> 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:** Longevity & Senolytics **Published:** 2026-07-17 06:16 KST **Entry ID:** 45 **Tags:** #IPF #idiopathic pulmonary fibrosis #pulmonary fibrosis #lung fibrosis #fibrosis #T cell #T-cell multiomic #T-cell subsets #epithelial cell #T-cell-epithelial interaction #Treg #regulatory T cell --- ## 🔬 Today's Top Findings ### 1. T-cell Multiomic Analysis Identifies Subsets and Mechanisms of Interaction with Epithelial Cells in Idiopathic Pulmonary Fibrosis (GSE326573, score 6, n=59, Homo sapiens, T-cell multiomic + protein-design, pdat 2026/07/14 = 3 days ago, the freshest large-cohort T-cell multiomic + IPF hit in the 2026-07-17 scan and the largest n-of-any IPF dataset surfaced this cycle) ### 2. IGFBP5 Derived From Endothelial Cells Drive Vascular Invasion and Liver Metastasis of Colorectal Cancer by Activating the ITGB3/PI3K/AKT Axis (GSE333995, score 6, n=9, Homo sapiens, single-cell, pdat 2026/07/15 = 2 days ago, the freshest score-6 endothelial-derived IGFBP5 + colorectal-cancer liver-metastasis hit in the scan) ### 3. Spatial transcriptomics and scRNA-sequencing on gastrocnemius muscle form B6-mdx and D2-mdx mice (GSE297388, score 7, n=8, Mus musculus, single-cell + spatial, pdat 2026/07/01 = 16 days ago, the freshest score-7 DMD-mouse-model + muscle single-cell + spatial hit in the scan) ## 📋 Synthesis Three freshly surfaced, novel Brown Biotech signals from the 2026-07-17 06:00 KST watcher scan (105 hits across 27 queries, collected_at 2026-07-16 UTC; all three primary signals are NOVEL versus yesterday's id:44 digest [GSE337336 mycosis-fungoides + GSE328275 TNBC CD45+ + GSE328422 LN-metastasis spatio-temporal] and absent from the retained id:40-id:44 window). All three converge on Brown Biotech's bioinformatics + longevity + refractory-cancer + fibrosis + multi-omics lanes with strong aging-biology angles: (1) a fresh large-cohort T-cell multiomic dissection of idiopathic-pulmonary-fibrosis (IPF) T-cell–epithelial-cell interaction mechanisms (GSE326573, n=59 Homo sapiens T-cell multiomic, pdat 2026/07/14 = 3 days ago) — the freshest large-n IPF T-cell-multiomic dataset surfaced this cycle and a direct bioinformatics + IPF + fibrosis + T-cell-reprogramming input; (2) endothelial-derived IGFBP5 driving vascular invasion and liver metastasis in colorectal cancer via the ITGB3/PI3K/AKT axis (GSE333995, n=9 Homo sapiens single-cell, pdat 2026/07/15 = 2 days ago) — the freshest score-6 endothelial-derived IGFBP5 + colorectal-cancer liver-metastasis + ITGB3/PI3K/AKT hit and a direct refractory-cancer + metastasis + AI-drug-discovery input for target nomination; and (3) spatial transcriptomics + scRNA-seq of gastrocnemius muscle from B6-mdx and D2-mdx Duchenne-muscular-dystrophy mouse models (GSE297388, n=8 Mus musculus, pdat 2026/07/01 = 16 days ago) — the freshest score-7 DMD-mouse-model + muscle single-cell + spatial hit and a direct longevity + sarcopenia + muscular-dystrophy + anti-aging + bioinformatics input for muscle-aging foundational dissection. --- ## 🎯 Highlights ### 1. T-cell Multiomic Analysis Identifies Subsets and Mechanisms of Interaction with Epithelial Cells in Idiopathic Pulmonary Fibrosis (GSE326573, score 6, n=59, pdat 2026/07/14 = 3 days ago, T-cell multiomic + protein-design, Homo sapiens, clean license, raw files available, suppfile H5): the FRESHEST large-cohort T-cell multiomic + IPF hit in the entire 2026-07-17 scan (n=59 = the largest single-IPF dataset surfaced this cycle) and a direct bioinformatics + IPF / fibrosis + T-cell-reprogramming + immunology-of-fibrosis input for Brown Biotech's IPF + fibrosis + longevity + immunology lane; idiopathic pulmonary fibrosis (IPF, 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; T-cell contribution to IPF pathobiology has been increasingly recognized with tissue-resident memory T cells (TRM, CD69+/CD103+ lung-resident CD8+ T cells), regulatory T cells (Treg, FOXP3+/CD25+/CD4+), exhausted T cells (Tex, PD-1+/TIM-3+/LAG-3+), Th17 cells (IL-17-producing pro-fibrotic CD4+ effectors), and Tfh cells (follicular helper T cells supporting tertiary-lymphoid-structure formation) all implicated in IPF progression versus resolution; the n=59 T-cell multiomic design (likely paired single-cell RNA-seq + T-cell-receptor [TCR] sequencing + CITE-seq / cellular-indexing-of-transcriptomes-and-epitopes-by-sequencing + ATAC-seq or hash-tagging across IPF-vs-control lung-tissue biopsies with paired airway-epithelial-cell sorting) delivers direct dissection of (a) IPF-versus-control T-cell-subset compositional shifts including Treg/TRM/Tex/Th17/Tfh proportion changes, (b) clonally-expanded versus polyclonal T-cell population architecture with TCR-repertoire diversity metrics, (c) T-cell-effector-function polarization including cytokine-output signatures (IFN-gamma, IL-4, IL-17, IL-10, IL-13, TGF-beta) and cytolytic-granule expression, (d) T-cell–epithelial-cell interaction mechanisms including ligand-receptor-pair inference (Niches / CellChat / CellPhoneDB frameworks) + spatial-proximity analysis + co-culture-validation hits, and (e) clinical-correlative endotyping identifying T-cell-subset-patterns that associate with rapid-progressing versus slow-progressing IPF trajectories — directly actionable for Brown Biotech's IPF + fibrosis + immunology-of-fibrosis + T-cell-reprogramming + anti-fibrotic-immunotherapy lane where new biologics targeting CCR2/CCR5 (cenicriviroc), JAK1/JAK3 (tofacitinib, baricitinib, nintedanib-JAK combinations), IL-4/IL-13 (dupilumab, lebrikizumab), IL-11, or lysyl-oxidase-like-2 (LOXL2, simtuzumab) are in active clinical or pre-clinical development. Dataset: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE326573. ### 2. IGFBP5 Derived From Endothelial Cells Drive Vascular Invasion and Liver Metastasis of Colorectal Cancer by Activating the ITGB3/PI3K/AKT Axis (GSE333995, score 6, n=9, pdat 2026/07/15 = 2 days ago, single-cell, Homo sapiens, clean license, raw files available, suppfile XLS): the FRESHEST score-6 endothelial-derived IGFBP5 + colorectal-cancer liver-metastasis + ITGB3/PI3K/AKT-axis hit in the entire 2026-07-17 scan and a direct refractory-cancer + metastasis + AI-drug-discovery + target-nomination input for Brown Biotech's refractory-cancer + colorectal-cancer + liver-metastasis + endothelium-targeted-therapy lane; colorectal cancer (CRC, ~1.9M new cases/year globally, ~900K deaths/year, 3rd-most-common cancer and 2nd-leading cause of cancer-related mortality) is the most-lethal gastrointestinal malignancy with liver as the dominant metastatic site (~50% of metastatic CRC patients develop liver metastases, mCRC, with 5-year overall survival <15% for unresectable disease) and a critical unmet need for anti-metastatic therapeutics beyond anti-VEGF (bevacizumab), anti-EGFR (cetuximab, panitumumab — KRAS-wild-type-only), anti-VEGFR (regorafenib, ramucirumab), and trifluridine/tipiracil (Lonsurf) + fruquintinib (FRESCO-2 trial); IGFBP5 (insulin-like growth factor binding protein 5, a secreted glycoprotein that binds IGF-1/IGF-2 with high affinity and modulates IGF-receptor signaling + has IGF-independent roles in cell-adhesion + migration + senescence) is emerging as a metastasis-driver with elevated circulating IGFBP5 levels in metastatic-cancer patients + tumor-stroma crosstalk roles; the ITGB3/PI3K/AKT axis (integrin beta 3 → focal-adhesion-kinase [FAK] → PI3K → AKT → mTOR survival-and-proliferation signaling) is the canonical cell-adhesion + survival pathway in cancer-cell vascular-invasion and a direct therapeutic-target nomination axis with alpelisib (PI3K-alpha inhibitor), capivasertib (AKT inhibitor, FDA-approved 2023 for HR+/HER2- breast cancer with PIK3CA/AKT1/PTEN alterations), and the inavolisib + ARV-471 combinations in active clinical development; the n=9 single-cell design (likely paired primary-CRC + liver-metastatic-CRC + matched normal-liver + portal-vein-endothelial-cell scRNA-seq from a small but well-characterized CRC cohort with paired bulk-RNA-seq validation) delivers direct dissection of (a) endothelial-cell-state shifts in the metastatic niche including tip-cell-versus-stalk-cell + arterial-versus-venous-versus-capillary + angiogenic-versus-quescent endothelial heterogeneity, (b) IGFBP5 ligand-receptor-pair identification with downstream ITGB3 engagement validation, (c) cancer-cell-intrinsic ITGB3/PI3K/AKT activation-state mapping using phospho-signaling readouts (pAKT-S473, pS6, p4EBP1), and (d) vascular-invasion-vs-established-metastasis transition-state dissection — directly actionable for Brown Biotech's CRC + liver-metastasis + anti-angiogenic + ITGB3/PI3K/AKT-target-nomination + refractory-cancer lane. Dataset: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE333995. ### 3. Spatial transcriptomics and scRNA-sequencing on gastrocnemius muscle form B6-mdx and D2-mdx mice (GSE297388, score 7, n=8, pdat 2026/07/01 = 16 days ago, single-cell + spatial, Mus musculus, clean license, raw files available, suppfile CSV/JPG/JSON/MTX/PNG/TSV): the FRESHEST score-7 DMD-mouse-model + skeletal-muscle single-cell + spatial hit in the entire 2026-07-17 scan and a direct longevity + sarcopenia + Duchenne-muscular-dystrophy + muscle-regenerative-biology + anti-aging input for Brown Biotech's longevity + sarcopenia + muscular-dystrophy + muscle-aging lane; Duchenne muscular dystrophy (DMD, X-linked recessive, ~1 in 3,500-5,000 live male births, caused by out-of-frame dystrophin [DMD gene on Xp21] mutations leading to complete absence of functional dystrophin protein in skeletal + cardiac + smooth muscle) is the most-common + most-severe childhood muscular dystrophy with progressive muscle-wasting, loss-of-ambulation by age 12, and cardiopulmonary-failure-mediated death typically by age 20-30; the B6-mdx (C57BL/10ScSn-Dmdmdx/J, the canonical DMD-model on a C57BL/10 background with mild phenotype) and D2-mdx (DBA/2J-mdx, the more-severe DMD-model on a DBA/2 background with pronounced fibrosis + inflammation + functional-impairment) genetic-background contrast is a powerful experimental system for dissecting genetic-modifier effects on DMD severity (the canonical latent-TGF-beta-binding-protein-4 [LTBP4] + osteopontin [SPP1] + Sgcd + Jag1/Notch genetic-modifier landscape); the n=8 paired-design (likely paired scRNA-seq + Visium spatial-transcriptomics from gastrocnemius muscle across B6-mdx-vs-D2-mdx-vs-B6-WT-vs-D2-WT conditions with paired histology validation) delivers direct dissection of (a) muscle-stem-cell [satellite cell, PAX7+] compartment changes including self-renewal-versus-differentiation fate decisions in dystrophic-versus-control muscle, (b) fibro-adipogenic-progenitor [FAP, PDGFRA+] activation-state shifts driving the dystrophic-muscle fibrosis that distinguishes D2-mdx from B6-mdx, (c) macrophage polarization (M1-versus-M2 + CD68+ pan-macrophage + MHC-II+ inflammatory versus CD206+ anti-inflammatory) controlling regeneration-versus-fibrosis balance, (d) myofiber-type composition changes (type-IIa + type-IIx fast-twitch vs type-I slow-twitch), and (e) the genetic-modifier-driven molecular-signatures that nominate new therapeutic-target axes for DMD including galectin-3 (LGALS3) inhibitors (GB1107, GB1211 in active clinical development), myostatin [MSTN/GDF8] inhibitors (bimagrumab, domagrozumab, apitegromab), GDF11 modulation, and utrophin [UTRN] upregulators — directly actionable for Brown Biotech's longevity + sarcopenia + anti-aging + muscle-aging + muscular-dystrophy + muscle-regenerative-biology lane. Dataset: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE297388. ### 4. Combined signal: bioinformatics / IPF / fibrosis / T-cell-multiomic (GSE326573, score 6, n=59 Homo sapiens T-cell multiomic + protein-design, pdat 2026/07/14 = 3 days ago, the freshest large-cohort T-cell multiomic + IPF hit in the scan and the largest single-IPF dataset surfaced this cycle, T-cell-subset-and-mechanism dissection of IPF T-cell-epithelial-cell interaction with direct anti-fibrotic-immunotherapy + Treg/TRM/Tex/Th17/Tfh reprogramming nomination, direct BB IPF + fibrosis + longevity + immunology-of-fibrosis + T-cell-reprogramming lane input) + bioinformatics / refractory-cancer / colorectal-cancer / liver-metastasis / AI-drug-discovery / target-nomination (GSE333995, score 6, n=9 Homo sapiens single-cell, pdat 2026/07/15 = 2 days ago, the freshest score-6 endothelial-derived IGFBP5 + colorectal-cancer liver-metastasis + ITGB3/PI3K/AKT-axis hit in the scan, vascular-invasion-and-liver-metastasis dissection with direct PI3K/AKT + ITGB3 axis therapeutic nomination pairing with alpelisib + capivasertib + inavolisib development landscape, direct BB refractory-cancer + CRC + liver-metastasis + AI-drug-discovery + target-nomination + endothelium-targeted-therapy lane input) + bioinformatics / longevity / sarcopenia / Duchenne-muscular-dystrophy / muscle-aging / anti-aging (GSE297388, score 7, n=8 Mus musculus single-cell + spatial, pdat 2026/07/01 = 16 days ago, the freshest score-7 DMD-mouse-model + muscle single-cell + spatial hit in the scan, B6-mdx-vs-D2-mdx genetic-modifier dissection of muscle-regenerative-biology + FAP + macrophage + satellite-cell compartments with direct galectin-3 + myostatin + GDF11 + utrophin therapeutic nomination, direct BB longevity + sarcopenia + muscle-aging + muscular-dystrophy + anti-aging lane input) — three orthogonal modalities spanning 3 of 6 Brown Biotech coverage categories (bioinformatics + longevity + ai-drug-discovery) with ALL THREE primary signals NOVEL versus yesterday's id:44 digest (GSE337336 mycosis-fungoides + GSE328275 TNBC CD45+ + GSE328422 LN-metastasis spatio-temporal) and absent from the retained id:40-id:44 window; the watcher's 2026-07-17 scan ran on its normal 06:00 KST cadence and emitted 105 hits with 13 score-9 entries (3 already featured in id:44 = GSE277080 + GSE328275 + GSE328422 recycled, plus GSE308147 + GSE308148 spatial-benchmarking hits, plus GSE337336 mycosis-fungoides recycled from id:44, plus GSE311507 HNSCC OXPHOS recycled from id:42, plus the GSE281462-5 heart-failure bundle recycled from id:41, plus GSE292589 IFN-I IPF recycled from id:40 — leaving 13-9 = 4 truly novel score-9 entries today that mostly converge on spatial-benchmarking methodology papers rather than disease-biology findings) and 12 score-7 entries dominated by single-cell + spatial datasets (the 3 featured today span scRNA-seq + T-cell-multiomic + spatial — a balanced multi-modal slate); all three featured datasets are public GEO records with raw or semi-raw files available (GSE326573 H5 + GSE333995 XLS + GSE297388 CSV/JPG/JSON/MTX/PNG/TSV), Homo sapiens-or-Mus musculus, and span the freshness range pdat 2026/07/01 (16 days ago) to pdat 2026/07/15 (2 days ago) with a 13-day freshness window that emphasizes actionable-now re-analysis targets over academic-methodology only papers. --- ## 💼 Next Steps - **[Request bioinformatics / IPF T-cell multiomic brief](https://brownbio.tech/multiomics#brief)** - **[Request refractory-cancer / CRC IGFBP5 liver-metastasis brief](https://brownbio.tech/services/ai-drug-discovery#brief)** - **[Request longevity / DMD muscle spatial brief](https://brownbio.tech/services/biostatx#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:** 2026-07-17 06:16 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 — 2026-07-17
PubMed/GEO scan · research-watcher · 06:00 KST