Articles tagged with Tumor Growth
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Researchers have identified LP-284 as a novel acylfulvene compound with anti-tumor activity against non-Hodgkin's lymphoma. The compound exerts nanomolar potency in 15 NHL cell lines and prolongs survival of mantle cell lymphoma xenograft mice, making it a potential therapeutic option for patients with HR or TC-NER deficiency.
A keto diet may help reduce body weight and slow tumor growth in cancer patients. However, research found that this diet can cause early-onset cachexia, a lethal wasting disease, in mice with pancreatic and colorectal cancer. Pairing keto with corticosteroids prevented cachexia in mice, allowing them to live longer.
Researchers achieve 3D printing within mini-organs growing in hydrogels, allowing for precise control over shape, activity, and tissue growth. This breakthrough enables the creation of realistic models of organs and disease, with potential applications in cancer research and treatment.
Researchers studied breast cancer cells that spread through the body and found a key mechanism driving their growth. The study reveals how cancer cells employ 'plasticity' to adopt properties promoting metastatic growth.
Cancer cells in brain tumors produce lipids at higher rates than surrounding healthy tissue, offering clues for treatment strategies. The study provides insights into the unique biochemical processes fueling cancer growth in the brain.
Researchers found that MALAT1 inhibition decreased BRAF RNA and protein levels, while increasing correlation with MAPK-associated genes. MALAT1-ASO treatment also reduced melanoma cell growth and tumor size in xenograft models.
A recent study led by UCLA researchers has identified a potential new strategy for treating glioblastoma by targeting a specific metabolic process in cancer cells. The study found that disrupting this process could make glioblastoma cells more vulnerable to cell death, offering hope for new treatment options.
Researchers found that distant cancers alter liver function by inducing fat accumulation and inflammation in liver cells. The process involves secretion of extracellular vesicles containing fatty acids, which reprogram the liver to resemble fatty liver disease.
Researchers have discovered that HER3 plays a crucial role in promoting cell survival in metastatic colorectal and pancreatic cancer. The surrounding liver microenvironment activates HER3, making it an emerging therapeutic target for these types of cancer.
Researchers have identified three subtypes of ovarian high-grade serous carcinoma (HGSC) based on genomic changes, which may help tailor therapies. The study's findings could improve treatment outcomes for patients with this aggressive subtype.
Researchers at Michigan Medicine have discovered a new nutrient source that pancreatic cancer cells use to grow in the absence of glucose. Uridine is found in the tumor microenvironment and its exact source remains unknown. Blocking uridine metabolism may lead to new treatment options for pancreatic cancer.
Glioblastoma steals cognitive faculties as it spreads, but its insidious ability to infiltrate neighboring networks may be its undoing. Researchers found neural activity can restructure connections in surrounding tissue, causing decline. The drug gabapentin blocks this growth-causing activity in mice with glioblastoma.
Scientists have identified a specific gene mutation that triggers an inflammatory cascade, driving the development of treatment-resistant cancers. The study reveals a molecular circuitry by which mutations in the STK11 gene cause inflammation to spiral out of control.
Brain cancer cells use mitochondria from healthy astrocytes to boost energy production and amplify cancer stem cells, making glioblastoma more deadly and difficult to treat. Researchers discovered that acquiring mitochondria is a common process in glioblastoma, with implications for developing new treatments.
Researchers at Baylor College of Medicine found that silencing gene p16 can drive colorectal cancer progression in animal models. A combined treatment strategy involving two drugs improved survival rates in tumor-bearing mice, offering new possibilities for targeted therapies.
A new study has provided insight into the mysterious evolution of DNA rings in tumors, revealing that nearly one-third of all tumors have these genetic structures. The researchers used a technology to trace the path of DNA ring development in neuroblastoma cells, finding that large rings contain cancer genes spurring cell growth.
Researchers developed a method to predict DCIS progression to invasive breast cancer using mice with human DCIS cells. The study found molecular similarities between humans and mice, including the presence of HER2 protein increasing breast cancer risk.
Researchers have highlighted the importance of stromal vitamin A pathway in regulating IL-6 expression in colorectal cancer-associated fibroblasts. The study found that disrupting retinol-mediated IL-6 expression could be a potential approach to target CAFs during CRC treatment.
A new study has shown that FAPI PET imaging is superior to standard FDG PET in evaluating multiple types of cancer. A newly designed FAP-targeted treatment also suppressed tumor growth in several common cancers, suggesting a powerful tool for the field of clinical nuclear medicine.
Researchers have identified ATAD3A as a molecular determinant that favors the development of head and neck cancer. The protein is involved in various cellular processes, including energy metabolism and apoptosis. Targeting ATAD3A could offer a novel approach to developing effective anti-cancer therapeutics.
The guideline provides guidance on definitive local therapy options for non-small cell lung cancer with limited extracranial metastases. It emphasizes the need for a patient-centered, multidisciplinary approach to treatment decisions.
A novel cell signaling pathway has been identified that could be targeted to treat aggressive pancreatic cancers. The High Mobility Group A1 (HMGA1) protein functions as a 'molecular switch' that activates genes required for tumor growth and invasion. Silencing HMGA1 or disrupting FGF19 signals in mouse models resulted in decreased tum...
A team of researchers has discovered that a naturally produced chemical in the body helps glioblastoma cells go unrecognized by the immune system. The findings could lead to the development of new and more effective treatments for this aggressive brain cancer.
Acute myeloid leukemia is a cancer that affects blood cells and can lead to infection, anemia, and easy bleeding. The Georgia Cancer Center has received a $2.3 million grant to study how cancer cells resist treatment and propose new options to improve patient survival.
Scientists discovered that deleting a protein called sphingosine kinase 2 (SphK2) reprograms the tumor microenvironment, decreasing S1P levels and increasing p53 tumor suppressor gene accumulation. This creates an inhospitable environment for aggressive breast tumors.
Cancer-associated fibroblasts (CAFs) are a type of cell that plays a crucial role in the tumor microenvironment. The authors suggest that understanding CAFs is essential for developing effective cancer therapies. Research targeting CAFs has shown promise, but challenges remain due to their complex nature.
Researchers found that neutrophils can be pro- or anti-tumour depending on their surface markers, and those fighting tumours share cytotoxic power with neutrophils in bacterial infections. Blocking these anti-tumour neutrophils eliminates treatment benefits.
Researchers at Georgia Institute of Technology developed a synthetic tumor model to understand the impact of microenvironment on targeted therapies for Activated B Cell-like Diffuse Large B cell lymphoma. The model showed promise in demonstrating how combining therapeutics can overcome tumor resistance to inhibitors.
Researchers developed a 3D cell culture system to test fibroblast inhibitors with anti-cancer drugs. Combining nintedanib with cisplatin increased the latter's efficacy in suppressing cancer growth and invasion. The study provides a promising tool for preclinical drug testing.
Researchers at University of California San Diego School of Medicine found a significant reduction in disease growth when combining immunotherapy with chemotherapy in patients with advanced endometrial cancer. The study resulted in a 70% risk reduction in the deficient mismatch repair group.
Scientists have identified a new molecule that could help distinguish and treat patients with a specific subgroup of medulloblastoma, the most common malignant brain tumor in children. The discovery points to potential targeted therapies using a drug or drugs to block the molecule's activity.
Researchers at the Salk Institute discovered that combining two therapeutic drugs, entinostat and trametinib, can significantly reduce tumor volume and number in mice with LKB1-mutated non-small cell lung cancer. The findings could lead to clinical trials in humans and potentially transform treatment for cancers beyond NSCLC.
Researchers from Swansea University and Université Grenoble Alpes demonstrate the effectiveness of selenium nanoparticles in killing ovarian cancer cell models. The study reveals a novel biological mechanism underlying the anti-cancer effect, involving histone methylatransferases and epigenetic processes.
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.
Two compounds, A5 and C1, have shown promising results in inhibiting the growth of glioblastoma cells, a type of aggressive brain cancer. Further research is needed to confirm their effectiveness on normal nerve cells and to move towards clinical trials.
Researchers discovered that quiescent ovarian cancer cells secrete follistatin, which induces resistance in neighboring cells and worsens survival rates. Targeting this protein may improve chemotherapy response and boost survival in patients with aggressive ovarian cancer.
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 explore cellular senescence's complex relationship with growth stimulation and cell cycle arrest, revealing potential anti-aging drug targets. Understanding these mechanisms is crucial for developing new treatments for age-related diseases.
Researchers discovered a new personalized immunotherapy combination that treats aggressive forms of advanced prostate cancer. By blocking PD-1-expressing macrophages and Wnt/β-catenin pathway activation, the therapy significantly improves response rates in PTEN-deficient cancers.
Researchers at VCU Massey Cancer Center found that simultaneous activation of Prdm16 and Smad4 proteins slows down pancreatic cancer progression. The study suggests a novel therapeutic approach to tackle this deadly disease.
Researchers at Indiana University School of Medicine have identified a new type of cell called the vasculogenic fibroblast, which can help create new blood vessels for treatment. This discovery could lead to improved treatments for ischemic diseases such as diabetic wounds.
A recent study suggests that routine evaluation of HER2 expression in ductal carcinoma in situ (DCIS) is crucial to avoid under or overtreatment. The research found a significant association between HER2 overexpression and a higher risk of recurrence, as well as improved radiotherapy outcomes.
Researchers at NUS Cancer Science Institute discover FAM3C in tumor-derived extracellular vesicles promotes distant lung tumour colonization. FAM3C enhances cellular transformation and stimulates metastasis potential, offering new therapeutic strategy targets.
Researchers at Scripps Research found that a 'poisoned' form of the DNA methyltransferase 3B protein can promote cancer growth by allowing cancer-causing genes to turn on. A new drug candidate, DBIC, was developed to revert the protein to its normal form, preventing tumor formation in mice with colon cancer.
Researchers have developed a novel prognostic index to predict survival outcomes in gastric cancer patients. The inflammation-combined prognostic index (ICPI) combines three biomarkers - lymphocyte-to-monocyte ratio, neutrophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio - to provide a personalized prognosis for each patient.
A deeper understanding of tumor cell responses to treatment is crucial for improving therapy effectiveness. Researchers at the Max Planck Institute discovered that physical interactions between cells can allow treatment-resistant cells to survive despite growing slower than non-resistant cells. This balance between mechanical cell-cell...
Researchers at Uppsala University developed a prognostic method using a combination of immune cells to provide clearer disease prognoses and predict which patients will respond best to immunotherapy. The method was shown to be associated with patient fate in several types of cancer.
Researchers investigated the effects of everolimus on the STAT3/HIF-1α/VEGF pathway in TP53 mutant cell lines and xenograft models. Everolimus treatment significantly inhibited cell growth and reduced tumor angiogenesis and lymphangiogenesis.
Researchers found that primary cancer tumors have a sluggish conversion of nutrients to usable cellular energy, conserving energy for growth and metastasis. The discovery has vast implications for anti-cancer strategies, directing attention to slow energy metabolism.
Pusan National University researchers have identified a novel gene, SURF4, that regulates cell death and differentiation in acute myeloid leukemia (AML). The study found that suppressing SURF4 expression increases cell differentiation, cell death, and accumulation of ROS, leading to arrested tumor growth in mice.
A research team from HKUMed identified chronic Type I Interferon signalling as a driver of CD8+ T cell exhaustion and therapy resistance. The study highlights the harmful effect of IFN-I on tumour-killing CD8+ T cells, providing new insights into immunotherapy improvement.
Using artificial human skin, researchers have successfully blocked invasive growth in a skin cancer model by targeting the TGF beta pathway. The study aims to develop new skin cancer therapies using existing drugs that can block these signalling pathways.
Researchers found that certain gene signaling pathways, such as interferon γ and beta-catenin, can lead to tumor hyperprogression after immunotherapy. Targeting these pathways may prevent hyperprogression in preclinical models.
Researchers found that regorafenib, a dual PDGFR α/β inhibitor, modifies the cancer microenvironment and enhances the efficacy of anti-PD-1 immunotherapy in advanced gastric cancers. This combination therapy boosts tumor infiltrating immune cells and reduces tumor fibroblasts.
Scientists at Cold Spring Harbor Laboratory have found a way to reprogram cells causing Ewing sarcoma to behave like normal connective tissue cells. By blocking the protein ETV6, cancer cells can be forced to take on a new identity and grow less aggressively.
A study of 184 grade I and II meningiomas found associations between specific tumor mutations and increased or decreased recurrence rates. Mutations in ATM and CREBBP were linked to accelerated recurrence, while POLE mutations showed protective effects, highlighting potential targets for intervention.
A computational model predicts brain tumour growth using MRI data, providing valuable insights for clinicians. The study uses anonymous patient data to develop a predictive model for glioblastoma multiforme (GBM) growth, which can be used to inform treatment decisions.
Researchers found that inhibiting HSF1 signaling reduces hepatoblastoma growth and induces apoptosis, suggesting it as a viable pharmacologic target. The study also identified HSF1's role in tumor aggressiveness and its potential association with mortality.
Researchers found that EWS::FLI1 induces Slit2 expression, which activates Robo receptors and enhances Ewing sarcoma growth. Silencing Slit2 strongly inhibited Ewing sarcoma cell growth, providing an opportunity for targeted therapy.
A new method utilizes an unnatural sugar to anchor cytokines to T cells, enhancing their functions without systemic side-effects. The approach has shown promise in stimulating the host immune system against tumor cells and inhibiting tumor growth in mice with melanoma.