rajEndiran

🧬✨ POLE-mutated endometrial cancer → ultramutated biology & excellent survival 🌟 ➡️ Molecular confirmation is key ➡️ Enables safe treatment de-escalation 🎯 🔗 bit.ly/4bTxUBF @pedroramirezMD @HsuMd @JayrajAarthi @AndreFernandes2 @IGCSociety @ESGO_society @ENYGO_official @OncoAlert @IJGCfellows @GynMe4 @RParejaGineOnco @lchiv4 @annafagottimd @HousseinELHAJJ3 @AinhoaMada @luribero26 @beatesarta @AlwynDO @PeppeParisi_ @ilkerselcukmd @VinTarantino @NSeminario27498 @dranushak88 #IJGConline #Research #Prevention #Treatment #Diagnostic #GynCancer #GynOnc #WomenHealth #SoMe #SoMe4GynOnc

The newly-described solid and granular/oncocytic lung adenocarcinomas (SAGAs). Recent case (adrenal met) illustrating their distinct morphology: granular-vacuolated-clear cytoplasm + macronucleoli. Focal mucin is common (best by mucin stains). sciencedirect.com/science/articl…

Hepatic Mesenchymal Hamartoma (HMH) pathology #pathology

PD-L1 predicts in metastatic… but not early cancer. Why? • Metastatic → exhausted immunity • Needs PD-L1 removal • Early → strong immunity • Builds new response • Same shield, different outcome #MVOnco #Oncology #Immunotherapy

WHO 2021 changed glioma forever Same histology ≠ same treatment • IDH, 1p/19q, MGMT drive decisions • From observation → RT → chemo → delay strategies Think molecular → treat smarter 🧠 #MVOnco #NeuroOncology #Glioma

WHO changed glioma classification forever • Molecular first, not histology • IDH defines biology • Grade ≠ disease • Grade 1 = only circumscribed Simple way to remember 👇 #MVOnco #Glioma #NeuroOncology #MedEd #Oncology

@MunchManju95 using big big ... words ..... kind of u ..... Keep up the good work ....😎🥰

What else one need It is of great honor when your inspiration himself likes and reposts your post.Sir is the one who introduced me to "TWITTER" for studing pathology.Sir once again proves how humble he is. Thanks sir this means a lot to me.This motivates me to work hard even🙏

Approach to Thrombocytopenia and Platelet Transfusion 📝✅ Thrombocytopenia (TP) is a localization problem. In anemia, the early signal is often MCV + retics. In TP, the early signal is often clinical context, which then guides mechanistic localization. Via- @WilliamAird4

Flash card on Leukemia #examnotes📝 #pathoflashcard ❌📝🎓🔬❌

Multiple Myeloma ITE/Board pearls (Follow ASCO/ASH/NCCN guidelines for latest updates) 🧠The "M-S-M" Ladder 🪜🦀 1. MGUS: Minimal (<10% cells, <3g M-protein, no CRAB). 2. Smoldering: Significant (10–60% cells, ≥3g M-protein, but still no CRAB). 3.Myeloma: Malignant (≥10% cells plus CRAB or SLiM). 🧠If scan is bland, think myeloma in the land🏖️ (Doesn’t MAKE → poor osteoblast activity → bone scan can be normal) 🧠⚡️17-4-16: The High-Risk Highway🛣️ 17: del(17p) – (Loss of TP53, the most aggressive). 4: t(4;14) – High-risk translocation. 16: t(14;16) – High-risk translocation. 🧬 Epidemiology & Basics ->Median age ~65–70; male predominance;  ->Black patients ≈2–3× incidence vs White ->Always preceded by MGUS → Smoldering → Myeloma. ->Clonal plasma cell malignancy producing monoclonal immunoglobulin (M‑protein). ->M‑protein types: IgG (~50%), IgA (~20%), light‑chain only (~20–25%); type not prognostic, used for response monitoring. 🩸 CRAB + SLiM – Diagnosis C: Hypercalcemia (osteolysis). R: Renal failure (light‑chain cast nephropathy, Bence Jones). A: Anemia (marrow replacement). B: Bone lesions (purely osteolytic; punched‑out skull). SLiM biomarkers (myeloma‑defining, no CRAB needed) S: ≥60% clonal marrow plasma cells. Li: FLC ratio ≥100. M: >1 focal lesion on MRI. 📌Key exam contrasts ->Myeloma lesions: purely osteolytic → bone scan can be normal. Preferred imaging: WB CT, PET‑CT, MRI spine. 🧪 Workup & Classic Board Traps ->SPEP alone detects ~80% → add immunofixation + serum free light chains → ~97–98% detection. ->Suspected myeloma with negative SPEP → order serum free light chain assay ± 24‑h UPEP. ->Nonsecretory myeloma (~1–2%): no M‑protein; diagnosis by marrow + imaging. ->Marrow: ≥10% clonal plasma cells; ~96% have marrow involvement. 🧬 Cytogenetics & Prognosis Primary (early) events – 2 big groups 1️⃣ IGH translocations (~50%): t(11;14), t(4;14), t(14;16), t(14;20), t(6;14) – usually mutually exclusive. 2️⃣ Hyperdiploid (~50%): trisomies of odd chromosomes (3,5,7,9,11,15); better prognosis. 📌High‑risk cytogenetics (boards 🫶) 1. del(17p), t(4;14), t(14;16), 1q gain/amplification. 2. Standard‑risk: t(11;14), t(6;14), hyperdiploid. 3. Double-/triple‑hit: multiple high‑risk lesions → very poor prognosis. 💊 Treatment – Frontline Therapy evolution: Doublets → Triplets (VRd) → Quadruplets now standard. Current standard (transplant‑eligible): 1️⃣ Determine eligibility (≈<73–75 y, fit). 2️⃣ Induction: Quadruplet Dara‑VRd (Daratumumab + Bortezomib + Lenalidomide + Dex). 3️⃣ Stem cell collection. 4️⃣ ASCT (early vs delayed); improves PFS, not OS. 5️⃣ Maintenance: Maintainance Standard risk: Lenalidomide. High risk: Lenalidomide + Bortezomib. Non‑transplant/frail: Quadruplet (shorter) or triplet (e.g., VRd or DRd) → maintenance. 🔁 Relapse Strategy Key concept: chronic relapsing disease; each remission shorter. First relapse – depends on Lenalidomide exposure/resistance: ->Len‑sensitive: Dara‑Len‑Dex; Carfilzomib‑Len‑Dex; Elo‑Len‑Dex, etc. ->Len‑refractory: switch to pomalidomide or carfilzomib backbone (e.g., Dara‑Poma‑Dex, Dara/Isa‑Car‑Dex). I->f stem cells stored → ASCT at first relapse. Late‑line immunotherapy: ->CAR‑T (BCMA): Cilta‑cel, Ide‑cel; ORR ~80–90%, remissions ~1–1.5 yrs. ->Bispecifics: Teclistamab, Elranatamab (BCMA); Talquetamab (GPRC5D); ORR ~70%, “off‑the‑shelf,” immediate use. Both: watch for CRS & neurotoxicity; infection risk high. 🛡️ Supportive & Drug‑Specific Toxicity (High‑Yield) 1. IMiDs (Len/Poma) → VTE risk → anticoag prophylaxis (ASA vs LMWH/DOAC). 2. Bortezomib → peripheral neuropathy → give SC, weekly, dose‑reduce if needed. 3. Carfilzomib → cardiomyopathy, HF, HTN → monitor CV status ± echo. 4. CD38 mAbs, CAR‑T, bispecifics → infections → antibacterial/viral prophylaxis, IVIG if severe hypogammaglobulinemia. 🔥 Ultra High‑Yield One‑Liners 1. Myeloma always arises from MGUS. 2. CRAB not required for diagnosis in 2024+; SLiM biomarkers suffice. 3. Myeloma lesions = purely osteolytic; bone scan can be normal. 4. SPEP can miss light‑chain disease → always think serum free light chains. 5. ≥60% marrow plasma cells OR FLC ratio ≥100 OR >1 MRI focal lesion = myeloma even if asymptomatic. del(17p), t(4;14), t(14;16), 1q gain = high‑risk cytogenetics. 6. Dara‑VRd quadruplet = current frontline standard in fit patients. 7. ASCT: ↑PFS, not OS; can be early or delayed (but don’t delay in high‑risk) 8. Lenalidomide maintenance improves PFS and OS; add bortezomib for high‑risk. 9. Venetoclax particularly active in t(11;14) myeloma. 🔖Follow Insta @ HemOnc_dr/ Twitter @MamthaB #Myeloma #HemOnc #MedEd #BoardReview #FOAMed #MedTwitter #OncTwitter #MedEd #Hematology #BoardReview #ITE #USMLE #FOAMed #Myeloma @IMFmyeloma @TheMMRF @MyelomaBeacon @NCCNorg @ASH_hematology @OncLive @TargetedOnc @TwoOncDocs @MedTwits @FOAMem @SagarLonialMD @NoopurRajeMD @VincentRK @realbowtiedoc @HemOncFellows @IMG_Oncologists @hemeoncfellow @OncoAlert @ASCO @ASCOPost

Paratesticular Fibrous Pseudotumor (PFP) #pathology

Recently started signing out endometrial biopsies... you get this slide (pic 1) and think: 'Is that fat? Perforation?!' 😱 Nope—this is pseudolipomatosis! An artifact with optically clear vacuoles mimicking adipocytes How to tell pseudolipomatosis vs real adipose tissue? → See Pic 2 Common sources of true fat in endometrial bx? → Pic 3 What real fat actually looks like here? → Pic 4 Great paper by Bahmad et al at Archives of Pathology doi.org/10.5858/arpa.2… #everydayGYN #pathology #PathX

I love this comment from Perplexity .....

4 members of a family

#PathQuiz 🔬🦴 A) Synovial sarcoma B) Osteofibrous dysplasia C) Ewing sarcoma D) Adamantinoma #Pathology #BonePath #Sarcoma Clue in caption 🧐

Mapping the WHO CNS5 Integrated Diagnosis CNS pathology #pathology

🩸 Chronic Lymphocytic Leukemia (CLL) – Board‑Style at a Glance (Follow ASCO/ASH/NCCN for latest updates) 🎯 CLL = CD5⁺ B‑cell leukemia. 13q = good, 17p = bad, mutated IGHV = good. Don’t treat at dx; treat when symptomatic. BTKi = nodes down, lymphocytes up. Richter = DLBCL. 💫“Mantra: Do NOT treat at dx; treat when symptomatic.💫 ->Most common adult leukemia; median age ~72 ->Older patient + lymphocytosis → think CLL ->Indolent mature B‑cell neoplasm; complications from immune dysfunction 1️⃣ Diagnosis ->Flow only: clonal CD5⁺ CD19⁺ CD23⁺ B cells ≥5 × 10⁹/L. ->Smudge cells on smear/CT not routinely needed. <5 × 10⁹/L + no LAD = MBL; <5 × 10⁹/L + LAD = SLL. 2️⃣ Genetics & Risk del(13q) 👍 best; trisomy 12 😐; del(11q) 👎; del(17p)/TP53 = worst, chemo‑resistant. Mutated IGHV = indolent; unmutated = aggressive. CD49d = strongest flow‑based prognostic marker. 💡 CD5⁺ B cell = think CLL. 3️⃣ When to Treat ->Treat the patient, not the lymphocyte count. ->Start therapy for: marrow failure (Hb <11, Plt <100k), bulky LAD/organomegaly, B‑symptoms, refractory autoimmune cytopenias. Rai 0–IV “0 = lymphocytosis only “III–IV = cytopenias from marrow failure Binet “A/B = ≤ or ≥3 areas, no cytopenias” “C = anemia and/or thrombocytopenia” 4️⃣ Therapy Choice: Frontline options: BTK inhibitors (ibrutinib, acalabrutinib, zanubrutinib) = continuous; venetoclax + anti‑CD20 = fixed duration (1–2 yrs, deep MRD Continuous vs Fixed 1. BTKi (acalabrutinib/zanubrutinib): BCR signaling block, continuous, nodes shrink + lymphocytes rise, risks = AFib, HTN, bleeding, hold 3–7 days pre‑op. 2. Venetoclax + anti‑CD20 (Obinutuzumab/Rituximab): BCL2 inhibition, 1‑2 yr fixed, high uMRD, must use 5‑week TLS ramp‑up.neutropenia main issue; excellent in mutated IGHV. 🚨17p = bad actor; BTKi preferred; del(17p) still high‑risk on ven. 5️⃣ Complications 1. Infections (top killer) → vaccinate (no live vaccines). 2. Autoimmune cytopenias (AIHA, ITP) from T‑cell dysfunction. 3. Second cancers (↑ skin SCC 5–10×) → annual derm exams. 4. Richter: CLL → DLBCL, rapid nodes + high LDH/SUV → trial/allo‑SCT. ⚡️ CLL in a blink: ->CD5⁺/CD23⁺ B‑cell → CLL. ->13q good, 17p bad. ->Venetoclax = TLS ramp‑up. ->BTKi = continuous, bleed risk around surgery. ->Richter = DLBCL, very poor prognosis. #MedTwitter #MedEd #HemOnc #OncTwitter #Leukemia #CLL #HemeOnc #BoardReview #USMLE #ABIM #FellowTwitter #InternalMedicine #FOAMed #OncoMedEd #CancerEducation @ASH_hematology @ASCOorg @theNCCN @EHA_Hematology @EuropeanHemOnc @CLLSociety @LeukemiaLymphoma @MDAndersonNews @DanaFarber @MayoClinic @ClevelandClinic @JCO_ASCO @BloodPortfolio @realbowtiedoc @IMG_Oncologists @HemOncFellows

🩸Hodgkin Lymphoma (HL)  ITE/Board review only 🧬 (Follow ASCO/ASH/NCCN for latest updates) Mnemonic🧠 📌''Bleomycin Blow up your lungs-watch for lung toxicity'' 📌"Popcorn is for the 20-Year-Olds"🍿 (LP (Lymphocyte-Predominant) cells look like popcorn. 20: They are CD20+ (unlike cHL). 📌Hodgkin🦉 = 15 & 30 party 🎉 1. Epidemiology & Pathology 🔬 ->Stats: ~8,830 cases/year (U.S.); bimodal age peaks (20–34 and 70+). 📊 ## cHL (95%): Characterized by Reed-Sternberg (HRS) cells.🦉 ->Markers: CD15+, CD30+, CD20-, PAX5 (weak). Subtypes:  1. Nodular Sclerosis (most common), 2.Mixed Cellularity (EBV+), 3.Lymphocyte-rich, 4. Lymphocyte-depleted. ## NLPHL-Nodular Lymphocyte-Predominant HL (NLPHL) – (5%): "Popcorn cells" 🍿(LP cells). ->Markers: CD20+, CD79a+, CD45+, CD15-/CD30-. ->Behavior: Indolent, like a B-cell Non-Hodgkin Lymphoma. 2. Early-Stage HL (Stage I–II) 📍 Stratified by  ->Favorable  ->Unfavorable (Risk factors: ESR >50, >2 nodal sites, or Bulky disease >10cm). GroupStandard Care 💊PET-Adapted Strategy 📡 -> Favorable: 2x ABVD + 20 Gy Radiation ->3x ABVD → If PET(-), omit Radiation. ->Unfavorable4x ABVD + 30 Gy Radiation ->2x ABVD → If PET(-), continue AVD; ->if PET(+), escalate. ->Bulky2+2 (2x BEACOPP + 2x ABVD)Focus on PET-negativity (Deauville 1–2) to omit RT. 3. Advanced-Stage HL (Stage III–IV) 🚀 The treatment landscape is shifting from traditional chemo to immunotherapy. ->Nivolumab + AVD (S1826 Trial): 🌟 New Emerging Standard. * PFS: 94% at 1 year. ->Pros: Better tolerated; less neuropathy and bone pain than Brentuximab. ->Brentuximab + AVD (ECHELON-1): 🎯 Established OS benefit. ->Cons: High peripheral neuropathy (~66%) and requires G-CSF (growth factor). ->RATHL (PET-Adapted): 2x ABVD → If PET(-) (DS 1–3), drop Bleomycin to avoid lung toxicity. 🫁 ->BrECADD: Highly effective BEACOPP modification; lower toxicity and 94% 4-year PFS. 4. Relapsed/Refractory (R/R) Strategy 🔄 The goal is a "Clean" PET before definitive therapy. Salvage Therapy:  ->Modern combos like Brentuximab + Nivolumab or Pembrolizumab + GVD (80–95% PET-negative rates). 🧪 Consolidation:  High-dose chemotherapy followed by Autologous Stem Cell Transplant (ASCT). 🏥 Maintenance: Post-ASCT Brentuximab for high-risk patients. 5.🎯 Key Toxicity Watch-list ⚠️ ->Bleomycin: Pulmonary fibrosis/toxicity 🫁 ->Brentuximab: Peripheral neuropathy (numbness/tingling). ⚡ ->Radiation: Secondary cancers (breast/thyroid) and CV disease. ❤️ ->Nivolumab: Immune-related adverse events (colitis, thyroiditis). ✨In short✨ Advanced cHL (III-IV) Preferred: 🥇 N-AVD (Cat 1) 🥈 BV-AVD (Cat 1) ✅ ABVD → PET-adapted Early Favorable: 2-4×ABVD ± ISRT Early Unfavorable: 4×ABVD + ISRT or PET-adapted 🚀 2026 Practice Shifts ->N-AVD dominance in advanced cHL (better tolerability than BV-AVD). ->Liquid biopsy integration (ctDNA MRD) for R/R therapy adaptation. ->RT minimization in early-stage via novel combos (92% CR, no FN). 🩸Bottom line: N-AVD is the 2026 advanced cHL regimen; early-stage moving toward chemo-only deep response; ctDNA will guide R/R decisions #HodgkinLymphoma #HemOnc #MedEd #Lymphoma #OncTwitter #ClinicalTrials #NCCN @NCCNorg @ASH_hematology @LymphomaHub @OncLive @TargetedOnc @ASCOPost @SWOG @COGorg @TwoOncDocs @UToledo @realbowtiedoc @OncBrothers @OncoAlert @oncodaily @IMG_Oncologists @HemOncFellows @hemeoncfellow

MPN (Myeloproliferative Neoplasms) Board/ITE Key Clinical Pearls 🩸🧬 Mnemonic🙂 “⚡JAK ate 🍁MAPL syrup when 📜CALR came to visit the 🏠MPN house'' MPN Categories 🔹 Chronic Myeloid Leukemia – BCR-ABL1 driven, highly treatable 🔹 Chronic Neutrophilic Leukemia – CSF3R mutation; transplant often needed 🔹 Chronic Eosinophilic Leukemia – clonal eosinophilia; transplant main option 🔹 JAK2-related MPNs: • Polycythemia Vera • Essential Thrombocythemia • Primary Myelofibrosis Driver Mutations 🧬 ⚡ JAK2 V617F – almost all PV, ~50% ET/PMF ⚡ CALR – common in JAK2-negative ET/PMF ⚡ MPL – less common ⚡ 10–20% triple-negative Diagnosis 🩺 • PV: ↑Hb + JAK2 → diagnosis likely • ET: mutation panel (JAK2/CALR/MPL) + CBC/smear • PMF:bone marrow + cytogenetics + NGS essential Not Every Erythrocytosis Is PV ⚠️ Common causes: 💊 SGLT2 inhibitors 💊 Testosterone ➡️ Check JAK2 first ➡️ Don’t stop beneficial meds automatically Major Risks in MPNs • Thrombosis • Symptoms / QoL 😴 • Leukemic transformation AML risk: • ET <5% • PV ~10% • PMF ~30% ET Management 🩸 🎯: prevent thrombosis PLT>450X109/L 🦶 Erythromelalgia, 🤕 Headache, 🩸 Clots 🔍 Diagnosis: BM Biopsy  with predominent predominant Risk factor: prior thrombosis Platelet number is not a risk factor for thrombosis!!! Treatment: 🟢 Low-risk (<60 no clot) → Aspirin 🔴 High-risk (>60 +/- clot) → Cyto reduction (Hydroxyurea) ± anticoagulation Aspirin strategy: • JAK2+ (High risk of thrombosis) → twice daily • Others → once daily • CALR type 2 / triple-negative → may skip aspirin The "Triple-A" Score: Modern prognosis in ET now uses Absolute Neutrophil, Monocyte, and Lymphocyte counts to identify patients who will live as long as the general population. PV Management 🧪 Low-risk: 🩸 Phlebotomy + Aspirin 🎯 Hct <45% or Females <16, Males <16.5 High-risk: 💊 Hydroxyurea (Cytoreductive therapy-1L) 💊 Interferon (alternative) 💊 Ruxolitinib (2L- line-✅ Pruritis, 📉 Decreases EFS) 💊 Buslphan (Older patients ) New therapy: 💉 Ropeginterferon-alfa (FDA approval recently) 💉 Rusfertide – hepcidin mimetic (reduces phlebotomy) Myelofibrosis 🔥 → Most aggressive MPN. Night Sweats, 🌡️ Fever, 🦴 Bone Pain, Weight Loss,  Organomegaly  Hepatomegaly &  Splenomegaly),  Cytopenia, insomnia, fatigue, early satiety, abdominal pain 📊 IPSS Scoring System: Risk Groups 📉🧬Worsening prognosis: CALR+ (22.7%-17.7 yr)—>JAK2+ (65%-9.2yr) or MPL+ (4%-3.2yr)—> Triple Negative. (8.6%) 🚨High Molecular risk: 🧬IDH1/2, EZH2, ASXL1, SRSF2 Only cure: 🏥 Allogeneic stem cell transplant If not eligible: ->Low risk/not symptomatic: observation ->Low risk/symptomatic: clinical trial/ruxolitinib/peginterferon /hydroxyuria ->High risk: transplant elgible-allo HSCT 💊 JAK inhibitors 1. Ruxolitinib – best tolerated and for spleen size and constitutional symptoms- Side effects-Zoster, TB activation, avoid interruptions causes SIRS so bridge with steroids 2. Momelotinib (MF+Anemia)(SE-Peripheral neuropathies) – helpful for anemia 3. Fedratinib-2L (SE-GI, WE (monitor thiamine) 4. Pacritinib (ACVR1- MF + platelets <50k or anemia) ->No constitutuation symptoms/splenomegaly 1. EPO>500mIU/ml→Luspatercept, danzol, iMids 2. EPO<500mIU/ML→ESA ➡️ Improve symptoms & spleen ❌ Do not cure disease Emerging Therapies 🚀 • Navitoclax • Pelabresib • Selinexor -CAR-T, CALR vaccines, TGF-β inhibitors- are in development 🧬 Clonal Eosinophilia 🧪 Key Molecular Screens 1. FIP1L1–PDGFRA: 🧬 (~10% of HES). Detect via FISH (look for CHIC2 deletion) or RNA-Seq. 2. PDGFRB: 🧬Often an MDS/MPN overlap. 3. FGFR1: 🧬🔥 (8p11 syndrome). Highly aggressive; often transforms to AML/Lymphoma. 4. JAK2 Rearrangements: 🧬 (Not V617F mutation!). 💊 Targeted Treatment Table ->FIP1L1–PDGFRA- Imatinib- Exquisitely sensitive (100mg dose) ->PDGFRB- Imatinib - High response rates 👍 ->FGFR1- Pemigatinib -Requires Chemo + Transplant ->JAK2 Rearr-Ruxolitinib -Specific for rearrangements- CEL-NOSCytoreduction 📉Diagnosis of exclusion 🔍 Chronic Neutrophilic Leukemia (CNL) 🩸 Hallmark: CSF3R mutation (G-CSF receptor). 🧬🔗 Presentation: Neutrophils/Bands >80% + Splenomegaly Treatment: Ruxolitinib  (Symptom relief) ➡️ SCT 🏥 (Curative). Systemic Mastocytosis (SM) 🐝 Hallmark: KIT D816V mutation. 🧬 Physical Exam: Darier Sign (rubbing skin causes hives) 🤏+ Urticaria Pigmentosa. Markers: Tryptase 📈, CD25, and CD117 (KIT). 🧪 Treatment: Avapritinib or Midostaurin 🎯. #Hematology #Oncology #MedEd #HemOnc #FOAMed #MPN #BoardReview #MedStudentTwitter #InternalMedicine #Pathology #MPN @ASH_hematology @MPNVoice @ASCOPost @IMG_Oncologists @OncoAlert @oncodaily @realbowtiedoc @VJHemOnc @JCO_ASCO @LeukemiaJnl #HemOnc #MedTwitter #FOAMed @HemOncFellows

Angiomyolipoma: Key Diagnostic Features Soft tissue pathology #pathology