Articles tagged with Tumor Growth
Cells undergoing EMT promote tumor growth by acquiring an endothelial phenotype or contributing to vascular transdifferentiation. FOXC2 is crucial for these processes.
A recent study published in the Oncogene Journal revealed that targeting HIF-1α significantly inhibited melanoma growth and amplified immune cell infiltration into tumour microenvironment. The discovery provides a valuable new target for making resistant melanomas more vulnerable to available anti-cancer treatments.
Researchers at the University of Texas M.D. Anderson Cancer Center have discovered that targeting the mitochondrial enzyme DHODH can induce ferroptosis and suppress tumor growth in cancer cells. The study suggests a new therapeutic strategy for inducing ferroptosis, which could have broad implications for treating various types of cancer.
Researchers found that autophagy selectively degrades PKA inhibitory subunit RIa, promoting mitochondrial metabolism and tumor cell growth. Suppression of AKAP11 levels in tumor cells prevents degradation and blocks PKA activation, inhibiting tumor cell growth.
A high-fat diet is associated with increased risk of late-onset colorectal cancer, particularly in obese female mice. The study reveals that excess body weight leads to tumor growth through inflammation, insulin-like growth factor release, and polarization of macrophages.
Researchers found that time-restricted feeding, a form of intermittent fasting aligned with circadian rhythms, improved metabolic health and reduced tumor growth in mice with obesity-driven postmenopausal breast cancer. Elevated insulin levels drove accelerated tumor growth, which was mitigated by reducing insulin levels.
Researchers at Duke University developed a predictive theory for tumor growth that approaches the subject from a new point of view, using thermodynamics and physical space. The results demonstrate how a tumor's growth is directly tied to its need to create greater access to flowing nutrients and conduits for removing refuse.
A team of engineers at Rensselaer Polytechnic Institute developed an in vitro lymphatic vessel model to study tumor emboli growth. Researchers found that the model showed different growth behaviors based on cell type, linked to force generation capability, and has implications for therapeutic design.
Dr. Benjamin Tu's research on cellular roles of small molecule metabolites has led to the discovery of a unique pathway supporting cancerous cell growth. His work challenges the long-held belief that metabolites are merely passive in their function, unveiling that they may drive key cellular processes.
Scientists have identified a new metabolic vulnerability in highly aggressive non-small cell lung cancer (NSCLC) tumors containing mutations in KRAS and LKB1. The hexosamine biosynthesis pathway is activated in these tumors, providing a potential target for therapy.
Researchers found that CRYM protein binds to hormone T3 and blocks cell membrane formation, inhibiting tumour growth. Lower CRYM levels are associated with poor prognosis.
Sertraline's anti-cancer activity is attributed to its ability to inhibit the production of serine and glycine, two amino acids that stimulate cancer cell growth. The substance has shown promise in inhibiting breast cancer cell growth when used in combination with other therapies.
Researchers found that chronic jet lag alters the microenvironment surrounding tumor cells, making it favorable for tumor growth, while hindering the body's natural immune defenses. This study adds to the growing scientific field of circadian disruption on health and wellbeing.
Research published in Nature Precision Oncology reveals that honeybee venom and its compound melittin rapidly destroy triple-negative and HER2-enriched breast cancer cells. The venom's potency allows for selective cell death with minimal effects on normal cells.
A team of scientists from UC San Diego identified a metabolic switch that decreases tumor growth in mice by restricting dietary amino acids. They found that restricting serine and glycine led to the production of toxic lipids that slow cancer progression.
Researchers found that TMEM165 expression levels alter N-linked glycosylation, promoting the invasion and growth of breast cancer cells. This study suggests a novel role for TMEM165 as a driver of tumor invasion and identifies it as a potential biomarker for breast carcinoma.
A study by Queen Mary University of London uncovers novel pathways controlling cancer progression, identifying Rac1 as a critical player in MET-driven processes. The findings may pave the way for more efficacious treatment regimens by targeting MET, PI3K, and mTOR.
A new study from Washington University School of Medicine has found that brain tumors in children with NF1 are driven by nearby noncancerous neurons and immune cells. The researchers discovered that targeting immune cells slows tumor growth in mice, pointing to potential new treatments.
Establishing an inducible BCL6 knock-out model allows studying the phenotype of BCL6 loss in DLBCL xenografts in vivo. The study demonstrates significant tumor growth inhibition and initial tumor stasis followed by slow tumor growth kinetics upon treatment with BCL6 degraders.
Researchers at Sanford Burnham Prebys Medical Discovery Institute found that prebiotics mucin and inulin slowed melanoma growth in mice by enhancing anti-tumor immunity. The study suggests a potential benefit of prebiotics in treating cancer or augmenting current therapies.
Researchers have discovered that inhibiting p38 reduces the growth of lung tumors in genetic mouse models. Lower levels of p38 in tumors are associated with a more favorable prognosis for patients.
Researchers at Boston University School of Medicine have discovered the protein c-Cbl has the ability to degrade PD-1, a critical immune checkpoint that helps cancer cells evade the immune system. This finding may lead to new therapies targeting c-Cbl to treat certain types of cancer, including melanoma and non-small lung cancer.
Researchers have identified a key protein, Importin-11, that transports the cancer-causing protein βcatenin into the nucleus of colon cancer cells. Inhibiting this transport step could block the growth of most colorectal cancers caused by elevated βcatenin levels.
Fibroblasts play a crucial role in wound healing but also facilitate tumor growth and metastases in breast cancer. Inhibiting inflammatory signaling pathways may prevent metastatic relapse, say researchers from Tel Aviv University.
Researchers at Stanford and UC-San Francisco have developed an experimental drug that targets lung cancer by neutralizing a single protein, slowing its growth. The decoy version of the receptor protein was engineered to preferentially bind to the protein, repelling other proteins involved in tumor growth.
Researchers at UNC Lineberger Comprehensive Cancer Center have identified a potential approach to block medulloblastoma growth by targeting the GSK-3 signaling pathway. By blocking this pathway, they may be able to control tumor growth and reduce debilitating side effects from radiation and chemotherapy.
A new study using big data reveals that many fundamental features of life, such as metabolism and growth, follow consistent relationships with body size across all creatures. This challenges the Metabolic Theory of Ecology and suggests a deep understanding of universal laws governing life's diversity.
Researchers at UNC Lineberger Comprehensive Cancer Center discovered a hyperactive cell signal contributing to tumor growth in aggressive blood cancer. They developed an experimental therapeutic compound, UNC3810A, that targeted and slowed tumor growth by blocking the hyperactive Tyro3 protein.
Researchers have identified an enzyme called LPCAT1 that plays a key role in tumor growth by changing the phospholipid composition of cancer cells' plasma membranes. When genetically depleted in mice, malignancies shrank dramatically, suggesting LPCAT1 as a potential new drug target for various cancer types.
Researchers at the University of Pennsylvania School of Medicine have identified a new pathway that works as a partner to MYC and may be its Achilles' Heel. By blocking the ATF4 gene, cancer cells produce too much protein and die due to stress. This finding could lead to a new therapeutic approach using existing inhibitors.
A high salt diet has been shown to inhibit tumor growth in mice by altering the function of certain immune cells called myeloid-derived suppressor cells. This effect could be beneficial for improving anti-cancer immunotherapies, but further research is needed to fully understand its therapeutic potential.
A study published in PLOS Medicine found that a computer-assisted diagnostic procedure can detect the growth of low-grade brain tumors earlier and at smaller volumes than current clinical methods. This could lead to reduced delays in detecting tumor growth and potentially improve patient outcomes.
Researchers at Penn Medicine found that chronic circadian disruption triggers cell proliferation and shifts the cell-cycle balance, leading to tumor growth. The study also suggests that timing cancer treatment according to an individual's circadian rhythm can improve disease outcomes.
A new study reveals that disrupting normal circadian rhythms promotes tumor growth and suppresses the effects of a tumor-fighting drug. Circadian rhythm disruption increases cell proliferation by activating key proteins involved in cell cycle regulation.
Researchers discovered that gasdermin E forms holes in cell membranes, leading to cell death and suppressing tumor growth. The protein's expression is lower in many types of cancer, suggesting it may be a useful target for improving cancer therapy.
Scientists at Hebrew University create decoy molecules that trick RNA-binding proteins into binding with them, inhibiting their cancer-promoting activity. The technology has shown promise in slowing or stopping the growth of brain and breast cancer cells in mice.
Researchers developed a new method to predict tumor growth rates using progression-free survival plots, reducing errors found in current methods. This improvement enables clinicians to schedule optimal screenings and set effective dosing regimens.
Researchers from Marshall University found that consuming two ounces of walnuts daily for two weeks changes gene expression in confirmed breast cancers, slowing growth and reducing survival risk. The study involved 10 women with breast lumps, who were randomized to walnut or control groups.
A mouse study suggests that time-restricted eating can delay the development of tumors and reduce tumor growth in obese mice with high-fat diets. The results imply that this intervention could be effective in preventing breast cancer.
A study by Weill Cornell Medicine found that consuming high-fructose corn syrup causes mice with colon cancer to develop larger tumors. The researchers discovered a molecular mechanism by which the sweetener fuels tumor growth and suggest blocking this effect could lead to new cancer treatments.
A new study suggests that enlarged prostates could impede tumor growth in prostate cancer patients. Computer simulations found that the mechanical stresses from an enlarging prostate keep tumors small. The findings challenge traditional treatments that involve downsizing the prostate.
A new study describes a novel approach to suppressing chemotherapy-induced tumor growth and recurrence in ovarian cancer. Researchers developed an anti-inflammatory drug called PTUPB that blocks the release of tumor-promoting chemicals by macrophages.
Researchers discovered Src activates mTORC1 through amino acid signals, found to be hyperactive in cancer. Src's malfunction leads to continuous signaling for cell growth and cancer progression.
A scientific study has found that sleep apnea can favor lung cancer growth in young individuals, suggesting that age may play a role in the disease's aggressiveness. The research team hopes to identify and prove physiopathological consequences of sleep apnea to develop personalized medicine strategies.
The study reveals how a fusion protein found in cancer cells enhances target gene expression by converting microsatellite repeats into active enhancers. Blocking this process prevents tumor growth.
A high-fat diet accelerates prostate cancer growth and increases immune cells that suppress the immune system. Anti-inflammatory drugs may have benefits for obese patients with prostate cancer.
Researchers discovered that FDA-approved kinase inhibitors can curb lung tumor growth in mouse models, offering new therapeutic avenues for a hard-to-treat form of lung cancer. The findings highlight the potential of targeting ERBB receptor tyrosine kinases and EGFR signaling pathways to develop alternative treatment strategies.
Scientists at German Cancer Research Center have discovered a new target for anti-angiogenic tumor therapy by deleting a signaling molecule in mice, leading to delayed tumor growth and limited metastases. The receptor Tie1 plays a crucial role in angiogenesis and is overexpressed in tumors.
A team of researchers is developing complex computer models to predict how cancer will progress in individual patients. They use advanced computing resources, including those at the Texas Advanced Computing Center, to analyze patient-specific data from imaging tests and biopsies, as well as other factors.
A new USC study reveals that tumor growth properties can influence response to cancer drugs. Researchers found certain parameters of tumor growth can forecast the effectiveness of anti-angiogenic treatment, allowing for more accurate predictions. This breakthrough has the potential to improve cancer therapy outcomes.
Researchers developed a mathematical model that simulates tumor growth and predicts response to cancer drugs. The model uses parameters of tumor growth to forecast treatment effectiveness, potentially leading to new strategies for predicting tumor response.
Researchers found that leftover cancer cell debris can stimulate tumor growth, but resolvins can block this response. The study suggests a new approach to enhance cancer therapy and prevent recurrence.
Researchers discovered that chemotherapy can stimulate tumor growth by inducing an inflammatory reaction in the body. Resolvins, a family of molecules, have been found to suppress this response, suggesting new ways to enhance cancer therapy effectiveness.
Research reveals that bone marrow-derived cells contribute to lung cancer progression by stimulating the production of specific neutrophils. These neutrophils exhibit increased expression of genes associated with tumor-promoting processes, leading to worse patient survival in a small study.
Researchers at Beth Israel Deaconess Medical Center have shown that chemotherapy-generated debris can stimulate tumor growth, but resolvins can suppress this effect. The findings offer a novel treatment approach to prevent cancer recurrence.
Researchers at NIST developed a novel method for measuring tumor growth using disposable diapers as 'phantoms' with water. Volumetric measurement proved more accurate than the traditional RECIST approach, potentially enabling earlier and more effective cancer screenings.
Researchers at RUDN University have synthesized new compounds with potential antitumor and antiviral activity from isoxazoles. The compounds, which include a central five-membered heterocycle, exhibit varying properties depending on the arrangement of substituents.
A study published in Cancer Research found that inhibiting two metabolic enzymes, NADK and KHK, reduced the growth of KRAS-mutant colorectal cancer cells in mice by approximately 50%. The research also identified new genes that, when inactivated, increased tumor growth in KRAS-mutant cancers.
Researchers at the University of Southern Denmark have discovered a new strategy to overcome resistance in lung cancer, which often leads to treatment failure. By combining an EGFR tyrosine kinase inhibitor with an AKT inhibitor, tumor growth can be arrested, potentially improving patient survival.
Epithelial tumours can grow independently of their microenvironment, driven by a feedback amplification loop that activates the JNK stress signalling pathway. This internal mechanism triggers proliferation in non-proliferating cells, leading to chromosomal instability and loss of epithelial polarity.