Articles tagged with Tumorigenesis
The Human Cancer Model Initiative released a compendium of more than 150 organoid models of 25 types of cancer, which are now available to scientists worldwide. These patient-derived organoids provide state-of-the-art research tools for accelerating discovery and developing personalized treatment strategies.
A new study reveals that the KDM3A/METTL16/PDK1 axis drives glycolysis and overcomes tyrosine kinase inhibitor resistance in non-small cell lung cancer. The research suggests that targeting this axis with PDK1 inhibitors could be a promising therapeutic strategy for overcoming acquired drug resistance.
A study by the CNIO group has identified a genetic signature in precancerous breast lesions that can predict which ones will evolve into invasive tumours. This discovery could help avoid over-treatment of women diagnosed with ductal carcinoma in situ, a common precancerous lesion.
Super-enhancers are densely clustered regions driving oncogene expression in cancer. Targeting BRD4, CDK7, and SE structure with small molecules and CRISPR may offer therapeutic benefits. Combination therapies aim to overcome resistance and improve outcomes.
The study reveals that MCL1 directly influences the mTORC1 complex, controlling bioenergetics and tumorigenesis in cancer cells. Genetic analyses also show that MCL1 inhibitors inhibit mTOR signaling, addressing a previously unresolved problem in cancer therapy.
The review highlights the complex relationship between mitochondria and tumorigenesis, exploring molecular mechanisms underlying this association. Mitochondrial dysfunction is linked to various cancers, and targeting mitochondria represents an ideal anti-tumor therapeutic approach.
A study found that higher consumption of ultraprocessed foods is associated with an increased risk of developing early-onset colorectal cancer precursors. The research highlights the importance of improving dietary quality to mitigate the rising burden of early-onset colorectal cancer.
Researchers at University of Texas M. D. Anderson Cancer Center discover that inflammation is responsible for driving the earliest stages of lung cancer, identifying potential targets for early intervention and suggesting a promising approach to intercepting lung cancer development.
Researchers discover that gray hair may be a result of a natural defense mechanism against cancer, where damaged stem cells undergo senescence-coupled differentiation, leading to graying. In contrast, bypassed stem cells can expand clonally and lead to tumor development.
Recent research highlights the crucial role of circadian rhythms in tumor biology, demonstrating their contribution to tumorigenesis, progression, and metastasis. Disruptions in these rhythms also influence the tumor immune microenvironment and the efficacy of anticancer therapies.
A new study has mapped genetic differences across children with Wilms tumour, a type of childhood kidney cancer, to understand how it develops and responds to treatment. The research suggests that inherited genetic changes predetermine tumour development, growth, and response to treatments.
Research suggests LKB1's paradoxical pro-tumorigenic properties highlight the need for targeted inhibitors. Studies indicate that LKB1 plays a crucial role in regulating AMPK and reactive oxygen species scavenging.
Researchers from Osaka University found that Foxo3 mediates erroneous cell elimination during vertebrate development, ensuring precise development and cancer prevention. The study identified a specific pathway involving Foxo3, N-cadherin, and reactive oxygen species to eliminate unfit cells with abnormal Shh activity levels.
Research highlights molecular chaperones' role in maintaining tumor suppressor stability and functional integrity. This understanding is crucial for developing targeted therapies for multiple cancers.
This study evaluated somatic copy number alterations (SCNAs) and mutation landscapes in malignant rhabdoid tumors before and after treatment. The results revealed recurrent SCNAs harboring genes involved in tumorigenesis, with some correlations between gene expression and tumor progression.
Researchers uncover how EBV infects host genome, leading to tumor formation and finding novel therapeutic targets. EBV-host interactions reveal epigenomic rewiring, dysregulated gene expression, and potential cancer treatment.
Researchers have uncovered the molecular and ultrastructural features of BCAS1+ cells in diffuse gliomas, highlighting their proliferative capacity and distribution. The study provides a comprehensive characterization of the BCAS1+ cell population within diffuse gliomas, shedding light on its role in tumor malignancy.
Researchers have identified macrocyclic compounds as a potential solution for targeting proteins critical to tumorigenesis, blocking nearly 80% of cancer's signature characteristic events. Additionally, these small compact molecules can effectively overcome drug resistance by binding to mutant proteins and inhibiting their activities.
A new study by Tulane University has identified a previously unknown molecular pathway that could halt lung cancer growth. The research found that protein RBM10 can suppress lung cancer by targeting the function of c-Myc, a protein that drives cancer cell growth and proliferation.
Researchers used base editors to introduce specific combinations of activating and inactivating mutations into healthy organoids, creating realistic models for various types of cancer. This allows for further investigation into the development and treatment of cancer, with potential applications including testing new drugs.
Researchers found that GPR141 enhances cell migration and proliferation in breast cancer by activating the p-mTOR/p53 signaling pathway. Silencing GPR141 restores p53 expression and attenuates tumor growth, suggesting its role in regulating breast cancer progression and metastasis.
Researchers found that necroptosis promotes metastasis in breast cancer models, and blocking it leads to inhibition of metastasis. Necroptosis may be a key factor in tumor progression, and targeting its regulators could be critical for mitigating metastasis.
Researchers found that p21 knockout mice experienced reduced senescent cell presence, alleviated chronic lung inflammation, and improved fitness. Resident epithelial and endothelial cells played a significant role in mediating the p21-dependent inflammatory response.
A study led by Tokyo University of Science researchers identified Dectin-1's role in promoting colorectal cancer by enhancing PGE2 production and suppressing IL-22BP expression. The study used mouse models and clinical samples to validate the findings, which have immediate clinical implications for CRC patients.
Researchers identified high expression of glypican-1 in primary solid tumors, correlating with poor prognosis in various cancer types. Suppression of GPC1 attenuated cancer cell proliferation, suggesting its potential as a novel diagnostic tool and target for therapy.
A recent study analyzed 7,301 metastatic breast cancer patients with MTAP loss, revealing younger age, higher TNBC cases, and BRCA1 mutations. The findings also suggest potential therapeutic agents targeting PRMT5 and MTA2 in MTAP-deficient cancers.
Researchers have identified mitochondrial signaling pathways as critical organelles that promote tumorigenesis and metastasis. In particular, the integrated stress response is found to engage with mitochondria to drive tumor growth, highlighting a new paradigm for understanding aggressive prostate cancer progression.
Researchers from Northwestern University discuss the multifaceted tumorigenic functions of EZH2, including its role in regulating translation and coactivating transcription. This new understanding may provide novel insights into advancing EZH2-targeting strategies for prostate cancer patients.
Researchers from Okayama University found that Actinidia arguta (Sarunashi) juice and its component isoquercetin inhibit lung cancer development in mice, accelerating DNA repair and suppressing Akt-mediated growth signaling. The study suggests Sarunashi juice as an attractive candidate for chemoprevention.
Researchers found that dietary saturated/trans fats, but not cholesterol, can trigger hepatic angiogenesis and lymphangiogenesis in mice, leading to the promotion of hepatic tumors. This process is driven by the JNK-HIF1α-VEGF-C axis.
A new review paper discusses the role of CDK4 in regulating the cell cycle and its involvement in cancer. The study highlights the importance of CDK4/6 inhibitors as treatments for ER+ breast cancer and their potential utility in multiple tumor types.
A retrospective study found that tumor hyaluronan levels are associated with improved time to progression in non-small cell lung cancer patients. HA-high tumors showed a trend towards improved clinical benefit, suggesting its potential as a prognostic biomarker and therapeutic target.
SLFN11 acts as a surveillance factor for protein homeostasis by alleviating proteotoxic stress derived from protein synthesis and maturation. Its lack makes cells vulnerable to anticancer drugs inducing ER and proteotoxic stress, leading to chemoresistance. SLFN11 is also involved in regulating immune response and inflammation.
Researchers from China have developed a novel bioconjugate that can suppress the growth of K-Ras mutant pancreatic tumors. The conjugate, which targets folate receptors and macropinocytosis, was found to be highly cytotoxic and effective at suppressing tumor growth.
Researchers identified a minimal set of defined factors that can convert normal human fibroblast cells to liver cancer cells, providing a mechanistic proof-of-principle for understanding why certain mutations cause cancer in particular tissues.
Researchers have determined the structure of human leukotriene B4 receptor 1 (hBLT1), a protein involved in inflammation and disease. The analysis reveals how the receptor recognizes its binding partners and interacts with them, opening up avenues for designing better drugs.
Researchers at the University of Helsinki have made a significant advance in fibroids research by identifying a new mechanism of tumorigenesis. Multiple tumors carried mutations in genes involved in histone trafficking, which affected gene expression levels and led to hereditary predisposition to the disease.
The loss of expression of a microtubule/tubulin binding protein, centrosomal protein 4.1-associated protein, causes increased EGFR levels and signaling in oral squamous cell carcinoma cells. Depletion of CPAP enhances tumorigenicity, while EGFR depletion attenuates EMT features.
The study investigates the cooperative effects of targeted deletions of tumor suppressors Rb1, Trp53, Men1, and Pten in neuroendocrine tumors in mice. The authors demonstrate that pRB has the strongest cooperative function with PTEN in suppressing Pit NETs and Menin and TRP53 in suppressing Pan NETs.
A study led by SUNY Downstate researchers found that inhibiting liver sphingolipid de novo synthesis in early life impairs adherens junctions and promotes tumorigenesis. Sphingomyelin supplementation partially corrects the defect, suggesting a potential therapeutic target for metabolic diseases.
Researchers found that dysbiosis enhances intestinal inflammation and increases risk of colon cancer, but treatment with antibiotics or fecal transplantation reduces disease risk. Gut bacterial communities play a crucial role in protecting against intestinal inflammation and tumorigenesis.
A research group at Case Western Reserve University found that Recql5 mutation had an important impact on tumorigenesis in the mouse GI tract. The study also suggested that Recql5 may be an important candidate for a colon cancer biomarker, and its expression was recently shown to affect sensitivity to camptothecin-based anticancer drugs.
Researchers investigated the roles of PTEN and TSC2 in tumorigenesis and found that TSC2 can suppress specific tumors caused by Pten heterozygosity. However, PTEN is haploinsufficient for repression of carcinogenesis resulting from Tsc2 heterozygosity.
Researchers found that Cripto overexpression inhibits Activin signaling, leading to increased tumor cell growth. Antibody blockade of Cripto suppresses tumor cell growth in xenograft models, suggesting a central role for Cripto in tumorigenesis.
Researchers found that MYC binds to the WRN gene promoter, activating WRN expression and promoting cellular senescence in tumor cells. This discovery suggests a potential therapeutic target for cancer treatment by inhibiting WRN in MYC-induced tumor cells.