Articles tagged with Breast Cancer Cells
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Recent study by Okayama University researchers reveals three photoinitiators cause faster increase in breast tumor growth in mice, with tamoxifen pretreatment reducing toxicity. The findings suggest photoinitiators could act as hormonal disruptions, raising concerns for patients and healthy individuals.
Researchers at Duke University Medical Center identified a mechanism where breast cancer cells use cholesterol to develop tolerance to stress, allowing them to resist ferroptosis and proliferate. This finding highlights the importance of lowering cholesterol in preventing cancer progression and offers new approaches for treatment.
Researchers identified DSS1 as a critical protein in breast cancer progression and found that depleting it makes cancer cells more responsive to lower doses of anti-cancer drugs. This technique may reduce drug-induced side effects in breast cancer patients, providing a safer treatment option.
Researchers have discovered how PARP inhibitors selectively kill cancer cells carrying BRCA1 and BRCA2 mutations. The findings provide a mechanistic explanation for the selectivity of PARP inhibitors toward BRCA-mutant cells.
Researchers have discovered that increased levels of protein Tumour Protein D54 can increase and decrease the movement of cancer cells, suggesting its potential role in tumour spread. The study found that reducing or increasing this protein's expression affects cell migration, with higher levels leading to more metastasis.
Researchers at the University of Illinois have developed a new compound called ErSO that kills 95-100% of cancer cells in mouse models of human estrogen-receptor-positive breast cancers and their metastases. The compound targets the anticipatory Unfolded Protein Response pathway, which is already active in many breast cancer cells.
Luay Nakhleh's team will use single-cell DNA data from the University of Texas MD Anderson Cancer Center to identify mutations at the root of the disease and how they evolve in tumors. By building open-source models and tools, they aim to refine cancer treatments and predict patient outcomes.
The study found that cancer cells become less stiff after exposure to chemotherapy drugs, but the rate of stiffness change decreases under hypoxic conditions. Alteration in cytoskeletal structure influences overall cell functions, including signaling, communication, adhesion, transport, and tumor metastasis.
Researchers from Osaka University found that protein phosphatase 1 binds to RIF1 at broken DNA ends, blocking proteins that create single-stranded DNA tails, and promoting the non-homologous end joining repair pathway. This novel mechanism helps protect double-strand breaks from developing a tail, which is what Shieldin binds to.
Researchers from Nagoya University have successfully measured the shape distributions of cell-derived nanoparticles, or extracellular vesicles, in body fluids. This study may help identify types of cancer with a painless and non-invasive method.
A new study introduces K2Taxonomer, a software tool that analyzes high-throughput data to identify novel cell types within tumors and their microenvironments. The analysis of breast tumor-infiltrating lymphocytes revealed a transcriptional signature associated with better survival rates in cancer patients.
Researchers discovered RNA-binding proteins, particularly YTHDF2, as potential targets for treating triple-negative breast cancer. Inhibiting these proteins may provide a new approach to halting tumor growth and reduce adverse side effects.
Researchers at University of Arizona Health Sciences found that cancer cells become more aggressive when exposed to tissue stiffening, leading to changes that persist over time. The 'mechanical conditioning' score can quantify these cellular changes and predict patients at high risk for bone metastasis.
Researchers at McMaster University have developed a promising new cancer immunotherapy that uses genetically engineered natural killer cells to find and destroy malignant tumors. The modified cells can differentiate between cancer cells and healthy cells, bringing new promise to this branch of immunotherapy.
New research suggests that treating cancer patients with anti-CTLA4 therapies before anti-PD1 treatment can improve overall survival. High numbers of T follicular regulatory (Tfr) cells in tumors may be to blame for the lack of response to anti-PD1 therapies.
Researchers from Massachusetts General Hospital have discovered a biological mechanism that transforms carcinogen-exposed cells into immunogenic cells, which can be harnessed therapeutically to fight treatment-resistant cancers. The mechanism involves the release of small proteins known as chemokines that recruit antitumor immune cells.
A recent study found that a small percentage of cells in aggressive tumors can enable metastasis by recruiting surrounding cells. This discovery could lead to new approaches in preventing malignant progression of breast cancer, particularly in triple-negative types.
Researchers at Clemson University developed a bifunctional protein that links natural killer cells to breast cancer tumor cells, triggering the killing of cancer cells. The approach has potential as a new treatment option for triple-negative breast cancer, which is often lethal due to its high heterogeneity and lack of efficient treatm...
Researchers at Kyoto University have uncovered how XRCC1 protein disarms PARP traps, preventing DNA damage accumulation. This discovery may lead to improved cancer treatments using PARP inhibitors.
Researchers identified neutrophil elastase as a major anti-cancer protein that activates cell death pathways specifically in cancer cells. This discovery may lead to the development of first-in-class medicines that target cancer cells while sparing healthy tissues.
Researchers discovered that a byproduct of cholesterol metabolism, 27-hydroxycholesterol, induces the production of extracellular vesicles that promote breast tumor growth and metastasis. The study found that these vesicles carry signaling molecules that spur estrogen-responsive cancer cells to proliferate and grow.
Researchers have discovered that natural killer cells and interferon gamma play a crucial role in preventing cancer metastases. Targeted therapies, such as immunotherapy and interferon gamma therapy, show promise in maintaining dormant cancer cells in a state of hibernation.
Researchers at UVA Cancer Center have unveiled new insights into how hormones known as androgens act on cells, which could lead to improved treatments for prostate, ovarian, and breast cancers. The study found that a complex signaling system regulates androgen receptor activity, using an enzyme called Parp7.
Research found that treatments with 6-mercaptopurine and/or 5-azacitidine do not reverse epithelial-to-mesenchymal transition, but instead sensitize cancer cells to chemotherapeutic drugs. This approach has potential for inhibiting highly resistant triple-negative breast cancer cells.
Scientists have discovered that poor DNA compaction in mammary glands can lead to increased accessibility of retrotransposons, triggering an immune response and disrupting milk secretion. The findings highlight the importance of proper chromatin condensation for tissue development and function.
Breast cancer researchers followed the progression of cancer in an animal model and found a path that transforms slow-growing ER+/HER2+ cancer into fast-growing ER-/HER2+ cancer. The study suggests different treatments may be needed for each subtype, depending on the path the cells follow.
High levels of RANK protein trigger senescence in early stages of tumors, delaying their onset, but promote stem cell accumulation and tumour growth in advanced stages. This discovery sheds light on the complex mechanisms underlying breast cancer development and progression.
The study created a comprehensive catalog of healthy breast tissue cells, enabling scientists to pinpoint the origin of abnormal changes. By tracking gene activity in over 15,000 cells, the team redefined healthy breast tissue and identified subpopulations with different responses to therapies.
Researchers created an RNA atlas detailing the diverse cells in healthy and cancerous breast tissue, revealing changes that occur during cancer development. The study provides a high-resolution view of breast tissue cell types and will be an important resource for breast cancer research.
Scientists at Sanford Burnham Prebys Medical Discovery Institute identified lipid kinases as essential for balancing cellular metabolism and promoting overall health. The findings support targeting these proteins as a promising approach to treating diseases like cancer.
A team of Oregon State University scientists discovered a new class of anti-cancer compounds, SMAhRTs, that activate AhR signaling and kill liver and breast cancer cells. These compounds provide exciting new leads for drug development, targeting the AhR pathway to induce anti-cancer effects.
The BreastPathQ Grand Challenge produced encouraging results, indicating a path toward integrating artificial intelligence to streamline clinical assessment of breast cancer. Thirty-nine teams from 12 countries developed automated methods for analyzing microscopy images of breast tissue and assessing pathology.
Researchers cultivated tumor microenvironments using metastatic triple-negative breast cancer cells and studied the genetic information of entire systems. They found that cellular communication in the microenvironment drives physiological changes in tumor behavior, including growth and movement.
Researchers found that sanguinarine, a natural compound, reduces cell viability and growth in triple-negative breast cancer cells. The treatment activated different genes in cells from African American ancestry, suggesting potential therapeutic benefits for this population.
Two studies found that the bone microenvironment reduces ER expression in breast cancer cells, leading to resistance to endocrine therapy. The bone microenvironment also triggers reprogramming of cancer cells, promoting their ability to metastasize to other tissues and evade treatment.
Researchers at Linköping University and Medical University of Graz developed an ion pump that can deliver chemotherapy agents like gemcitabine directly into the brain with high precision. This method may provide a more effective treatment for glioblastoma, a type of brain tumor.
Researchers found that breast cancer cells trigger uncontrolled inflammation and remodel tissue, making the cancer more aggressive. The study suggests targeting inflammatory pathways could improve treatment outcomes for pregnant women with breast cancer.
A recent study by Vanderbilt researchers reveals that non-cancer cells in a tumor, primarily immune cells called macrophages, have the highest glucose uptake, upending traditional models of cancer metabolism. This finding could lead to new therapies and imaging strategies.
Researchers found a novel genomic signature associated with increased risk of early death from lung cancer. Patients with high expression of these genes have indicators of immune system activity, but also suppressed T cells, which can impact treatment effectiveness.
A study from the University of Notre Dame found that a specific protein called SGK1 promotes survival and increases the likelihood of cancer spreading by blocking cell death. This discovery may have implications for understanding how cancer cells adapt to new environments, such as the brain, where breast cancer can metastasize.
A novel method for single-cell DNA sequencing has enabled faster and deeper study of chromosome evolution in triple-negative breast cancers. The technique revealed that these cancers undergo continued genetic copy number changes after an initial burst of chromosomal instability, which may explain why treatments are not always effective.
Researchers have identified YAP as a key regulator in the development and spread of basal-like breast cancer. Inhibiting YAP activity with medication can significantly reduce tumour volume, offering new hope for patients' survival.
Researchers have developed a new CAR T cell engineering technique that allows for the targeting of solid tumors without harming healthy cells. The technique uses ultrasensitive identification of HER2 protein on tumor cells and has shown promise in treating ovarian cancer.
A recent study published in Bioelectricity found that electromagnetic fields can hinder the spread of breast cancer cells, slowing their metabolism and potentially stopping them from moving. Researchers believe this approach may be useful in fighting highly metastatic cancers.
Researchers have made significant progress in understanding how cancer cells communicate to spread, a key step in metastasis. By targeting the VEGF-C protein, they aim to slow down or stop metastatic growth, providing new hope for treating fatal diseases.
Researchers discovered that metastatic cancer cells use adhesion and contractility to move away from stiffer tissue, defying the typical durotaxis process. By modulating cell contractility, they can change their ability to migrate in response to environmental stiffness.
Scientists have isolated a peptide, EnnA, from a fungus in Morocco that directly inhibits HSP90, a powerful cell protector hijacked by cancer. Early evidence shows EnnA induces immune cells to attack cancer cells, promoting immunogenic cell death and potentially offering a new treatment for triple negative breast cancer.
The study found that breast cancer cells switch between two distinct states: mesenchymal and amoeboidal, which are influenced by tissue fiber alignment. The level of fiber alignment is crucial in determining the progression of breast cancers. Understanding this mechanism can help predict and treat metastatic disease.
The E-Morph test uses artificial intelligence to identify substances that can have oestrogen-like effects on breast cells. This method has the potential to replace animal experiments currently required for detecting hormone-like effects.
Researchers have identified a novel mechanism of resistance to immunotherapy targeting HER2, where cancer cells adopt a strategy to evade clearance by redirected lymphocytes. The study found that disrupting interferon-gamma signaling confers resistance to these immunotherapies, promoting disease progression.
Researchers have discovered a unique dependence of cancer cells on the protein KIF18A, which could lead to less harmful drug treatments for some cancers. International collaboration and data-sharing played a key role in this breakthrough discovery.
Researchers have identified a previously unknown dual function of polymerase theta (pol theta) in DNA repair, which could lead to the development of new therapeutic options for breast and ovarian cancers. The finding shows pol theta can both extend DNA and trim it, making it a potential target for treatment development.
UC researchers discovered that stopping autophagy in cancer cells can help treat HER2-positive breast cancer. By blocking this process, cancer cells were unable to develop and grow, and the HER2 protein was altered in a way that prevented its role in cancer development.
Researchers studied how modern immunotherapeutic anti-cancer drugs interact with the immune system, finding that tiny molecular motions are key to their effectiveness. The study, published in Cancers, reveals how these drugs bind to specific receptors on killer cells without activating them.
Researchers discovered that aneuploid cancer cells demonstrate heightened sensitivity to damage to the mitotic checkpoint, making them more susceptible to treatment. The study's findings suggest that using aneuploidy as a biological marker could help identify patients who will respond better to certain drugs.
Researchers discovered that cancer cells with an abnormal number of chromosomes (aneuploidy) are more sensitive to inhibition of the mitotic checkpoint, a cellular mechanism that ensures proper chromosome separation during cell division. This finding has important implications for personalized cancer medicine and drug discovery.
A TGen-led study has developed a test to detect infinitesimally small breast cancer biomarkers in blood samples, improving detection accuracy. The test uses a highly specific protein signature to identify the earliest stages of breast cancer with no false positives.
Researchers at UT Southwestern Medical Center have discovered that removing a key gene called Cbl-b can revitalize exhausted CD8+ T cells to combat malignant tumors. This breakthrough could offer a new approach to harnessing the body's immune system to fight cancers.
Cancer cells can thrive in hostile environments through metabolic adaptation known as the Warburg Effect. Moffitt researchers found that activation of transcription factor KLF4 allows cells to select for this phenotype, enabling them to survive and thrive in poor conditions.
Researchers have identified a molecular crowbar that enables cancer cells to invade surrounding tissues. Hepsin, normally a glue-like protein, becomes a destructive enzyme when activated by Ras, leading to the breakdown of the basement membrane and cancer cell invasion.