> 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:** Bioinformatics & Multi-Omics **Published:** 2026-07-18 06:05 KST **Entry ID:** 46 **Tags:** #IPF #idiopathic pulmonary fibrosis #pulmonary fibrosis #lung fibrosis #fibrosis #myeloid #myeloid cell #monocyte #macrophage #alveolar macrophage #tissue-resident macrophage #TRM --- ## 🔬 Today's Top Findings ### 1. Type I interferon–activated myeloid states gate less-fibrotic IPF stages (GSE292589, score 9, n=4, Homo sapiens, single-cell + spatial, pdat 2026/07/10 = 8 days ago, the FRESHEST score-9 IPF + myeloid + IFN-I hit in the 2026-07-18 scan and the cleanest anti-fibrotic-myeloid atlas surfaced this cycle) ### 2. Visium HD single-cell spatial atlas of murine normal pancreas → pancreatitis → PDAC FFPE progression (GSE329811, score 7, n=10, Mus musculus, single-cell + spatial, pdat 2026/07/02 = 16 days ago, the freshest score-7 pancreatitis-to-PDAC spatial atlas in the scan) ### 3. PRMT1-mediated arginine methylation redirects SMAD4 toward a metastasis-promoting transcriptional output in pancreatic cancer (GSE338354, score 6, n=6, Homo sapiens, bulk RNA-seq, pdat 2026/07/16 = 2 days ago, the freshest PRMT1-SMAD4 pancreatic-metastasis target-nomination hit in the scan) ## 📋 Synthesis Three freshly surfaced, novel Brown Biotech signals from the 2026-07-18 06:00 KST watcher scan (105 hits across 27 queries, collected_at 2026-07-17 UTC; ALL THREE primary signals are NOVEL versus yesterday's id:45 digest [GSE326573 IPF T-cell multiomic + GSE333995 CRC IGFBP5 + GSE297388 DMD muscle spatial] and absent from the retained id:42–id:45 window). All three converge on Brown Biotech's bioinformatics + fibrosis + refractory-cancer lanes with strong anti-fibrotic-immunology and pancreatic-cancer target-nomination angles: (1) a fresh score-9 single-cell + spatial dissection of type-I-interferon–activated myeloid states in idiopathic pulmonary fibrosis showing protective association with less-fibrotic stages (GSE292589, n=4 Homo sapiens, pdat 2026/07/10 = 8 days ago) — the FRESHEST score-9 IPF + myeloid + IFN-I hit in the scan and a direct bioinformatics + IPF / fibrosis + anti-fibrotic-immunology input that complements yesterday's IPF T-cell-multiomic dataset (GSE326573) by adding the innate-immune / myeloid / IFN-axis counter-regulation angle; (2) a Visium-HD single-cell spatial atlas covering the murine normal pancreas → pancreatitis → PDAC FFPE progression continuum (GSE329811, n=10 Mus musculus, pdat 2026/07/02 = 16 days ago) — the freshest score-7 pancreatitis-to-PDAC spatial atlas in the scan and a direct refractory-cancer + pancreatic-cancer + inflammation-aging + pancreatitis-to-PDAC-transition input that opens a tractable QC-first re-analysis path for Brown Biotech's pancreatic-cancer + spatial-omics lane; and (3) PRMT1-mediated arginine methylation redirecting SMAD4 toward a metastasis-promoting transcriptional output in pancreatic cancer (GSE338354, n=6 Homo sapiens, pdat 2026/07/16 = 2 days ago) — the freshest PRMT1-SMAD4 pancreatic-metastasis target-nomination hit in the scan and a direct AI-drug-discovery + refractory-cancer + PRMT1-inhibitor-landscape + pancreatic-ductal-adenocarcinoma-metastasis input that pairs naturally with the type-I PRMT1-inhibitor development landscape (GSK3368715 / MRTX1719 / TNG462 / AM-9747 / PRT-543). --- ## 🎯 Highlights ### 1. Type-I-interferon–activated myeloid states gate less-fibrotic IPF stages (GSE292589, score 9, n=4, pdat 2026/07/10 = 8 days ago, single-cell + spatial, Homo sapiens, NCBI public repository, raw files available, suppfile TAR): the FRESHEST score-9 IPF + myeloid + IFN-I hit in the entire 2026-07-18 scan and a direct bioinformatics + IPF / fibrosis + anti-fibrotic-immunology input that pairs with yesterday's GSE326573 IPF T-cell-multiomic atlas by adding the innate-immune / myeloid counter-regulation angle; IPF (idiopathic pulmonary fibrosis, median survival 3–5 years from diagnosis, ~3M affected globally, prevalence ~20 per 100,000 in the US with rising incidence in older adults) is the most-lethal chronic fibrosing interstitial lung disease with only two approved disease-modifying therapies (pirfenidone + nintedanib) that slow but do not halt progression; type-I-interferon signaling in myeloid cells (canonical IFN-α/β → IFNAR1/IFNAR2 → TYK2/JAK1 → STAT1/STAT2 → IRF9 → ISG [interferon-stimulated gene] induction) is increasingly recognized as a protective anti-fibrotic axis that opposes TGF-β–driven fibroblast activation, and IFN-I–activated monocyte-derived macrophages and tissue-resident alveolar macrophages are emerging therapeutic-nomination targets for IPF + post-viral-fibrosis + post-acute-COVID-19-fibrosis; the n=4 paired single-cell + spatial design (likely paired scRNA-seq + spatial transcriptomics across IPF-versus-control lung biopsies stratified by fibrotic-stage severity using a standardized scoring framework) delivers direct dissection of (a) IFN-I–activated versus IFN-I–quiescent myeloid-state compositional shifts across less-fibrotic versus end-stage-fibrotic IPF stages, (b) ISG-high myeloid subsets' co-localization with epithelial-activation foci and fibroblastic foci in spatial tissue, (c) STAT1/STAT2/IRF7 regulon activity differences across myeloid states including IRF7-driven monocyte-derived macrophage polarization, and (d) cross-talk signatures between IFN-I–activated myeloid cells and the T-cell subsets catalogued in yesterday's GSE326573 T-cell-multiomic atlas — directly actionable for Brown Biotech's IPF + fibrosis + anti-fibrotic-immunology + innate-immune-reprogramming lane. Dataset: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE292589. ### 2. Visium HD single-cell spatial atlas of murine normal pancreas → pancreatitis → PDAC FFPE progression (GSE329811, score 7, n=10, pdat 2026/07/02 = 16 days ago, single-cell + spatial, Mus musculus, NCBI public repository, raw files available, suppfile H5/JPG/JSON/PNG/TIFF): the FRESHEST score-7 pancreatitis-to-PDAC spatial atlas in the entire 2026-07-18 scan and a direct refractory-cancer + pancreatic-cancer + inflammation-aging + pancreatitis-to-PDAC-transition input for Brown Biotech's pancreatic-cancer + spatial-omics + inflammation-aging lane; pancreatic ductal adenocarcinoma (PDAC, ~495,000 new cases/year globally, ~466,000 deaths/year, 4th-leading cause of cancer-related mortality in the US with 5-year overall survival <12% for metastatic disease and limited targeted-therapy options beyond FOLFIRINOX + gemcitabine/nab-paclitaxel + olaparib for BRCA1/2-mutated tumors + pembrolizumab for MSI-H tumors + larotrectinib/entrectinib for NTRK-fusion tumors) is the most-lethal common solid tumor and the focus of intense pre-malignant-detection + early-pancreatitis-intervention effort with chronic pancreatitis recognized as a major risk factor (RR ~13–19-fold for PDAC development); Visium HD (10x Genomics high-definition spatial-transcriptomics platform with sub-cellular-resolution targeted gene-panel readout enabling single-cell-scale cellular-resolution reconstruction from FFPE-compatible tissue sections) is the platform-of-choice for clinical-sample spatial profiling of FFPE archives; the n=10 progression-continuum design (likely normal pancreas → acute pancreatitis → chronic pancreatitis → PDAC with biological replication across conditions, all FFPE-compatible for clinical-translation potential) delivers direct dissection of (a) acinar-to-ductal metaplasia (ADM, the canonical pre-malignant trans-differentiation of acinar cells toward a ductal-like state in response to inflammatory injury) trajectory including KRT19+/SOX9+ ductal-state marker acquisition and zymogen-granule loss dynamics, (b) pancreatic stellate cell (PSC, the canonical PDAC-stroma myofibroblast precursor) activation-state shifts driving the desmoplastic-stroma hallmark of PDAC, (c) tumor-microenvironment compartmentalization including cancer-associated fibroblast (CAF) heterogeneity (myCAF versus iCAF versus apCAF subsets with distinct TGF-β– versus IL-6– versus MHC-II–driven polarization programs), and (d) tertiary-lymphoid-structure (TLS) formation and immune-exclusion patterns across the pancreatitis-to-PDAC transition — directly actionable for Brown Biotech's pancreatic-cancer + inflammation-aging + spatial-omics + early-detection lane. Dataset: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE329811. ### 3. PRMT1-mediated arginine methylation redirects SMAD4 toward a metastasis-promoting transcriptional output in pancreatic cancer (GSE338354, score 6, n=6, pdat 2026/07/16 = 2 days ago, bulk RNA-seq, Homo sapiens, NCBI public repository, raw files available, suppfile TXT): the FRESHEST PRMT1-SMAD4 pancreatic-metastasis target-nomination hit in the entire 2026-07-18 scan and a direct AI-drug-discovery + refractory-cancer + PRMT1-inhibitor-landscape + PDAC-metastasis input for Brown Biotech's pancreatic-cancer + AI-drug-discovery + target-nomination + epigenetic-therapy lane; PRMT1 (protein arginine methyltransferase 1, the major type-I protein arginine methyltransferase responsible for ~85% of cellular asymmetric-dimethyl-arginine [ADMA] marks on arginine-glycine-glycine [RGG] motifs in RNA-binding proteins, splicing factors, and transcription factors) is a master epigenetic regulator with emerging therapeutic-target nomination in cancer, including the canonical PRMT1/MAT2A/PRMT5 axis where MTAP-deletion cancers (~15% of all cancers, enriched in PDAC, mesothelioma, glioblastoma, and certain NSCLC subtypes) are uniquely vulnerable to MAT2A inhibition combined with PRMT5 inhibition (the MRTX1719 + TNG462 + AMG 193 development landscape); SMAD4 (the canonical co-SMAD transcription factor that mediates TGF-β signaling together with receptor-regulated SMADs SMAD2/SMAD3) is inactivated in ~55% of PDAC cases via homozygous deletion or truncating mutations, but a residual SMAD4-wild-type subset (~45%) maintains TGF-β–responsive transcriptional programs that can be redirected by PRMT1-mediated arginine methylation toward pro-metastatic versus tumor-suppressive outputs; the n=6 RNA-seq design (likely paired control-versus-PRMT1-knockdown/overexpression + SMAD4-wild-type versus SMAD4-mutant isogenic PDAC lines with or without TGF-β stimulation) delivers direct dissection of (a) PRMT1-dependent SMAD4 arginine-methylation sites (with R361 and adjacent RG/RGG motifs as likely candidate sites based on canonical SMAD-family arginine-methylation patterns), (b) PRMT1-driven transcriptional-output switching of SMAD4 target genes from canonical TGF-β tumor-suppressive programs (CDKN1A/p21, CDKN2B/p15, BAX) toward pro-metastatic programs (SNAI1, SNAI2, ZEB1, ZEB2, VIM, MMP9), and (c) synthetic-lethal partner nominations for PRMT1 inhibition including DNA-damage-response genes + splicing-factor vulnerabilities + SMAD4-wild-type-specific dependencies — directly actionable for Brown Biotech's pancreatic-cancer + PRMT1-target-nomination + epigenetic-therapy + AI-drug-discovery lane. Dataset: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338354. ### 4. Combined signal: bioinformatics / IPF / fibrosis / anti-fibrotic-immunology / myeloid-IFN-I (GSE292589, score 9, n=4 Homo sapiens single-cell + spatial, pdat 2026/07/10 = 8 days ago, the FRESHEST score-9 IPF + myeloid + IFN-I hit in the scan, anti-fibrotic-myeloid atlas with direct IFN-I–activated-monocyte-derived-macrophage + STAT1/STAT2/IRF7 regulon nomination pairing with the type-I-IFN therapeutic landscape, complements yesterday's GSE326573 IPF T-cell-multiomic atlas with the innate-immune counter-regulation angle, direct BB IPF + fibrosis + anti-fibrotic-immunology + innate-immune-reprogramming lane input) + bioinformatics / refractory-cancer / PDAC / spatial-omics / inflammation-aging (GSE329811, score 7, n=10 Mus musculus single-cell + spatial Visium HD FFPE, pdat 2026/07/02 = 16 days ago, the freshest score-7 pancreatitis-to-PDAC spatial atlas in the scan, normal-pancreas → pancreatitis → PDAC progression continuum with direct acinar-to-ductal-metaplasia + PSC + CAF + TLS dissection and clinical-FFPE-translation potential, direct BB pancreatic-cancer + spatial-omics + inflammation-aging + early-detection lane input) + AI-drug-discovery / refractory-cancer / PDAC-metastasis / PRMT1-inhibitor-landscape / target-nomination (GSE338354, score 6, n=6 Homo sapiens bulk RNA-seq, pdat 2026/07/16 = 2 days ago, the freshest PRMT1-SMAD4 pancreatic-metastasis target-nomination hit in the scan, PRMT1-mediated arginine methylation redirects SMAD4 toward pro-metastatic transcriptional output with direct PRMT1-inhibitor + MAT2A-inhibitor + MTAP-deletion synthetic-lethality nomination pairing with the GSK3368715 + MRTX1719 + TNG462 + PRT-543 development landscape, direct BB AI-drug-discovery + pancreatic-cancer + epigenetic-therapy + target-nomination lane input) — three orthogonal modalities spanning 2 of 6 Brown Biotech coverage categories (bioinformatics + ai-drug-discovery) with ALL THREE primary signals NOVEL versus yesterday's id:45 digest (GSE326573 IPF T-cell multiomic + GSE333995 CRC IGFBP5 + GSE297388 DMD muscle spatial) and absent from the retained id:42–id:45 window; the watcher's 2026-07-18 scan (Saturday, weekday-cadence-normal) ran on its normal 06:00 KST cadence and emitted 105 hits with 12 score-9 entries dominated by single-cell + spatial datasets; GSE292589 is the headline signal because it (a) directly complements yesterday's GSE326573 IPF T-cell-multiomic atlas with the missing myeloid / IFN-I innate-immune angle, (b) opens a tractable PRMT1-inhibitor + STAT1-agonist co-development angle via the IFN-I–myeloid-stromal cross-talk, and (c) is GEO-accessible with raw TAR files for immediate Brown Biotech intake; GSE329811 pairs inflammation-aging with pancreatic-cancer spatial-omics and is the cleanest FFPE-compatible Visium-HD PDAC atlas surfaced this cycle; GSE338354 is the freshest (pdat 2026/07/16 = 2 days ago) and pairs directly with the active PRMT1-inhibitor development landscape for target-nomination hand-off. --- ## 💼 Next Steps - **[Request bioinformatics / IPF IFN-I myeloid atlas brief](https://brownbio.tech/multiomics#brief)** - **[Request refractory-cancer / PDAC Visium HD spatial brief](https://brownbio.tech/multiomics#brief)** - **[Request AI drug discovery / PRMT1-SMAD4 pancreatic metastasis brief](https://brownbio.tech/services/ai-drug-discovery#brief)** - **[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:** 2026-07-18 06:05 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 — 2026-07-18
PubMed/GEO scan · research-watcher · 06:00 KST