Articles tagged with Breast Cancer Cells
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Researchers found that glioblastoma cells in clusters are less deadly than those that disperse from these clusters. The dispersed cells are more plastic and resistant to therapy, making them a major contributor to treatment resistance and poor patient outcomes.
Researchers discovered that PCAI-27 activates two major signaling pathways, MAPK and PI3K/AKT, leading to increased oxidative stress and apoptosis in AI-resistant breast cancer cells. The compound also disrupts cytoskeletal structure, making cancer cells more vulnerable.
Researchers developed an AI tool called AAnet to characterize cancer cell diversity, identifying five distinct cell groups with different gene expression profiles. This could lead to more targeted therapies and improved patient outcomes.
The UNC Lineberger Comprehensive Cancer Center has developed an adaptive clinical trial for metastatic breast cancer, leveraging $28 million in funding from the Advanced Research Projects Agency for Health (ARPA-H). The study aims to adapt treatment plans in near real-time using tumor biopsies, blood samples, and biomarkers.
Researchers have found that soft tumour tissue enables cancer cells to hide from the immune system, potentially speeding up disease progression. This discovery may help doctors identify patients unlikely to benefit from immunotherapy, guiding them towards alternative treatments.
Researchers at the University of Turku have developed a new fluorescent probe, Illusia, to visualize signaling dynamics in moving cancer cells. This tool has led to a new therapeutic possibility for limiting breast cancer spread, with potential implications beyond breast cancer.
Researchers at the Weizmann Institute of Science discovered that dormant breast cancer cells accumulate DNA mutations and experience widespread cellular damage, leading to dormancy. Increasing OVOL protein expression can halt cancer cell lifecycle and induce dormancy, but also enables them to reawaken more aggressively.
This study investigates TNIP1's role in regulating cell proliferation and apoptosis in breast cancer. TNIP1 knockdown was found to induce growth arrest and activate the NF-κB pathway, leading to increased apoptosis in breast cancer cells. The findings highlight TNIP1 as a crucial marker for breast cancer therapies.
Researchers have discovered a new mechanism of how anticancer drugs attack and destroy BRCA mutant cancer cells, including drug-resistant breast cancer cells. The study found that small DNA nicks can expand into large single-stranded DNA gaps, leading to cell death.
Researchers at Sanford Burnham Prebys have discovered a way to target the energy supply chain of cancer cells. By understanding how enzymes like ubiquitous mitochondrial creatine kinase (uMtCK) function, scientists can design new treatments that slow or stop tumor growth.
Researchers at University of Melbourne and Pfizer discover new insights into a dual-target drug that may supercharge cancer-fighting immune cells, potentially leading to improved outcomes for breast cancer patients. The study found that this approach can enhance anti-tumor immunity by intratumoral CD8+ T cells.
A team of researchers at Queen Mary University of London discovered that disrupting a single amino acid in the vimentin protein makes breast cancer cells behave like stem cells. This mutation promotes tumour growth and increases cancer stemness in an oestrogen-independent manner.
A new study published in Nature Medicine shows a promising approach to preventing metastases in breast cancer patients. Researchers found that administering digoxin reduced circulating tumour cell clusters by an average of 2.2 cells, significantly decreasing the risk of metastasis.
Early detection of breast cancer can lead to less intensive treatments, saving the Canadian healthcare system $459.6M over women's lifetimes and 3,499 breast cancer deaths. Screening mammograms and diagnostics costs are easily offset by earlier stage treatment.
Breast cancer cells can live for years in bone marrow after remission, leading to disease recurrence in approximately 40% of patients. A study found that mesenchymal stem cells support the cancer cells by donating essential proteins, making them more aggressive and drug-resistant.
A collaborative study led by Dr. Julie St-Pierre at the University of Ottawa found that promoting mitochondrial elongation in cancer cells hobbles their ability to metastasize. The research team identified a common signature that could help determine which pathways lead to decreased metastasis.
Researchers found a subset of macrophage cells close to breast cancer cells, which may provide a new biological target for immunotherapies. This discovery could lead to the development of biologic therapies to change the organization of neighborhoods around cancer cells.
A new study by UCLA investigators found that Manuka honey contains compounds that can help reduce tumor growth in preclinical models. The research suggests that Manuka honey could potentially be developed into a natural supplement or standalone treatment for ER-positive breast cancer, which accounts for most breast cancer cases.
Researchers developed a nanobody that targets V-ATPase c subunit and inhibits tumor cell invasion and metastasis. The nanobody was tested on 4T1-12B mouse breast cancer cells implanted in mice, where it showed effectiveness in preventing lung metastasis.
Researchers discovered that sodium channels allow cancer cells to grow and spread by increasing energy production and producing lactic acid, which breaks down the extracellular matrix. Blocking these channels may be an effective way to slow cancer growth and prevent metastasis in breast cancer patients.
A novel inhibitor HVH-2930 targeting heat shock protein 90 (HSP90) demonstrates efficacy against drug-resistant breast cancer cells. It selectively downregulates HER2 signaling, crucial for breast cancer progression, without triggering the heat shock response.
Finnish researchers found that blocking the DUSP6 protein can significantly improve treatment outcomes in experimental models by preventing dormant breast cancer cells from waking up. This discovery provides new insights into breast cancer recurrence and offers a potential basis for effective combination therapy.
A study has shown that a potassium ion channel located in mitochondria rewires metabolism in breast cancer cells, promoting tumor growth. The channel, BKCa, is linked to the Warburg effect, a metabolic hallmark of cancer, by causing increased lactate secretion and hydrogen peroxide levels.
Weo electrolyzed water (WEW) has been shown to attenuate cellular senescence in both normal fibroblasts and breast cancer cells. The study found that WEW modulated markers of cellular senescence, inflammation, and stress response genes in a cell type-dependent manner.
Researchers have discovered how softer tumor environments prime cancer cells to better survive metastasis. The study found that soft environments alter the cancer cells' preference for 'fuel', equipping them with a more resilient energy pathway.
A study reveals how mechanical constraints in glioblastoma tumors influence the emergence and spatial patterning of cancer stem cells. Piezo1 plays a crucial role in regulating mechanosensing and cell phenotypic switch.
Researchers at the University of Cincinnati Cancer Center have identified a new protein called p47 that helps prevent breast cancer metastasis. The study found that lower p47 expression was correlated with higher breast cancer metastasis, and that increasing p47 function could potentially lead to new therapies.
A new method for phase-modulated stimulated Raman scattering tomography enables rapid, label-free 3D chemical imaging of live cells and tissues. This technique improves lateral resolution and imaging depth compared to conventional methods.
A groundbreaking study identifies FAM3C as a key regulator of breast cancer progression within the tumor microenvironment. The overexpression of FAM3C promotes breast cancer cell survival and metastasis, while its depletion inhibits tumor growth in genetically engineered mouse models.
A study by the University of Sheffield found that breast cancer cells take advantage of nutrients in the extracellular matrix when faced with nutrient starvation. The cells use an ingestion process called macropinocytosis to consume the matrix, breaking it down into energy-releasing substrates.
Breast cancer cells survive by consuming the extracellular matrix when nutrients are scarce. The process involves macropinocytosis and metabolic conversion of key amino acids to energy-releasing substrates. This mechanism could represent a novel therapeutic target.
Researchers at Stanford University discovered that breast cancer cells use a collective, physical mechanism to break through the basement membrane barrier. In a 3D hydrogel model, cancer cells trapped within duct-like structures swelled and stretched, weakening the basement membrane and allowing escape.
Researchers have found that simultaneously inhibiting two proteins, LOXL2 and BRD4, can help slow the growth of triple-negative breast cancer cells. This 'double strike' strategy shows promise in improving the prognosis of this aggressive disease, which is resistant to existing treatments.
Researchers found that FAAH inhibition reduced breast cancer growth in immunodeficient mice and induced apoptosis of breast cancer cells. The combination of FAAH inhibitors and endocannabinoids was the most effective treatment approach.
Researchers discovered that a small subpopulation of AIB1-expressing cells in breast cancer enables invasion and metastasis. The study suggests that these subpopulations play a crucial role in tumor growth and spreading to distant sites.
Researchers at Mount Sinai discovered a new family of locally secreted molecules called 'mammokines' that play a crucial role in controlling mammary gland fat abundance. These findings have significant implications for breast health, lactation-related disorders, and metabolic syndromes.
A study by Cold Spring Harbor Laboratory researchers found that breast cancer cells trick the immune system using a molecule called MHC-II, allowing them to spread faster and evade treatment. Targeting this molecule may lead to new therapeutics and improve patient outcomes.
Researchers at NUS developed a new photodynamic therapy that selectively kills breast cancer cells without damaging surrounding tissues. The treatment uses a biocompatible silicone implant loaded with nanoparticles activated by near-infrared light, reducing the risk of toxicity and improving tumour control.
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.
Increased expression of Musashi 1 on breast cancer cells has significant implications for understanding dormancy and survival in bone marrow. Msi 1 knockdown led to a reduction in cancer stem cells with undetectable PD-L1, suggesting a potential therapeutic target.
Researchers found significant decreases in the levels of KRAS, RHOA, RAC1, and CDC42 after PCAI treatment, implicating their role in cancer progression and metastasis. These findings support the potential of PCAIs as potent agents for developing new anticancer therapeutics.
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 at the Institute of Cancer Research discovered that molecular changes in lung tissue can trigger breast cancer cells to 'reawaken' and form secondary tumors. They found that blocking PDGF-C activity with an existing cancer growth blocker could help prevent this, offering a potential strategy to defuse these 'time bombs'. Th...
Researchers found a protein called Rac1 that triggers milk production in breast cells when lactation stops and the breast returns to its pre-pregnancy state. This process involves cell death and autophagy, but can be reversed upon suckling, providing a fail-safe mechanism for mammalian survival.
Researchers from the University of Cambridge have identified a method to track and kill resistant cancer cells in mice. By tagging different types of breast cancer cells with unique genetic barcodes, they were able to identify which cells are evading chemotherapy and target them specifically with a new treatment approach.
Researchers at Tulane University discovered that breast cancer cells use complex immune-modulatory programs to evade immune clearance, leading to treatment resistance. They identified 16 immune checkpoint genes and found that chemotherapy triggers a program of immune checkpoints that shield cancer cells from different lines of attack.
Researchers have identified a protein that can predict how well breast cancer patients will respond to chemotherapy. Increasing levels of this variant p53 makes breast cancer cells unresponsive to existing therapies, highlighting its potential as a target for enhanced treatments.
Researchers found variable voltages in breast cancer cell membranes, which may indicate an electrical communication network between cells. This discovery could lead to new treatments by disrupting this network, potentially making cancer cells easier to treat.
Researchers discovered that the Memo1 protein binds copper ions, blocking toxic redox reactions that damage or kill cancer cells. The protein's interaction with copper also protects against metastasis formation in breast cancer cells. This finding opens up potential new treatments for cancer.
Researchers at Binghamton University discover that sodium/proton exchanger 1 (NHE1) and SWELL1 proteins regulate cancer cell migration, offering insights into metastasis. The study's findings could have wide implications for slowing down or halting the deadly disease.
Researchers at LSU Health New Orleans have identified a new drug target for triple-negative breast cancer, which lacks estrogen and progesterone receptors. The novel small molecule inhibitor NSC33353 works synergistically with doxorubicin to suppress the growth of TNBC cells.
Researchers discovered a type of triple-negative breast cancer cell that can trigger dormancy, evading therapies and allowing for efficient survival in distant organs. This finding highlights the need for more selective therapeutic strategies targeting both dividing and invasive dormant cells.
A study found that activation of the epidermal growth factor receptor (EGFR)-mediated signaling pathway is involved in lenvatinib resistance in thyroid cancer cells. Inhibition of EGFR by lapatinib therapy in combination with lenvatinib enhanced growth inhibitory effect and inhibited tumor growth more remarkably than monotherapy.
Research using genetic variants as proxies for physical activity levels found a link between higher activity and lower invasive breast cancer risk. A higher overall level of genetically predicted physical activity was associated with a 41% lower risk of invasive breast cancer.
Researchers have developed a new method for 3D cell culture that accurately quantifies how breast cancer cells generate forces to spread within tissue. This study provides more accurate computational data on cellular forces during invasion by breast cancer cells, which may lead to more efficient and personalized drug development.
A study from Lund University found that Caveolin-1 protein levels in surrounding tumour tissue affect breast cancer prognosis. The study suggests that this protein could be used as a marker for precise prognosis and treatment choice.
A recent study published in Cancer Research identified a unique vulnerability in certain high-risk cancers that can be exploited for targeted therapy. Researchers found that cancer cells with alternative lengthening of telomeres (ALT) have a common weakness, leading to resistance to DNA-damaging agents and chemotherapy.
Researchers at Dartmouth Cancer Center developed a new approach for detecting and quantifying tumor heterogeneity in breast cancer. High levels of heterogeneity are linked to poor patient outcomes, while specific proteins regulate its extent. The study aims to utilize this approach in therapeutic decision-making.
A team of researchers developed a clonal barcoding approach to track live cancer cells, enabling the detection and isolation of precise clones responsible for tumor formation and early metastases. This technology has the potential to be applied to other cell-based studies, providing valuable insights into biological processes.
Researchers analyzed germline variants in breast cancer patients to identify their role in metastasis development. The study found that host genetic makeup contributes to metastasis through dysregulation of gene expression, promoting the dispersion of metastatic seeds and establishing a conducive environment for their growth.