> 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:** 2026-08-22 06:06 KST
**Entry ID:** 76
**Tags:** #gse343490 #cas12a #combinatorial-knockout #combinatorial-crispr #crispr-screen #dna-damage-response #ddr #end-seq #dna-repair #dna-damage #senescence #ai-drug-discovery
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## 🔬 Today's Top Findings
### 1. Cas12a-based combinatorial knockout screens define the genetic architecture of the DNA Damage response [END-seq] (GSE343490, score 9, n=4, Homo sapiens, protein-design / END-seq, pdat 2026/08/20 = 2 days ago, raw BW files, the FRESHEST score-9 NOVEL Cas12a-combinatorial-CRISPR/DNA-damage-response/END-seq screen in the entire 2026-08-22 hits.jsonl and a direct AI-DD + longevity + DNA-damage-repair + senescence input for the BB AI-DD + longevity lane)
### 2. Multi-omic profiling of DNA damage-induced senescence in healthy and IPF primary human lung fibroblasts [RNA-seq + ATAC-seq companion] (GSE328392 + GSE328393, score 6/6, n=192/24, Homo sapiens, mixed-modality [RNA-seq + ATAC-seq], pdat 2026/08/19 = 3 days ago, raw H5AD/TSV/CSV, the FRESHEST NOVEL DNA-damage-induced-senescence / IPF-fibroblast / RNA-seq+ATAC-seq companion atlas in the entire 2026-08-22 hits.jsonl and a direct longevity + senescence + anti-fibrotic + IPF input for the BB longevity + anti-fibrotic lane)
### 3. Dosage of the fusion transcription factor PAX3::FOXO1 controls cell state in rhabdomyosarcoma [ChIP-Seq + scRNA-Seq + RNA-Seq companion] (GSE297125 + GSE297127 + GSE331041, score 6/6/6, n=24/9/20, Homo sapiens, mixed-modality [ChIP + scRNA + RNA-seq], pdat 2026/08/20 = 2 days ago, raw BED/BIGWIG/MTX/TSV/CSV, the FRESHEST NOVEL PAX3-FOXO1-dosage / fusion-TF / rhabdomyosarcoma cell-state / ChIP+scRNA+RNA-seq companion atlas in the entire 2026-08-22 hits.jsonl and a direct refractory pediatric cancer + AI-DD + fusion-TF input for the BB refractory-cancer + AI-DD lane)
## 📋 Synthesis
The 2026-08-22 06:00 KST research-watcher scan completed cleanly via `bash run.sh scan` after the §20 silent-failure fix: 106 fresh hits across 27 queries landed in `research-watcher/output/latest/hits.jsonl` (collected_at 2026-08-21T21:03Z), with the score-9 top-band RECYCLED at both accession and study-family level from id:71-id:75 (GSE277080, GSE311507, GSE328275, GSE328422, GSE337336, GSE292589, GSE306130+GSE316922+GSE318638, GSE281462-GSE281465, GSE334010, GSE331133, GSE310802, GSE341884, GSE343063) — but with a single FRESH score-9 accession (GSE343490) AND a cluster of FRESH score-6 companion atlases (GSE328392+GSE328393 DNA-damage-senescence-IPF; GSE297125+GSE297127+GSE331041 PAX3::FOXO1-rhabdomyosarcoma) surfacing as the actionable NOVEL harvest today. The three actionable NOVEL signals today come from the score 6–9 band after pdat-filter (≤5 days) + prior-id:71-id:75-dedupe: (1) **Cas12a-based combinatorial knockout screens define the genetic architecture of the DNA Damage response [END-seq]** (GSE343490, watcher score 9, n=4, Homo sapiens, protein-design / END-seq modality, pdat 2026/08/20 = 2 days ago, raw BW files available, raw_file_availability 'yes', watcher query 'OpenFold weights' — the FRESHEST score-9 NOVEL hit in the entire 2026-08-22 hits.jsonl); (2) **Multi-omic profiling of DNA damage-induced senescence in healthy and IPF primary human lung fibroblasts** as a coherent 2-dataset companion atlas (GSE328392, score 6, n=192, Homo sapiens, RNA-seq 'Expression profiling by high throughput sequencing', pdat 2026/08/19 = 3 days ago, raw H5AD/TSV files) + GSE328393 (score 6, n=24, Homo sapiens, ATAC-seq 'Genome binding/occupancy profiling by high throughput sequencing', pdat 2026/08/19 = 3 days ago, raw CSV/H5AD files — the ATAC-seq companion arm for chromatin-accessibility validation); (3) **Dosage of the fusion transcription factor PAX3::FOXO1 controls cell state in rhabdomyosarcoma** as a coherent 3-dataset companion atlas (GSE297125, score 6, n=24, Homo sapiens, ChIP-Seq 'Genome binding/occupancy profiling by high throughput sequencing', pdat 2026/08/20 = 2 days ago, raw BED/BIGWIG files) + GSE297127 (score 6, n=9, Homo sapiens, scRNA-Seq 'Expression profiling by high throughput sequencing', pdat 2026/08/20 = 2 days ago, raw MTX/TSV files) + GSE331041 (score 6, n=20, Homo sapiens, RNA-Seq 'Expression profiling by high throughput sequencing', pdat 2026/08/20 = 2 days ago, raw CSV files — the bulk-RNA-seq validation arm). All three signals are CLEAN NOVEL — absent from id:71-id:75 at both accession and study-family level (verified via `re.findall(r'GSE\\d+', id:75-page)` returning the 43 accession ladder plus the 3 NOVEL signals today; GSE343490 and the two 3-platform companion families are confirmed absent from id:71-id:75). Combined four-axis score (peptide / AI-agent infra / longevity / translational-fit): GSE343490 9/12 + GSE328392+GSE328393 9/12 + GSE297125+GSE297127+GSE331041 7/12 = 25/36 — well above the goal-criterion threshold and approaching the highest fresh-ladder day in id:71-id:75. The DNA-damage-response + senescence + Cas12a-combinatorial-CRISPR + fusion-TF-dosage cluster is the dominant BB-relevant NOVEL harvest today (3/3 signals today touch the DNA-damage / senescence / fusion-TF axis), and the rhabdomyosarcoma pediatric-cancer lane is fresh for the first time in id:71-id:75 (0/3 in id:71-id:75 had any rhabdomyosarcoma / fusion-TF-dosage atlas). Recommended BB move: (a) ingest GSE343490 raw BW files to reconstruct the Cas12a-combinatorial-knockout DDR-genetic-architecture screen and benchmark against the existing BB DNA-damage / senescence / AI-DD reference panel for a unified DNA-repair-network + senescence-driver + combinatorial-CRISPR-target-nomination brief; (b) ingest GSE328392 H5AD/TSV + GSE328393 CSV/H5AD raw files to reconstruct the DNA-damage-induced senescence RNA-seq + ATAC-seq multi-omic atlas in healthy vs IPF primary human lung fibroblasts (the 'senescence-program-divergence' angle is directly relevant to the existing BB longevity + anti-fibrotic + IPF + CTHRC1+-fibroblast atlas panel from id:74 GSE272972 + id:72 GSE292589 Type-I-IFN-IPF); (c) ingest GSE297125 BED/BIGWIG + GSE297127 MTX/TSV + GSE331041 CSV raw files to reconstruct the PAX3::FOXO1-dosage ChIP-seq + scRNA-seq + bulk-RNA-seq companion atlas and benchmark against the existing BB refractory-cancer + AI-DD panel (id:73 GSE343502 ECM/YAP-TEAD prostate, id:71 GSE289506 CLL-ex-vivo, id:68 GSE343370+GSE343371 MSKCC dual-barcoding) for a unified pediatric-rhabdomyosarcoma + fusion-TF-dosage + cell-state-biology brief.
---
## 🎯 Highlights
### 1. Signal 1 — Bioinformatics + AI Drug Discovery + Longevity / Cas12a-based combinatorial knockout screens define the genetic architecture of the DNA Damage response [END-seq combinatorial CRISPR screen]: GSE343490 (watcher score 9, n=4, Homo sapiens, 'Other' gds_type, pdat 2026/08/20 = 2 days ago, raw BW files available, raw_file_availability 'yes', collected_at 2026-08-21T21:03:01Z, watcher query 'OpenFold weights') is the FRESHEST score-9 NOVEL hit in the entire 2026-08-22 hits.jsonl and a direct AI-DD + longevity + DNA-damage-repair + senescence input for the BB AI-DD + longevity lane. The DNA damage response (DDR) is the coordinated cellular network that detects DNA lesions (single-strand breaks [SSBs], double-strand breaks [DSBs], base modifications, crosslinks, replication stress), signals via the ATM-Chk2 / ATR-Chk1 / DNA-PKcs kinase cascades, and executes repair through homologous recombination (HR, BRCA1/BRCA2/PALB2/RAD51), non-homologous end joining (NHEJ, KU70/KU80/DNA-PKcs/XRCC4/Lig4), mismatch repair (MMR, MLH1/MSH2/MSH6/PMS2), nucleotide-excision repair (NER, XPA-XPG), base-excision repair (BER, PARP1/Polβ/Lig3/XRCC1), and Fanconi anemia (FA, FANCA-FANCG + FANCM-FAAP24) pathways — and DDR failure drives both cancer (deficiencies in HR or MMR drive genomic-instability-driven oncogenesis) and aging (accumulating unrepaired DNA damage is the 'DNA-damage-aging' hypothesis, with persistent lesions driving cellular senescence via p16INK4a / p21CIP1 / p53 activation, SASP induction, and stem-cell exhaustion — the canonical aging hallmark per López-Otín 2013/2023). Cas12a (Cpf1) is the Class-2 Type-V-A CRISPR nuclease (orthogonal to Cas9, recognizes TTTT-PAM, generates staggered cuts ~19-bp downstream of PAM) that has emerged as the preferred nuclease for combinatorial pooled CRISPR screens because a single Cas12a-guide-array transcript can deliver 3-4 distinct guides per cell (the Cas12a crRNA-array processing by the nuclease itself enables multiplexed-guide delivery in a single transcript, a feature Cas9 lacks without engineered tRNA-processing or Csy4-RNAi systems) — and the END-seq (Exonuclease-Directed Double-Strand Break Sequencing, detection of DSBs via exonuclease-mediated resection-end capture) modality directly maps DSB positions genome-wide at single-nucleotide resolution. The GEO title reports a Cas12a-based combinatorial knockout screen with END-seq readout that defines the genetic architecture of the DNA-damage response — an n=4 design (likely 2 conditions × 2 replicates: untreated vs DDR-inducing agent like etoposide / olaparib / aphidicolin / hydroxyurea, profiled by END-seq) that maps how combinatorial-gene knockout (pairs or triplets) reshapes the DDR genetic-interaction network and DSB-position landscape. The combinatorial-knockout angle is the freshest BB signal: classical CRISPR screens test single-gene knockouts, but genetic interactions (synthetic lethality, synthetic viability, epistasis, buffering, synergism) are the true architecture of cellular-response networks — and Cas12a-array combinatorial screens are the only scalable approach to map this architecture at genome-wide depth. Recommended BB move: ingest as handoff brief for the AI-DD + longevity + DDR lane; the END-seq + Cas12a-combinatorial-CRISPR angle is directly relevant to (i) synthetic-lethality target nomination for the BB refractory-cancer lane (BRCA-mutant HR-deficient tumors, MSI-high MMR-deficient tumors, FA-pathway-deficient tumors, PARP-inhibitor combinations), (ii) DDR-aging biomarker discovery (the 'DNA-damage-aging' hallmark is the most-actionable longevity axis per recent geroscience reviews), and (iii) BB's combinatorial-genetic-interaction-AI-DD platform opportunity (a curated DDR genetic-interaction map is the foundation for next-generation virtual-screening and target-prioritization models).
### 2. Signal 2 — Longevity + Anti-Fibrotic + Bioinformatics / Multi-omic profiling of DNA damage-induced senescence in healthy and IPF primary human lung fibroblasts [RNA-seq + ATAC-seq companion atlas]: GSE328392 (watcher score 6, n=192, Homo sapiens, RNA-seq 'Expression profiling by high throughput sequencing', pdat 2026/08/19 = 3 days ago, raw H5AD/TSV files available, raw_file_availability 'yes', watcher query 'lung fibrosis single-cell') + GSE328393 (watcher score 6, n=24, Homo sapiens, ATAC-seq 'Genome binding/occupancy profiling by high throughput sequencing', pdat 2026/08/19 = 3 days ago, raw CSV/H5AD files available, raw_file_availability 'yes', watcher query 'lung fibrosis single-cell') form the FRESHEST NOVEL DNA-damage-induced-senescence / IPF-fibroblast / RNA-seq+ATAC-seq companion atlas in the entire 2026-08-22 hits.jsonl and a direct longevity + senescence + anti-fibrotic + IPF input for the BB longevity + anti-fibrotic lane. Cellular senescence is the irreversible cell-cycle arrest triggered by diverse stressors (DNA damage, oncogenic stress, oxidative stress, mitochondrial dysfunction, telomere attrition, paracrine inflammation) and is one of the canonical 'hallmarks of aging' (López-Otín 2013/2023) — with the SASP (senescence-associated secretory phenotype, comprising IL-6, IL-8, IL-1α/β, TNFα, TGF-β1, GDF15, PAI-1/SERPINE1, MMPs, fibronectin) as the central effector that propagates senescence to neighboring cells, drives chronic tissue inflammation ('inflammaging'), and paradoxically contributes to both anti-tumor surveillance (senescent-cell clearance by NK cells and macrophages) and pro-fibrotic tissue remodeling (senescent fibroblasts are the dominant source of pathologic ECM in IPF, MASH, systemic sclerosis, and age-related skin/lung/kidney fibrosis). Idiopathic pulmonary fibrosis (IPF) is the prototypical aging-related fibrotic disease (~3M cases worldwide, incidence ~10-20 per 100K in adults >65y, median survival 3-5 years from diagnosis, ~50% mortality at 5 years even with antifibrotic therapy nintedanib/pirfenidone) and is driven by pathologic accumulation of senescent fibroblasts that produce excess ECM (collagen I/III/IV, fibronectin, hyaluronan), secrete pro-fibrotic SASP factors, and resist apoptosis — making fibroblast-senescence a top-priority anti-fibrotic drug-target class (the senolytic + senomorphic pipeline: navitoclax/ABT-263 BCL2/BCL-xL inhibitor, dasatinib + quercetin, fisetin, UBX0101, UNITY Biotechnology UBX1325, Oisín Biotechnologies senolytic gene therapy, Cleara Biotech FOXO4-DRI peptide, Androvia Life Sciences fertility-senolytics). The GEO title reports a multi-omic profiling of DNA-damage-induced senescence in healthy and IPF primary human lung fibroblasts with parallel RNA-seq + ATAC-seq design — a 192-sample RNA-seq + 24-sample ATAC-seq companion design (likely etoposide- or doxorubicin-induced senescence vs uninjured control, in primary human lung fibroblasts from healthy donors vs IPF patients, profiled for transcriptome + chromatin-accessibility divergence) that maps how the senescence program differs between healthy and IPF-derived fibroblasts and how the chromatin landscape (ATAC-seq peaks at senescence-driver loci: CDKN1A/p21CIP1, CDKN2A/p16INK4a, SASP-genes IL6/IL8/CXCL1/CCL2, ECM-genes COL1A1/COL3A1/FN1) is differentially remodeled. The healthy-vs-IPF-donor comparison angle is the freshest signal: most prior senescence-atlas work uses healthy donor cells and asks how senescence is induced, but the IPF-vs-healthy comparison asks whether IPF fibroblasts are PRE-DISPOSED to senescence (constitutively higher baseline p16/p21, lower LaminB1, more SASP-positive cells even at baseline) or whether they ACCELERATE into senescence upon the same stress — and the parallel ATAC-seq arm enables identification of the chromatin-accessibility 'senescence-priming' signature that distinguishes IPF from healthy fibroblasts (likely involving open chromatin at SASP loci + closed chromatin at proliferation-fate loci). Recommended BB move: ingest as handoff brief for the longevity + anti-fibrotic + IPF + senescence lane; the healthy-vs-IPF donor comparison + RNA-seq+ATAC-seq companion design is directly complementary to (i) id:74 GSE272972 CTHRC1+/TGF-β1/mTORC1 IPF pathologic-fibroblast atlas, (ii) id:72 GSE292589 Type-I-IFN-activated-myeloid IPF stage-stratification atlas, (iii) the BB senolytic + senomorphic pipeline (BCL-xL inhibitors, FOXO4-DRI, dasatinib+quercetin) for biomarker-stratified trial-design, and (iv) the BB DNA-damage / Cas12a-combinatorial-screen atlas from today's Signal 1 (GSE343490) for a unified DDR-senescence-IPF genetic-architecture reference panel.
### 3. Signal 3 — Refractory Cancer + AI Drug Discovery / Dosage of the fusion transcription factor PAX3::FOXO1 controls cell state in rhabdomyosarcoma [ChIP-Seq + scRNA-Seq + RNA-Seq 3-platform companion atlas]: GSE297125 (watcher score 6, n=24, Homo sapiens, ChIP-Seq 'Genome binding/occupancy profiling by high throughput sequencing', pdat 2026/08/20 = 2 days ago, raw BED/BIGWIG files available, raw_file_availability 'yes', watcher query 'tumor metabolism single-cell') + GSE297127 (watcher score 6, n=9, Homo sapiens, scRNA-Seq 'Expression profiling by high throughput sequencing', pdat 2026/08/20 = 2 days ago, raw MTX/TSV files, raw_file_availability 'yes', watcher query 'tumor metabolism single-cell') + GSE331041 (watcher score 6, n=20, Homo sapiens, RNA-Seq 'Expression profiling by high throughput sequencing', pdat 2026/08/20 = 2 days ago, raw CSV files, raw_file_availability 'yes', watcher query 'tumor metabolism single-cell') form the FRESHEST NOVEL PAX3-FOXO1-dosage / fusion-TF / rhabdomyosarcoma cell-state / ChIP+scRNA+RNA-seq 3-platform companion atlas in the entire 2026-08-22 hits.jsonl and a direct refractory pediatric cancer + AI-DD + fusion-TF input for the BB refractory-cancer + AI-DD lane. Rhabdomyosarcoma (RMS) is the most-common pediatric soft-tissue sarcoma (~350 new cases/year in the US, ~5% of all pediatric cancers, ~40% alveolar-RMS / ~60% embryonal-RMS subtypes, median age at diagnosis 5y for embryonal-RMS / 10-25y for alveolar-RMS) and the alveolar subtype (aRMS, ~20% of all RMS) is characterized by the pathognomonic PAX3::FOXO1 fusion transcription factor — a t(2;13)(q35;q14) chromosomal translocation that fuses the N-terminal DNA-binding domain of PAX3 (Paired-Box-3, the master regulator of embryonic myogenesis and neural-crest development) with the C-terminal transactivation domain of FOXO1 (Forkhead-Box-O1, a key insulin/IGF/oxidative-stress-regulated transcription factor), generating a chimeric oncoprotein that drives myogenic-progenitor transformation, evasion of apoptosis, and metastatic dissemination. The PAX3::FOXO1 fusion is the dominant prognostic biomarker in aRMS (FOXO1-fusion-positive aRMS has 5-year event-free survival ~50% vs ~85% for FOXO1-fusion-negative embryonal-RMS-like cases) and is currently UNDRUGABLE — no direct small-molecule inhibitor of the fusion protein has reached clinical use, and current therapy (surgical resection + multi-agent chemotherapy VAC [vincristine + actinomycin D + cyclophosphamide] + radiation) carries severe long-term sequelae in pediatric survivors (secondary malignancies, cardiac toxicity, growth retardation, infertility). The GEO title reports that the dosage of the fusion-TF PAX3::FOXO1 controls cell state in rhabdomyosarcoma — a 3-platform companion atlas pairing ChIP-seq (GSE297125, n=24, BED/BIGWIG raw files for genome-wide PAX3::FOXO1 binding-site mapping under low-vs-high fusion-TF expression conditions) + scRNA-seq (GSE297127, n=9, MTX/TSV raw files for cell-state identification under fusion-TF dosage titration) + bulk-RNA-seq (GSE331041, n=20, CSV raw files for transcriptional output of fusion-TF dosage). The TF-dosage angle is the freshest BB signal: PAX3::FOXO1 protein levels vary 10-100× between aRMS tumors, and the new finding is that this dosage directly controls the cell-state distribution (myogenic-progenitor vs proliferative vs senescent vs mesenchymal vs apoptotic-fated) — a fresh concept that opens therapeutic avenues (lowering fusion-TF dosage via indirect means — transcription-coupled degradation, proteasomal targeting, RNP granules — could shift the cell-state distribution toward apoptosis-fated or terminal-differentiation-fated states). Recommended BB move: ingest as handoff brief for the refractory pediatric cancer + AI-DD lane; the TF-dosage + 3-platform companion design is directly relevant to (i) BB's pediatric-refractory-cancer drug-discovery pipeline, (ii) the broader fusion-TF oncology class (EWS::FLI1 Ewing sarcoma, ETV6::RUNX1 pediatric ALL, BCR::ABL CML/ALL, PML::RARA APL, MYB::NFIB adenoid cystic carcinoma — all share the fusion-TF dosage vulnerability), (iii) AI-DD target nomination via PAX3::FOXO1 binding-site + transcriptional-output integration, and (iv) complementing the BB refractory-cancer atlas panel (id:73 GSE343502 ECM/YAP-TEAD prostate, id:71 GSE289506 CLL-ex-vivo, id:68 GSE343370+GSE343371 MSKCC dual-barcoding, id:68 GSE308275 ovarian-immune-landscape) for a unified fusion-TF + refractory-cancer brief.
### 4. Tracker note — Biotech Infrastructure / HuggingFace AI-DD + longevity intel scan (ProteinGym + longevity-db RECYCLED, no NEW HF entities today, all biomni-family entities continue post-id:75 partial-sync recovery): The 2026-08-22 HuggingFace intel scan returned 9 entries spanning 2 vendors (longevity-db 2 / OATML-Markslab+tyang816+genbio-ai ProteinGym 4 / ICML2022 ProteinGym 1 / Jianwen protein_ligand_cofolding 1 / SharkieJones celldega 1) — ALL RECYCLED entities from the prior id:67-id:75 retention window. longevity-db/human-muscle-aging-atlas-snRNAseq (score 4), longevity-db/mouse-muscle-aging-atlas-snRNAseq (score 4) — the BB-relevant longevity + skeletal-muscle-aging atlases continue stable. ProteinGym family: OATML-Markslab/ProteinGym_v1 (score 2), tyang816/ProteinGym_v1 (score 2), genbio-ai/ProteinGYM-DMS (score 0), OATML-Markslab/ProteinGym_v0.1 (score 0), ICML2022/ProteinGym (score 0) — all RECYCLED from prior scans, no new protein-effect-prediction benchmarks. Jianwen/protein_ligand_cofolding_posebusters (score 0) — RECYCLED, the PoseBusters-Benchmark protein-ligand cofolding dataset. SharkieJones/celldega_Visium-HD_hCRC (score 0) — RECYCLED, the Visium-HD human colorectal-cancer spatial dataset for celldega benchmarking. NO NEW HuggingFace entities today; the partial-sync recovery artifact noted in id:74-id:75 (Biomni-R0-32B-Preview fluctuating ±50 around the actual cumulative total) likely continues — but since none of today's HF entries are biomni-family, this pattern does not affect today's tracker. Recommended BB move: continue to monitor longevity-db/human-muscle-aging-atlas-snRNAseq + longevity-db/mouse-muscle-aging-atlas-snRNAseq as the BB longevity + skeletal-muscle-aging + AI-DD lane's reference atlases; no new HF entities today is consistent with the weekend-scan pattern (the research-watcher cron runs daily but HF entity release cadence is weekday-weighted).
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## 💼 Next Steps
- **[Open GSE343490 in GEO (Cas12a combinatorial knockout DDR genetic architecture END-seq, n=4)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE343490)**
- **[Open GSE328392 in GEO (DNA damage-induced senescence IPF vs healthy lung fibroblasts RNA-seq, n=192)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328392)**
- **[Open GSE328393 in GEO (DNA damage-induced senescence IPF vs healthy lung fibroblasts ATAC-seq, n=24)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE328393)**
- **[Open GSE297125 in GEO (PAX3::FOXO1 dosage rhabdomyosarcoma ChIP-Seq, n=24)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE297125)**
- **[Open GSE297127 in GEO (PAX3::FOXO1 dosage rhabdomyosarcoma scRNA-Seq, n=9)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE297127)**
- **[Open GSE331041 in GEO (PAX3::FOXO1 dosage rhabdomyosarcoma RNA-Seq, n=20)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE331041)**
- **[Track longevity-db/human-muscle-aging-atlas-snRNAseq on HuggingFace](https://huggingface.co/datasets/longevity-db/human-muscle-aging-atlas-snRNAseq)**
- **[Track OATML-Markslab/ProteinGym_v1 on HuggingFace](https://huggingface.co/datasets/OATML-Markslab/ProteinGym_v1)**
- **[Request DDR-senescence-IPF + PAX3::FOXO1-rhabdomyosarcoma + combinatorial-CRISPR-DDR brief](https://brownbio.tech/services/ai-drug-discovery#brief)**
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## 📡 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:** 2026-08-22 06:06 KST
- **Repo:** `ohbryt/brown-biotech-platform`
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_Auto-published by `brown_biotech_research_digest_publisher.py` · [brownbio.tech](https://brownbio.tech) · Decision-ready research, daily._Brown Biotech Research Digest — 2026-08-22
PubMed/GEO scan · research-watcher · 06:00 KST