track to OPN-6602 for RRMM. An oral EP300/CBP bromodomain inhibitor. Not a bispecific. Not a CAR-T. Myeloma therapy in 2026 is dominated by BCMA-targeting immunotherapy — bispecifics, CAR-T, ADCs. Incredible responses. But we all can agree, we're watching the same pattern: deep responses, eventual relapse, and a narrowing set of options for patients who've exhausted the immunotherapy playbook. OPN-6602 targets a completely different vulnerability. EP300 and CBP are transcriptional coactivators that myeloma cells depend on to keep IRF4 and MYC running. Block those bromodomains → IRF4 and MYC collapse → cell cycle arrest and apoptosis. Oral, selective (>200-fold over BET bromodomains), and mechanism-independent of prior therapy. Preclinical (ASH 2024): • 71% tumor growth inhibition as single agent • 100% TGI with dexamethasone • Activity in models resistant to standard-of-care Phase 1b (NCT06433947) is enrolling — single agent + dex in RRMM ≥4 prior lines. Orphan Drug designation already in hand (Jan 2025). Fast Track granted April 2026. Feels like we've been talking about "what comes after immunotherapy" for two years. Epigenetic targeting of myeloma's core transcriptional addiction might be part of that answer. Early days. But the biology is clean, and the unmet need is real. #Myeloma #mmsm #HemOnc @FDAOncology @opnabio @TargetedOnc @OncologyTimes @Myeloma_Society @MMRFTeam4Cures

🩸 Marginal Zone Lymphoma (MZL): 50 Pearls Review Series Alderuccio JP, Noy A. The treatment of marginal zone lymphoma. Blood. 2026;147(2):115–122. 1️⃣ MZL is an indolent B-cell non-Hodgkin lymphoma with a generally favorable prognosis. 2️⃣ It comprises three subtypes: extranodal (EMZL), nodal (NMZL), and splenic (SMZL). 3️⃣ EMZL, also known as MALT lymphoma, is the most common subtype. 4️⃣ Chronic antigenic stimulation plays a central role in pathogenesis. 5️⃣ The disease typically exhibits an indolent clinical course. 🔬 Biology & Immunophenotype 6️⃣ Typical markers: CD19⁺, CD20⁺, CD79a⁺, and PAX5⁺. 7️⃣ Usually negative for CD5, CD10, Cyclin D1, and LEF1. 8️⃣ EMZL arises from mucosa-associated lymphoid tissue. 9️⃣ NMZL presents primarily with lymphadenopathy. 🔟 SMZL commonly involves spleen, bone marrow, and peripheral blood. 🧬 Molecular Features 1️⃣1️⃣ NOTCH2 and KLF2 mutations are characteristic of MZL. 1️⃣2️⃣ KMT2D (MLL2) mutations are frequently observed. 1️⃣3️⃣ PTPRD abnormalities are enriched in nodal MZL. 1️⃣4️⃣ t(11;18)(q21;q21) predicts resistance to H. pylori eradication. 1️⃣5️⃣ SMZL exhibits distinct genomic clusters influencing survival. 🌍 Etiology & Associations 1️⃣6️⃣ H. pylori infection is strongly linked to gastric EMZL. 1️⃣7️⃣ Hepatitis C virus is associated with SMZL. 1️⃣8️⃣ Sjögren syndrome predisposes to salivary gland MALT lymphoma. 1️⃣9️⃣ Hashimoto thyroiditis is linked to thyroid EMZL. 2️⃣0️⃣ Autoimmune diseases contribute to lymphomagenesis. 🩺 Clinical Presentation 2️⃣1️⃣ EMZL is often localized at diagnosis. 2️⃣2️⃣ NMZL usually presents with disseminated nodal disease. 2️⃣3️⃣ SMZL presents with splenomegaly and cytopenias. 2️⃣4️⃣ Bone marrow involvement is common in SMZL. 2️⃣5️⃣ B symptoms are uncommon but may occur. 📊 Diagnosis & Staging 2️⃣6️⃣ Diagnosis requires histopathology and immunophenotyping. 2️⃣7️⃣ PET/CT demonstrates FDG avidity in most cases. 2️⃣8️⃣ Lugano classification is used for staging. 2️⃣9️⃣ GELF criteria help determine treatment initiation. 3️⃣0️⃣ Biopsy is essential to exclude transformation. 💊 Treatment – Early Stage 3️⃣1️⃣ H. pylori eradication is first-line therapy for gastric EMZL. 3️⃣2️⃣ Radiotherapy (24–30 Gy) is highly effective for localized disease. 3️⃣3️⃣ Observation is appropriate for asymptomatic patients. 3️⃣4️⃣ Rituximab is used when radiotherapy is not feasible. 3️⃣5️⃣ Antibiotic therapy may induce durable remissions. 💉 Treatment – Advanced Stage 3️⃣6️⃣ Bendamustine plus rituximab is a preferred frontline regimen. 3️⃣7️⃣ Rituximab monotherapy is effective in frail patients. 3️⃣8️⃣ Rituximab is first-line therapy for symptomatic SMZL. 3️⃣9️⃣ Splenectomy is reserved for selected SMZL cases. 4️⃣0️⃣ Lenalidomide plus rituximab is an effective chemo-free option. 🔁 Relapsed/Refractory Disease 4️⃣1️⃣ Zanubrutinib is an FDA-approved BTK inhibitor for R/R MZL. 4️⃣2️⃣ Acalabrutinib and pirtobrutinib show promising activity. 4️⃣3️⃣ CAR-T therapy demonstrates high response rates in R/R MZL. 4️⃣4️⃣ Bispecific antibodies (e.g., mosunetuzumab) show encouraging results. 4️⃣5️⃣ Antibody-drug conjugates are emerging therapeutic options. 📈 Prognosis & Future Directions 4️⃣6️⃣ Median overall survival often exceeds 8–10 years. 4️⃣7️⃣ POD24 is associated with inferior outcomes. 4️⃣8️⃣ Transformation to aggressive lymphoma can occur. 4️⃣9️⃣ Circulating tumor DNA is an emerging biomarker. 5️⃣0️⃣ Personalized and targeted therapies are shaping the future of MZL. ⸻ 📚 References •Alderuccio JP, Noy A. The treatment of marginal zone lymphoma. Blood. 2026;147(2):115–122. •NCCN Clinical Practice Guidelines in Oncology: B-Cell Lymphomas. •ESMO Clinical Practice Guidelines for Marginal Zone Lymphoma.

🧵1/ BCMA CAR-T resistance in Multiple Myeloma — what are we missing? Despite transformative responses with ide-cel & cilta-cel, most patients relapse. 👉 Resistance is NOT one mechanism — it’s multifactorial. Let’s break it down 👇 #mmsm #myeloma #MedEd #medtwitter #USMIRC @USMIRCNEWS @US_HMC @MedwatchKate @Larvol @OncoAlert

Dietary habits are not a major risk factor for MGUS overall and unlikely to be a major causative factor in the development of MM #mmsm #iStopMM @BloodCancerJnl @SaemundurMD nature.com/articles/s4140…