Multiomics, computational biology, and ancestry-specific genomics are transforming proactive cancer care with new insights into tumor biology and targeted therapies.
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American Association for Cancer Research · Oncology · ISSN 0008-5472, 1538-7445
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Multiomics, computational biology, and ancestry-specific genomics are transforming proactive cancer care with new insights into tumor biology and targeted therapies.
EZH2 inhibition triggers a metabolic stress response in TNBC, increasing glutaminolysis and making tumors more vulnerable to glutaminase inhibitors.
Targeting cell cycle regulators CDK4/6 and CDK2 overcomes resistance to KRAS inhibitors in pancreatic and lung cancers, achieving durable tumor control.
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IL-1α drives expansion of SLC2A1highSPP1highIFNlow myeloid cells, promoting immune escape and malignant transformation in pre-cancerous head and neck lesions.
Placenta-related PEG10 promotes hepatocellular carcinoma progression by inhibiting mRNA decay and enhancing glucose metabolism, with overexpression linked to poor prognosis.
EZH2 inhibition triggers a metabolic stress response in TNBC, increasing glutaminolysis and making tumors more vulnerable to glutaminase inhibitors.
Acidic tumor microenvironment activates p300, causing a 50% reduction in PARPi effectiveness in epithelial ovarian cancer.
The ITCC-P4 platform developed 353 pediatric cancer PDX models, enabling preclinical testing and biomarker discovery for high-risk solid tumors.
ScanTCR achieves over 90% accuracy in early cancer detection across seven cancer types by analyzing the full TCR repertoire in peripheral blood.
ALKBH5-driven epitranscriptomic changes in cancer-associated fibroblasts promote pancreatic cancer metastasis independently of primary tumor growth.
Cancers exhibit a four-fold higher mutation burden than normal tissues across five organs, driven by individual baseline mutation rate differences.
PDE5a inhibitors like sildenafil reduce cancer metastasis by disrupting NPC1-mediated cholesterol trafficking, causing lysosomal cholesterol accumulation and impairing cell migration.
TLR9 agonists enhance adoptive T cell therapy by activating a B cell-CD2 costimulatory pathway, leading to improved tumor control and T cell function.
High-risk rhabdomyosarcomas share a common neural-like cell state, regardless of FOXO1 fusion status, revealing a convergent transcriptional phenotype in lethal cases.
Targeting cystine addiction reduces lung metastasis in MYC-driven breast cancer by exploiting a unique metabolic vulnerability.
Obesity and aging increase tissue-resident Akkermansia muciniphila in breast tissue by up to 50%, promoting oxidative stress and elevating postmenopausal breast cancer risk.
Targeting cell cycle regulators CDK4/6 and CDK2 overcomes resistance to KRAS inhibitors in pancreatic and lung cancers, achieving durable tumor control.
Natural killer and CD8+ T cells cooperate to convert poorly infiltrated tumors into inflamed, immune-responsive environments, with NK cell infiltration occurring early after vaccination.
Macrophage-induced senescent cancer-associated fibroblasts drive 78% chemoresistance in colorectal cancer via SASP factors IL6 and CXCL12.
Mapping intra-tumoral drug distribution reveals significant barriers, with variability across patients and tumor regions, limiting therapeutic success in cancer treatment.
MYC drives tissue-specific and systemic metabolic reprogramming in tumors, creating context-dependent vulnerabilities that can be targeted for therapy.
Targeting WRN helicase in MSI colorectal cancer induces immune activation by releasing extrachromosomal circular DNA, enhancing antitumor responses.
CDK2 inhibitors induce RB-independent tumor suppression in CDK4/6 inhibitor-resistant HR+/HER2- breast cancer, with disease stabilization observed in patients.
KRASG12R pancreatic cancer cells develop resistance to daraxonrasib via EGFR/RASWT signaling, enabling effective trametinib-based therapy and extending patient survival to 40 months.
Exercise reduces stromal fibroblasts and inflammatory signals in pancreatic cancer, with a 50% decrease in αSMA+ cells linked to microbial metabolites.
High MYC expression drives ribophagy-induced rRNA breakdown, causing cell death in hepatocellular carcinoma under glutamine deprivation, with 70% sensitivity linked to MYC levels.
PLAU⁺ fibroblasts drive chemoresistance in lung adenocarcinoma by activating a CXCL5-CLGN pathway, with high CLGN levels linked to poor patient survival.
Impaired NAD⁺ regeneration via the mevalonate pathway reduces serine biosynthesis by 50% and increases neuroblastoma cell sensitivity to PHGDH inhibition.
ClpP agonist IMP125 rewires the metabolic-immune axis in AML, reducing tumor oxygen consumption and enhancing T-cell function.
Inhibiting translesion synthesis enhances PARP inhibitor effectiveness, preventing resistance in BRCA-deficient ovarian cancer by delaying tumor relapse and promoting sustained regression.
Spatial colocalization of CD24+ tumor cells and BGN+ CAFs predicts breast cancer recurrence after BCS with high accuracy.
A machine learning framework called EXPRESSO accurately predicts treatment responses across nine cancer types using tumor transcriptomics, outperforming existing signatures in 91 cohorts.
MITF-regulated PD-L1 expression in melanocytes protects against UVB-induced immune attack, linking photoprotection to immune tolerance and melanoma risk.
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