Cancer Cells and Metastasis

The paper infers EMT dynamics from cell cycle profiles using a hidden Markov model, showing it can reconstruct EMT trajectories from cell cycle data alone.

The paper uses live single-cell imaging to show cancer stem cells form spatial niches and undergo reprogramming influenced by both lineage and cell-cell interactions.

The paper develops a mouse model of metastatic dormancy and identifies unique phenotypic and molecular features of dormant metastases controlled by the immune system.

This study identifies immune mimicry in breast cancer cells, where neoplastic cells express leukocyte receptors, enhancing tumor aggressiveness and therapy resistance.

This study shows cancer cells follow intrinsic self-organized programs that coordinate tumor cell state transitions during growth, revealing mechanical gradients and stereotyped patterns of heterogeneity and plasticity.

This study shows that CENP-A, a centromeric histone variant, epigenetically regulates epithelial-mesenchymal plasticity and heterogeneity in human cells through non-centromeric mechanisms.

The paper introduces the SITE platform for live-cell ex vivo modeling of cancer and TME interactions, revealing tissue-specific dynamics and ERK signaling patterns in breast cancer.

This study shows that capillary constrictions reprogram melanoma cells to a tumorigenic cancer stem cell-like state via PIEZO1 mechanosensing.

This study identifies metastasis-initiating osteosarcoma subpopulations that interact with lung and tumor cells to form a metastatic niche, highlighting tumor-stromal interactions as key drivers of metastasis.

This study shows ERK3 promotes TNBC progression through EMT plasticity and collective migration, linking it to poor clinical outcomes.

This study shows primary cilia in TNBC cells contribute to chemoresistance by supporting EMT-driven heterogeneity and stemness, and inhibiting ciliogenesis reduces this resistance.

This study shows that Sox10 deletion in luminal cells of HER2+ mice prevents tumor initiation and reprograms tumor cells to a basal phenotype.

The paper identifies L1CAM-driven planar cell polarity signaling as a mechanism promoting SOX2+ metastatic progenitors in lung adenocarcinoma.

This study identifies early transcriptional signatures of drug resistance in cancer and across species, showing conservation and predictive value for treatment response.

This study identifies multiple metastatic cell states in TNBC through EMT plasticity, showing that metastatic competence arises from diverse EMT programs rather than a single phenotype.

This study shows that fine needle aspiration biopsy (FNAB) effectively harvests cells for patient-derived organoids modeling breast ductal carcinoma in situ, with faster growth times compared to core needle biopsy.

This study uses deep learning and spatial data to show how tumor architecture and cell states co-evolve, influencing colorectal cancer outcomes.

This study uses lineage tracing and single-cell analysis to show tumor plasticity precedes stable immune evasion, with AP-1 regulating EMT stabilization during immunotherapy.

This study identifies GSTT1HighCD133High cells as a stem-like subpopulation in pancreatic cancer that is sensitive to FGFR inhibitors, highlighting a therapeutic target.

This paper introduces a breast organoid model that captures tissue organogenesis with high-resolution live imaging, revealing novel morphogenesis processes and stromal generation.

The paper shows that transient CB2R activation in breast cancer cells leads to irreversible luminal differentiation through chromatin remodeling, enhancing tamoxifen response and reducing resistance.

This study shows that lung epithelial cells promote breast cancer metastasis through wound repair mechanisms, and targeting CREB signaling with PDE4 inhibitors can reduce metastatic outgrowth.

The paper identifies neurogenesis-related gene expression as a clone-specific hallmark of brain metastasis in breast cancer using a new optical barcoding tool.

This paper demonstrates that targeting the tumor microenvironment, specifically cancer-associated fibroblasts, with a novel nanotherapeutic called Penetrium can overcome resistance and metastasis in cancer models.

This study identifies SNO-COX-2 as a biomarker for mesenchymal phenotypes in breast cancer, showing its microenvironmental regulation and association with invasive growth.

The paper shows that cell-free chromatin particles from cancer patients can transform mouse fibroblasts into cancer stem cells capable of forming tumors and expressing germline markers.

The paper establishes a large-scale biobank of GEA patient-derived organoids that accurately model tumor features and drug responses, enabling personalized treatment strategies.

This study shows Regnase-1 promotes tumor-initiating activity in NSCLC by suppressing the SOX2 pathway, and its inhibition reduces tumor growth and enhances anti-cancer immunity.