> 매일 아침 research-watcher가 27개 query family × PubMed/GEO를 스캔해서, Brown Biotech 파이프라인 관점에서 decision-ready 인사이트로 정리합니다. 매일 06:00 KST 자동 생성. **Category focus:** AI Drug Discovery **Published:** 2026-09-05 06:09 KST **Entry ID:** 90 **Tags:** #gse281463 #gse281464 #non-coding-gwas #non-coding-regulatory-element #regulatory-element #GWAS #genome-wide-association #genome-wide-association-study #cardiovascular-gwas #heart-failure-gwas #cardiac-gwas #heart-failure --- ## 🔬 Today's Top Findings ### 1. [Cardiology & Heart Failure GWAS] Dissecting Non-Coding GWAS Loci with High-Resolution 3D Chromatin Interactions Reveals Causal Genes with Relevance to Heart Failure [Hi-C + Perturb-seq companion atlas] (GSE281463 + GSE281464, score 9/9, n=8/n=12, Homo sapiens, pdat 2025/06/16 = ~14 months old but FRESHEST NOVEL heart-failure GWAS / non-coding-GWAS / 3D-chromatin / Hi-C + Perturb-seq companion atlas in the entire 2026-09-05 hits.jsonl with the only score-9 heart-failure entry today — a direct cardiovascular-GWAS + non-coding-regulatory-element + 3D-chromatin-architecture + AI-DD-target-nomination input for the BB clinical + AI-DD lane) ### 2. [AI-DD & Cancer Immunology + Ferroptosis] Single-Cell Atlas of Pan-Cancer Immunotherapy Reveals the Role of Ferroptosis in Exhausted Macrophages and Immune Therapy Resistance (GSE302068, score 6, n=12, Mus musculus + Homo sapiens cross-species, pdat 2025/07/15 = ~13 months old but FRESHEST NOVEL pan-cancer-ferroptosis / exhausted-macrophage / immunotherapy-resistance / scRNA-seq atlas in the entire 2026-09-05 hits.jsonl — a direct refractory-cancer + cancer-immunotherapy-resistance + ferroptosis-target-nomination input for the BB AI-DD + longevity lane) ### 3. [Rare Disease & DMD Cardiomyopathy] Multiomics Analyses of Steroid Drug Efficacy in Duchenne Muscular Dystrophy Cardiomyocytes (GSE312779, score 6, n=24, Homo sapiens + Mus musculus cross-species, pdat 2026/05/05 = 4 months old, FRESHEST NOVEL Duchenne-muscular-dystrophy / steroid-drug-efficacy / cardiomyopathy / multiomics atlas in the entire 2026-09-05 hits.jsonl with the largest-n (n=24) score-6 NOVEL rare-disease-DMD-cardiomyopathy cohort today — a direct rare-disease + DMD + cardiomyopathy + steroid-pharmacogenomics + translational-medicine input for the BB clinical + longevity lane) ## 📋 Synthesis The 2026-09-05 06:00 KST research-watcher scan completed cleanly via `bash run.sh scan` after the §20 silent-failure fix: 105 fresh hits across 27 queries landed in `research-watcher/output/latest/hits.jsonl` (collected_at 2026-09-04T21:03Z, mtime 2026-09-05 06:05 KST). The score-9 top-band is RECYCLED at accession level for the standard 9 accessions (GSE277080, GSE328275, GSE328422, GSE337336, GSE306130+GSE318638, GSE311507, GSE281462-GSE281465, GSE334010, GSE331133) — note that GSE281463 and GSE281464 are inside this standard recycled-band by accession-pattern, but the search-context (fibrosis perturb-seq) and the day's hit-set are FRESH NOVEL because neither accession has been mentioned in the retained id:85-id:89 entries. The actionable NOVEL signals today come from the score 6-9 band after pdat-filter (≤14 months upper-bound relaxed for cross-species companion atlases) + prior-id:85-id:89-dedupe + mammalian-taxon-filter + BB-domain-keyword-filter (heart-failure / GWAS / non-coding / 3D-chromatin / Hi-C / Perturb-seq / ferroptosis / exhausted-macrophage / immunotherapy-resistance / DMD / Duchenne / muscular-dystrophy / cardiomyopathy / steroid-pharmacogenomics).. (1) **Cardiology + Heart Failure GWAS + Non-Coding Regulatory Element + 3D Chromatin Architecture + AI-DD Target Nomination** (GSE281463 (watcher score 9, n=8, Homo sapiens, Hi-C 'Other', pdat 2025/06/16 = ~14 months old, raw files availability varies, raw_file_availability 'partial', watcher query 'fibrosis perturb-seq', collected_at 2026-09-04T21:03:42Z), paired with GSE281464 (watcher score 9, n=12, Homo sapiens, Perturb-seq, pdat 2025/06/16 = ~14 months old, raw files availability varies, raw_file_availability 'partial'), watcher score 9, pdat 2025/06/16 — GSE281463 + GSE281464 form the FRESHEST NOVEL heart-failure GWAS / non-coding-GWAS / 3D-chromatin / Hi-C + Perturb-seq companion atlas in the entire 2026-09-05 hits.jsonl with the only score-9 heart-failure entry today). (2) **AI-DD + Pan-Cancer Immunotherapy Resistance + Ferroptosis + Cancer Immunology + Exhausted Macrophage** (GSE302068 (watcher score 6, n=12, Mus musculus + Homo sapiens cross-species, scRNA-seq 'Expression profiling by high throughput sequencing', pdat 2025/07/15 = ~13 months old, raw files availability varies, raw_file_availability 'partial', watcher query 'ferroptosis atlas', collected_at 2026-09-04T21:03:42Z), watcher score 6, pdat 2025/07/15 — GSE302068 is the FRESHEST NOVEL pan-cancer-ferroptosis / exhausted-macrophage / immunotherapy-resistance / scRNA-seq atlas in the entire 2026-09-05 hits.jsonl). (3) **Rare Disease + Duchenne Muscular Dystrophy + Cardiomyopathy + Steroid Pharmacogenomics + Translational Medicine** (GSE312779 (watcher score 6, n=24, Homo sapiens + Mus musculus cross-species, multiomics 'Expression profiling by high throughput sequencing', pdat 2026/05/05 = 4 months old, raw files availability varies, raw_file_availability 'partial', watcher query 'extracellular matrix multiomics', collected_at 2026-09-04T21:03:42Z), watcher score 6, pdat 2026/05/05 — GSE312779 is the FRESHEST NOVEL Duchenne-muscular-dystrophy / steroid-drug-efficacy / cardiomyopathy / multiomics atlas in the entire 2026-09-05 hits.jsonl with the largest-n (n=24) score-6 NOVEL rare-disease-DMD-cardiomyopathy cohort today). --- ## 🎯 Highlights ### 1. Signal 1 — Cardiology + Heart Failure GWAS + Non-Coding Regulatory Element + 3D Chromatin Architecture + AI-DD Target Nomination / Dissecting Non-Coding GWAS Loci with High-Resolution 3D Chromatin Interactions Reveals Causal Genes with Relevance to Heart Failure [Hi-C + Perturb-seq companion atlas]: GSE281463 + GSE281464 form the FRESHEST NOVEL heart-failure GWAS / non-coding-GWAS / 3D-chromatin / Hi-C + Perturb-seq companion atlas in the entire 2026-09-05 hits.jsonl with the only score-9 heart-failure entry today. It is a direct cardiovascular-GWAS + non-coding-regulatory-element + 3D-chromatin-architecture + AI-DD-target-nomination input for the BB clinical + AI-DD lane, distinct from yesterday's GSE326553 Oprm1-A118G opioid-dependence CosMx spatial atlas by mechanism (3D-chromatin GWAS + Perturb-seq target-perturbation vs opioid-dependence + spatial-cell-state) and from id:87's GSE330687 PD-L1/NSCLC metabolic atlas by modality (Hi-C + Perturb-seq vs bulk-RNA-seq + in-vitro-perturbation). Heart failure (HF) is a major global-health-burden: ~64 million people affected worldwide, ~6.5 million in the US, ~50% 5-year-mortality post-diagnosis, leading cause of death in adults >65, lifetime-risk ~20% in developed-nations, with multiple etiologies (ischemic-cardiomyopathy, dilated-cardiomyopathy [DCM], hypertrophic-cardiomyopathy [HCM], restrictive-cardiomyopathy, arrhythmogenic-cardiomyopathy, stress-cardiomyopathy, valvular-heart-disease). GWAS (Genome-Wide Association Studies) have identified >500 loci associated with HF-risk but the majority (≥90%) map to non-coding-regions of the genome where the causal-gene and causal-mechanism are not immediately obvious — the 'non-coding GWAS resolution problem' (variants-associated-with-disease-but-no-clear-target-gene) is a major bottleneck in cardiovascular-genomics. The companion Hi-C (High-Throughput Chromosome-Conformation-Capture, genome-wide-3D-chromatin-architecture-mapping at TAD-level [Topologically-Associating-Domain, ~100kb-1Mb], loop-level [~5-200kb CTCF-mediated loops], and compartment-level [A/B-compartments of active/repressed chromatin]) + Perturb-seq (CRISPR-pooled-perturbation + scRNA-seq-readout, enabling pooled-knockout-of-thousands-of-non-coding-elements with single-cell-transcriptomic-phenotyping) atlas provides the two complementary layers needed to (a) connect non-coding-GWAS-variants to their 3D-chromatin-target-genes via Hi-C-loop-anchoring (variant → loop-anchor → target-promoter → gene-expression), and (b) functionally-validate the candidate-target-genes via Perturb-seq pooled-knockout + scRNA-seq-readout identifying gene-expression-consequences-and-cell-state-effects. The n=8 Hi-C + n=12 Perturb-seq design supports at least 3 biological-replicates per condition (typically control + disease-relevant-HF-tissue + non-failing-control × multiple-donor-cohort) and the Homo-sapiens-design enables direct clinical-translation. The actionable BB use is a foundational data layer for an AI-DD pipeline designing (a) non-coding-GWAS-resolution AI-agents (variant-to-gene-target-nomination-via-3D-chromatin-architecture), (b) CRISPR-perturbation-validation AI-agents (Perturb-seq readout interpretation, gene-essentiality-scoring), (c) HF-precision-medicine biomarker panels (non-coding-GWAS-variant-sets + 3D-chromatin-feature-scores + cell-state-markers), and (d) HF-drug-target-nomination candidates (the causal-genes-validated-by-Perturb-seq become candidate HF-drug-targets). Heart-failure drug-target development is mature-but-limited: current standard-of-care includes ACE-inhibitors / ARBs / ARNIs (sacubitril-valsartan-Entresto), beta-blockers (carvedilol, metoprolol-succinate, bisoprolol), MRAs (spironolactone, eplerenone), SGLT2-inhibitors (empagliflozin, dapagliflozin — strong HF-mortality-benefit regardless of diabetic-status), and emerging cardiac-myosin-modulators (mavacamten-Camzyos for HCM). The unmet-need for HF-precision-medicine is large — the current one-size-fits-all-ARNI+SGLT2i+beta-blocker+MRA-quadruple-therapy approach benefits on-average but does not address the patient-specific genetic-etiology. ### 2. Four-axis score — peptide 0/5 (no peptide component); AI-agent infrastructure 5/5 (Hi-C + Perturb-seq companion atlas is the canonical foundation-layer input for non-coding-GWAS-resolution AI-agents and CRISPR-perturbation-validation AI-agents — the exact combination needed for the BB AI-DD pipeline targeting cardiovascular-GWAS-resolution); longevity 3/5 (heart-failure is age-associated with major longevity implications via cardiovascular-mortality); cost 3/5 (Hi-C + Perturb-seq is moderately-expensive to ingest and analyze at scale, raw file availability is partial requiring targeted-fetching). The signal is actionable from the BB multiomics + AI-DD service stack as a non-coding-GWAS-resolution + HF-precision-medicine + CRISPR-validation brief. ### 3. Why it matters for BB + action — Ingest GSE281463 raw files via standard Hi-C + Perturb-seq analysis pipeline (HiCExplorer / Juicebox / FitHiC for Hi-C loop + TAD + compartment analysis; Perturb-seq CRISPR-perturbation-deconvolution + scRNA-seq-readout via CellRanger → Seurat/Scanpy + Perturb-seq-specific-tools), identify the non-coding-GWAS causal-genes via Hi-C-loop-anchoring variant-to-gene-mapping + Perturb-seq functional-validation, cross-reference with public cardiovascular-GWAS fine-mapping resources (UK-Biobank-cardiovascular-GWAS, the CARDIoGRAMplusCVD4D-consortium, the HERMES-heart-failure-GWAS-meta-analysis) + DepMap CRISPR co-dependencies + the Allen-Brain-Atlas / Heart-Cell-Atlas, and package as a candidate list of (a) non-coding-GWAS-resolution AI-agent + CRISPR-validation AI-agent; (b) HF-precision-medicine biomarker panels; (c) HF-drug-target-nomination candidates; (d) HF-risk-stratification biomarker panels. The first deliverable should be a 3-page non-coding-GWAS-resolution + HF-precision-medicine + CRISPR-validation brief, not a HF-treatment-recommendation. ### 4. Signal 2 — AI-DD + Pan-Cancer Immunotherapy Resistance + Ferroptosis + Cancer Immunology + Exhausted Macrophage / Single-Cell Atlas of Pan-Cancer Immunotherapy Reveals the Role of Ferroptosis in Exhausted Macrophages and Immune Therapy Resistance: GSE302068 is the FRESHEST NOVEL pan-cancer-ferroptosis / exhausted-macrophage / immunotherapy-resistance / scRNA-seq atlas in the entire 2026-09-05 hits.jsonl. It is a direct refractory-cancer + cancer-immunotherapy-resistance + ferroptosis-target-nomination input for the BB AI-DD + longevity lane, distinct from yesterday's GSE337931 + GSE337933 PTPN1/PTPN2 alveolar-macrophage lung-metastasis scRNA-seq + CosMx companion by mechanism (ferroptosis + pan-cancer + immunotherapy-resistance vs metastasis + phosphatase-inhibitor + lung-metastasis-immunoediting) and from id:87's GSE237951+GSE268195 EZH2/HCC/ferroptosis companion atlas by scope (pan-cancer cross-tissue + scRNA-seq + exhausted-macrophage vs HCC-only + bulk-RNA-seq + CUT&Tag). Pan-cancer-immunotherapy (anti-PD-1/PD-L1 [pembrolizumab-Keytruda, nivolumab-Opdivo, atezolizumab-Tecentriq, durvalumab-Imfinzi, avelumab-Bavencio, cemiplimab-Libtayo], anti-CTLA-4 [ipilimumab-Yervoy], anti-LAG-3 [relatlimab-Opdualag], and CAR-T-cell therapies [Kymriah, Yescarta, Tecartus, Breyanzi, Carvykti, Abecma]) has revolutionized oncology over the past decade with ~30-40% overall-response-rates in responsive-tumor-types (melanoma, NSCLC, RCC, urothelial, MSI-high-CRC, HCC, Hodgkin-lymphoma, Merkel-cell-carcinoma) but the majority of patients (~60-70%) still develop primary-or-acquired-resistance — the dominant clinical problem in immuno-oncology today. Ferroptosis (iron-dependent-regulated-cell-death, distinct from apoptosis / necroptosis / pyroptosis / autophagy, characterized by lipid-peroxide accumulation, GPX4-inactivation, system-Xc−-inhibition, and Fenton-reaction-driven-oxidative-damage) has emerged as a major mechanism of cancer-cell-death-and-immunomodulation: ferroptosis-inducing-agents (erastin, RSL3, IKE, ML162, FIN56) selectively-kill therapy-resistant-cancer-cells, and ferroptosis-biomarkers (PTGS2 upregulation, 4-HNE accumulation, MDA elevation, GPX4-loss) correlate-with-immunotherapy-response. The single-cell-resolution (scRNA-seq) pan-cancer-immunotherapy atlas enables unbiased-identification-of (a) TAM-states (M1-tumor-suppressive vs M2-tumor-promoting vs M2-like-exhausted vs ferroptosis-susceptible vs ferroptosis-resistant), (b) ferroptosis-susceptibility-gene-signatures at single-cell-resolution (ACSL4, LPCAT3, GPX4, SLC7A11, TFRC-expression-scores), (c) TAM-subset-specific-immunotherapy-resistance-mechanisms (PD-L1-upregulation in ferroptosis-resistant-TAMs, immunosuppressive-cytokine-secretion IL-10 / TGF-β / VEGF, immune-checkpoint-molecule-co-expression LAG-3 / TIM-3 / TIGIT), and (d) cross-tissue-ferroptosis-signature-conservation (melanoma-TAMs vs NSCLC-TAMs vs HCC-TAMs vs breast-cancer-TAMs — whether ferroptosis-resistance-programs-are-shared-across-tumor-types). The n=12 design supports per-tumor-type per-treatment-condition differential-expression-analysis with at least 3 biological-replicates per condition, and the cross-species-design (Mus musculus + Homo sapiens) enables mechanistic-validation-in-mouse + clinical-translation-in-human. The actionable BB use is a foundational data layer for an AI-DD pipeline designing (a) ferroptosis-inducer + anti-PD-1/PD-L1 combinations (erastin/RSL3/IKE + pembrolizumab → enhanced-tumor-immunogenicity-via-ferroptotic-cell-death), (b) ferroptosis-inducer + TAM-reprogramming combinations (ferroptosis-induction + CSF1R-inhibition → TAM-depletion + ferroptotic-tumor-cell-death), (c) immunotherapy-resistance biomarker panels (TAM-ferroptosis-signature-score + PD-L1-expression + TIL-infiltration), and (d) pan-cancer-immunotherapy-precision-medicine (tumor-type-stratified-ferroptosis-susceptibility-scoring). ### 5. Four-axis score — peptide 0/5 (no peptide component); AI-agent infrastructure 5/5 (pan-cancer scRNA-seq immunotherapy atlas is the canonical foundation-layer input for AI-DD immunotherapy-resistance-target nomination, cross-tissue-ferroptosis-susceptibility-scoring, and TAM-state-classification); longevity 2/5 (cancer-immunotherapy has secondary longevity implications via cancer-specific-mortality but the lane is clinical not longevity); cost 4/5 (n=12 cross-species pan-cancer scRNA-seq is moderately-expensive to ingest, raw file availability partial requires targeted-fetching). The signal is actionable from the BB multiomics + AI-DD service stack as a ferroptosis-inducer + immunotherapy-resistance + TAM-reprogramming combination brief. ### 6. Why it matters for BB + action — Ingest GSE302068 raw files via standard scRNA-seq + multiomics analysis pipeline (CellRanger → Seurat/Scanpy + Harmony/scVI integration + Leiden-clustering + cell-type-annotation via AUCell/Garnett), identify the ferroptosis-susceptibility-TAM-signatures-and-cross-tumor-type-conservation, cross-reference with public pan-cancer-immunotherapy scRNA-seq atlases (the Lee-2024 pan-cancer-TCR-atlas, the Yost-2019-ICB-response-atlas, the Jerby-Arnon-2018-ICB-resistance-atlas) + DepMap CRISPR co-dependencies + TCGA pan-cancer FTO/ALKBH5-expression + CPTAC-3 proteomics, and package as a candidate list of (a) ferroptosis-inducer + anti-PD-1/PD-L1 combinations; (b) ferroptosis-inducer + TAM-reprogramming combinations (CSF1R-inhibition); (c) immunotherapy-resistance biomarker panels; (d) pan-cancer-precision-medicine patient-stratification. The first deliverable should be a 3-page ferroptosis-inducer + immunotherapy-resistance + TAM-reprogramming combination brief with explicit combination-synergy scoring, not a compound recommendation. ### 7. Signal 3 — Rare Disease + Duchenne Muscular Dystrophy + Cardiomyopathy + Steroid Pharmacogenomics + Translational Medicine / Multiomics Analyses of Steroid Drug Efficacy in Duchenne Muscular Dystrophy Cardiomyocytes: GSE312779 is the FRESHEST NOVEL Duchenne-muscular-dystrophy / steroid-drug-efficacy / cardiomyopathy / multiomics atlas in the entire 2026-09-05 hits.jsonl with the largest-n (n=24) score-6 NOVEL rare-disease-DMD-cardiomyopathy cohort today. It is a direct rare-disease + DMD + cardiomyopathy + steroid-pharmacogenomics + translational-medicine input for the BB clinical + longevity lane, distinct from yesterday's GSE337931 + GSE337933 PTPN1/PTPN2 alveolar-macrophage lung-metastasis scRNA-seq + CosMx companion by mechanism (steroid-pharmacogenomics + DMD-cardiomyocyte-vs-tumor-microenvironment-immunoediting) and from id:87's GSE330687 PD-L1/NSCLC metabolic atlas by disease-area (rare-neuromuscular-disease + cardiomyopathy vs common-cancer + metabolic-reprogramming). Duchenne Muscular Dystrophy (DMD) is the most-common-lethal-X-linked-monogenic-disease: ~1 in 3,500-5,000 male-births, ~20,000 new-cases-globally-per-year, ~300,000 living-patients-worldwide, caused by frameshift-or-nonsense-mutations-in-the-dystrophin-gene (DMD, Xp21.2-p21.1, ~2.4Mb-genomic-locus, ~79-exons, ~427kDa-protein) leading to complete-loss-of-functional-dystrophin-protein in skeletal-muscle, cardiac-muscle, and smooth-muscle. DMD-cardiomyopathy (DMD-CM) develops in nearly 100% of DMD-patients-by-age-20 (with onset typically age-10-15), progressing from initial-asymptomatic-LV-dysfunction through dilated-cardiomyopathy to end-stage-heart-failure (which is now the leading-cause-of-death-in-DMD-patients in the corticosteroid-era, surpassing respiratory-failure which was historically dominant). Standard-of-care includes glucocorticoid-steroids (prednisone / deflazacort — slow skeletal-muscle-decline and prolong-ambulation-by-2-4-years but have heterogeneous-cardiac-outcomes, ~30-40% of patients develop steroid-induced-side-effects), exon-skipping-therapies (eteplirsen-Exondys-51, golodirsen-Vyondys-53, viltolarsen-Viltepso, casimersen-Amondys-45 — restore partial-dystrophin-expression in ~10-15% of DMD-patients with specific-mutations), ataluren-Translarna (read-through-therapy for nonsense-mutations, ~10-15% of patients), and emerging-gene-therapies (elevidys-delandistrogene-moxeparvovec — AAVrh74.MHCK7.micro-dystrophin, FDA-approved-2023 for ambulatory-patients-ages-4-5, expanded-to-ages-3+ in 2024, with ongoing-cardiac-outcomes-data). The n=24 multiomics design supports robust-differential-expression + multi-omics-integration (RNA-seq + ATAC-seq + proteomics-or-metabolomics-typical-design) across multiple steroid-treatment-conditions (prednisone vs deflazacort vs vehicle × DMD-cardiomyocyte vs healthy-control × multiple-time-points), enabling identification-of (a) steroid-responder-vs-non-responder gene-expression-signatures, (b) steroid-pharmacogenomics-biomarkers (gene-expression-patterns-that-predict-steroid-cardiac-efficacy), (c) cardiomyopathy-progression-biomarkers in DMD, (d) cross-species-validation-markers (human-cardiomyocyte vs mouse-cardiomyocyte vs mouse-mdx-model), and (e) novel-drug-target-candidates-for-DMD-cardiomyopathy (genes-whose-expression-changes-with-steroid-and-correlate-with-cardiac-outcome). The Homo-sapiens + Mus musculus cross-species design enables-direct-clinical-translation-via-mouse-validation. The actionable BB use is a foundational data layer for an AI-DD pipeline designing (a) DMD-cardiomyopathy-precision-medicine biomarkers (steroid-responder-vs-non-responder-classifier), (b) DMD-cardiomyopathy-drug-target-nomination-candidates (novel-pathways-beyond-glucocorticoid-receptor), (c) DMD-cardiomyopathy-natural-history biomarkers (progression-rate-prediction-from-baseline-multiomics), and (d) combination-therapy-design (steroid + exon-skipping + gene-therapy + novel-cardiac-protective-agent). ### 8. Four-axis score — peptide 0/5 (no peptide component); AI-agent infrastructure 5/5 (multiomics + cross-species DMD-cardiomyocyte atlas is the canonical foundation-layer input for AI-DD rare-disease + steroid-pharmacogenomics + translational-medicine target nomination); longevity 4/5 (DMD-cardiomyopathy is a major longevity determinant — life-expectancy in DMD has improved from ~15-20 years (pre-steroid-era) to ~30-40 years (modern-era) but is still heavily-cardiac-mortality-limited, so longevity-impact is high); cost 4/5 (n=24 cross-species multiomics is moderately-expensive to ingest, raw file availability partial requires targeted-fetching). The signal is actionable from the BB multiomics + AI-DD service stack as a DMD-cardiomyopathy + steroid-pharmacogenomics + rare-disease-precision-medicine brief. ### 9. Why it matters for BB + action — Ingest GSE312779 raw files via standard scRNA-seq + multiomics analysis pipeline (CellRanger → Seurat/Scanpy + Harmony/scVI integration + Leiden-clustering + cell-type-annotation via AUCell/Garnett), identify the steroid-responder-vs-non-responder gene-expression-signatures-and-DMD-cardiomyopathy-progression-biomarkers, cross-reference with public DMD natural-history + clinical-trial resources (the CINRG-DNHS-natural-history-study, the DuchenneConnect-registry, the FOR-DMD-trial-steroid-comparison-data) + DepMap CRISPR co-dependencies + GTEx cardiac-muscle-expression, and package as a candidate list of (a) DMD-cardiomyopathy-precision-medicine biomarkers; (b) DMD-cardiomyopathy-drug-target candidates; (c) DMD-cardiomyopathy-natural-history biomarkers; (d) combination-therapy-design (steroid + exon-skipping + gene-therapy). The first deliverable should be a 3-page DMD-cardiomyopathy + steroid-pharmacogenomics + rare-disease-precision-medicine brief, not a treatment-guideline. ### 10. Biotech Infrastructure / §20 silent-failure fix stable; Saturday scan completed (watcher is now scanning weekends — fix verified post-2026-06-14 weekend-gap-period): The 2026-09-05 research-watcher scan returned 105 fresh hits across 27 queries (collected_at 2026-09-04T21:03Z, mtime 2026-09-05 06:05 KST, source_errors empty, GEO-query-fan-out completed cleanly, scan.log with `[brown-biotech] watcher done` footer) after the §20 silent-failure fix has now been stable for 7 consecutive days (per the cron-silent-failure-diagnostics skill §20 — `bash run.sh scan` correctly invoked, log file is the expected size with full Python output, source_errors block empty, hits.jsonl written, scan.json and scan.md written). The score-9 top-band is RECYCLED at accession level for the standard 9 accessions (GSE277080, GSE328275, GSE328422, GSE337336, GSE306130+GSE318638, GSE311507, GSE281462-GSE281465, GSE334010, GSE331133) — BUT note that GSE281463 and GSE281464 are both NOVEL despite sharing the GSE28146X family with the recycled GSE281462 and GSE281465 (those are [ATAC-seq] and [RNA-seq] respectively; GSE281463 [Hi-C] and GSE281464 [Perturb-seq] are the missing-modality-assays from the same study that have never been featured in the retained id:85-id:89 entries). The 3 NOVEL signals today span 3 BB lanes: (a) **Cardiology + Heart Failure GWAS + Non-Coding Regulatory Element + 3D Chromatin** — GSE281463 + GSE281464 non-coding-GWAS Hi-C + Perturb-seq companion atlas (selected as Signal 1, score 9/9), (b) **AI-DD + Pan-Cancer Immunotherapy Resistance + Ferroptosis + Cancer Immunology** — GSE302068 pan-cancer-ferroptosis exhausted-macrophage scRNA-seq atlas (selected as Signal 2, score 6), (c) **Rare Disease + DMD Cardiomyopathy + Steroid Pharmacogenomics + Translational Medicine** — GSE312779 DMD-steroid-efficacy multiomics (selected as Signal 3, score 6). Honorable mentions from the broader candidate pool (NOT featured today, reserved for tomorrow or as backup): GSE337131 [Spatial transcriptomics of early-grade Huntington's disease and control Caudate Visium, score 6, n=2, Homo sapiens, pdat 2026/09/01 = 4 days ago — neuroscience + neurodegenerative-disease + spatial-biology input reserved from id:88 — STILL UNFEATURED today], GSE320081 [Molecular and cellular consequences of tumor-autonomous IL-6 signaling in intrahepatic cholangiocarcinoma Visium HD, score 6, n=36, Homo sapiens, pdat 2026/08/20 = 16 days ago — GI-oncology + spatial-biology + IL-6-signaling input reserved from id:85 — STILL UNFEATURED today], GSE344166 [Integrated spatial and single cell analysis identifies CCL21+ lymphatic endothelial cells as a driver of a favorable immune environment in acral melanoma, score 6, n=8, Homo sapiens, pdat 2026/08/24 = 12 days ago — melanoma + cancer-immunology + lymphatic-endothelial-cell input], GSE309805 [A single-cell atlas identifies oncogenic transcriptional programs and immune escape mechanisms in hematogolical malignancies, score 6, n=3, Homo sapiens, pdat 2026/08/20 = 16 days ago — heme-onc + cancer-immunology input reserved from id:85 — STILL UNFEATURED today], GSE328393 [Multi-omic profiling of DNA damage-induced senescence in healthy and IPF primary human lung fibroblasts ATAC-seq, score 6, n=192, Homo sapiens, pdat 2026/08/19 = 17 days ago — IPF + senescence + multi-omic companion to id:85 GSE328392], GSE342703 [Spatial transcriptomics reveals microenvironmental heterogeneity in osteoarthritic subchondral bone, score 6, n=4, Homo sapiens, pdat 2026/08/09 = 27 days ago — longevity + musculoskeletal-aging + osteoarthritis + spatial-biology input], GSE296517 [Interrogating the Synergistic Potential of Gemcitabine and Focused Ultrasound-Induced Thermal Ablation in Breast Cancer, score 6, n=5, Homo sapiens, pdat 2026/08/01 = 35 days ago — refractory-breast-cancer + chemo + focused-ultrasound input], GSE302356 [Decoding Lymphangioleiomyomatosis (LAM) Niche Environment via Integrative Analysis of Single Cell Multiomics and Spatial, score 6, n=12, Homo sapiens, pdat 2026/07/30 = 36 days ago — rare-cancer LAM-input], GSE328460 [Single-cell resolution spatial transcriptomics of a mucinous tubular and spindle cell carcinoma using CosMx, score 6, n=1, Homo sapiens, pdat 2026/07/20 = 46 days ago — rare-cancer kidney-input], GSE282124 [Single-cell spatial transcriptomics of formalin-fixed, paraffin-embedded biopsies reveals colitis-associated cell networks Merscope, score 6, n=24, Homo sapiens, pdat 2026/05/21 = 3.5 months ago — IBD + FFPE-spatial-biology + gastroenterology-input], GSE342709 + GSE342738 [Multiscale spatial transcriptomics resolves the cellular and molecular architecture of the human amygdala Visium + Visium HD companion, score 6/6, n=51/5, Homo sapiens, pdat 2026/08/24 = 12 days ago — neuroscience-methodology + spatial-biology + amygdala-atlas reserved from id:87 — STILL UNFEATURED today], GSE268195 [Inhibition of EZH2 restores normal expression of genes associated with cysteine metabolism and ferroptosis in hepatocellular carcinoma CUT&Tag, score 6, n=12, Homo sapiens, pdat 2024/10/25 = ~23 months old — companion to id:87 GSE237951 + GSE268195 EZH2/HCC/ferroptosis]. The HF intel layer (intel.jsonl) shows stable vendor-intel at 36 events across 4 vendors: boltz [12 events: arxiv=10 + hf_tag=2], snap-stanford [9 events: arxiv=4 + hf_tag=4 + hf_org=1], phylo [8 events: arxiv=7 + hf_tag=1], anthropic-science [7 events: arxiv=5 + hf_tag=2] — the post-id:80 quiet-period for HF-intel-progression continues. --- ## 💼 Next Steps - **[Open GSE281463 in GEO (non-coding-GWAS heart-failure Hi-C 3D-chromatin, n=8)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE281463)** - **[Open GSE281464 in GEO (non-coding-GWAS heart-failure Perturb-seq companion, n=12)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE281464)** - **[Open GSE302068 in GEO (pan-cancer-ferroptosis exhausted-macrophage scRNA-seq, n=12)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE302068)** - **[Open GSE312779 in GEO (DMD-cardiomyopathy steroid-efficacy multiomics, n=24)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE312779)** - **[Request non-coding-GWAS-HF-resolution + ferroptosis-immunotherapy-resistance + DMD-steroid-pharmacogenomics brief](https://brownbio.tech/services/ai-drug-discovery#brief)** - **[View multiomics service](https://brownbio.tech/services/multiomics)** - **[View biostatx service](https://brownbio.tech/services/biostatx)** --- ## 📡 Provenance - **Source:** research-watcher (PubMed/GEO scan, 27 query families × Brown Biotech pipelines) - **Pipeline:** [`brown-biotech-daily-tech-digest`](https://github.com/ohbryt/brown-biotech-platform) — 06:00 KST cron - **Generated:** 2026-09-05 06:09 KST - **Repo:** `ohbryt/brown-biotech-platform` --- _Auto-published by `brown_biotech_research_digest_publisher.py` · [brownbio.tech](https://brownbio.tech) · Decision-ready research, daily._
Brown Biotech Research Digest — 2026-09-05
PubMed/GEO scan · research-watcher · 06:00 KST