Articles tagged with Breast Cancer Cells
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A new study suggests that lower doses of parabens, commonly found in personal care products, may stimulate breast cancer cell growth at concentrations 100 times lower than previously thought. The researchers also found that parabens can interact with other agents to increase breast cancer risk.
Breast cancer researcher Dr Michalak aims to understand how normal and cancerous cells develop in the breast to identify suspicious tumors and develop better treatments. Her study focuses on epigenetic modifiers, which can influence DNA behavior, and may hold clues to preventing tumor spread.
Researchers at The Scripps Research Institute have discovered a way to convert leukemia cells into cancer-killing immune cells using a rare human antibody. The induced NK cells can detect and eliminate cancer cells, offering a potential new therapy for leukemia and possibly other cancers.
A new study reveals how breast cancer cells become desensitized to lapatinib, a common cancer drug, by turning FOXO into an oncogene c-Myc. The researchers hope to develop new tools to fix this adaptation pathway and improve therapy for HER2+ breast cancer.
Researchers at the University of Manchester and Nottingham are developing a gel that mimics human breast tissue, enabling the growth of breast cell models in the lab. This will help understand the influence of the breast matrix on breast cancer progression, potentially leading to new approaches to prevention and treatment.
Researchers found that a tolerant immune system, characterized by high levels of regulatory T cells, increases the risk of certain types of cancer. The study analyzed blood samples from EPIC participants with cancer and controls, revealing a strong link between immunotolerance and increased lung and colon cancer risks.
A team of researchers found specific variations in RNA splicing that may play a role in converting normal breast cells into tumors. The study identifies potential targets for therapies in some forms of breast cancer.
Researchers discovered genetic alterations in healthy breast cells associated with an increased risk of non-familial breast cancer. These findings can be used for future improvements in diagnostics to identify women at high risk before the tumor forms.
Scientists have developed a new toolkit to examine the BRCA1 protein and its associated parts in near-native environments. This allows for direct visualization of macromolecular regulatory complexes in human patient-derived cancer cells, providing valuable insights into the molecular mechanisms underlying breast cancer.
Researchers have identified a molecular pathway that explains how tamoxifen-resistant breast cancer cells develop. The 'feedback loop' involves the HOXB7 protein, which helps activate genes that promote cancer growth. Targeting MYC protein, which is involved in this pathway, may lead to new treatments for tamoxifen-resistant cancers.
Scientists from UC San Francisco capture and study individual metastatic breast cancer cells, finding they express genes similar to mammary stem cells, which could lead to targeted therapies. The research suggests a new approach to understanding how cancer spreads and developing effective treatments.
Researchers discovered a new method to attack cancer cells by targeting the SAS1B protein, which appears on cancer cells but not healthy tissue. This approach could lead to reduced side effects and improved fertility preservation for female patients.
Researchers at Salk Institute discovered a single master gene, Sox10, that controls the formation of mobile cancer factories. High levels of Sox10 in breast cancer tissue enable these stem-like cells to rapidly produce variants that can survive and spread to other tissues.
Researchers discovered that cell programs controlling normal mammary gland stem cells differ from those regulating cancer stem cells, which arise in a distinct layer of tissue. This finding could lead to new cancer treatments by targeting the specific differences between normal and cancer cells.
Researchers have found that combining aspirin with immunotherapy can slow cancer growth and unleash the immune system's full power. By stopping the production of PGE2, a molecule that dampens down the immune response, COX inhibitors like aspirin may lift the protective barrier around tumors, making cancer more susceptible to treatment
Research reveals mutant p53 proteins use epigenetics to drive aggressive cancer growth by targeting key genes and enzymes, such as MLL1 and MOZ. Inhibiting these regulators may lead to combinatorial epigenetic therapies for treating difficult-to-treat cancers.
Researchers have created a technique to build tiny models of human tissues, called organoids, using a process that turns human cells into biological equivalents of LEGO bricks. These mini-tissues can be used to study how structural features affect normal growth or go awry in cancer.
Research suggests that fetal microchimerism can have both cooperative and competitive effects on maternal health, depending on the context. Fetal cells may provide benefits by migrating to damaged tissue and repairing it, while also contributing to inflammatory responses and autoimmunity in some cases.
Researchers at the University of Illinois have developed a new technique to create synthetic tissue environments that can realistically recreate microenvironments found in biology. This allows for more accurate study of tumor growth and behavior, and has potential applications in drug screening and personalized medicine.
Researchers identified a unique doorway in the blood vessel wall that allows breast cancer cells to spread to other parts of the body. The discovery could lead to new treatments and better predict whether breast cancer will spread.
A recent study by Fen Wang and Wallace McKeehan reveals that errors in FGF transmission can activate dormant stem cells, leading to cancer. The research supports the existing theory that cancer is a stem cell disease and holds promise for future cancer therapies.
A new cancer drug candidate, MCB-613, stimulates proteins crucial for tumor growth, causing cell stress and death. It efficiently kills human cancer cells while sparing normal cells, showing promise as a treatment for a range of cancers.
A team of researchers at Washington State University has discovered a novel structural function of the protein ATF5, which guides transcription and provides structure within the centrosome. This finding sheds light on the role of ATF5 in cell division and its potential implications for cancer growth and disease treatment.
Researchers used Liquid STEM to study HER2 dimers in breast cancer cells, finding that a sub-population without these dimers may have self-renewing properties and be resistant to HER2-antibody therapy. This discovery could provide new insights into drug resistance and tumor growth.
A new study by MD Anderson researchers found that protein 14-3-3 sigma opposes and reverses tumor-promoting metabolic programs in breast cancer. The study revealed that 14-3-3 sigma suppresses cancer glycosis, preventing tumors from converting glucose into pyruvate.
A low-methionine diet can increase the vulnerability of triple-negative breast cancer cells to targeted therapies. Researchers found that depriving cancer cells of methionine triggers an increase in a receptor on the cell's surface, making them more sensitive to treatments.
A new study at the University of Wisconsin-Madison has linked a vaccine targeting cancer cells with an altered enzyme that breaks apart RNA, causing cell death. The vaccine targets a carbohydrate called Globo H, which is abundant in many tumors.
Researchers at the University of Warwick have discovered a new cell structure called the mesh, which helps hold together cells and is partly made of protein TACC3 found to change in certain cancers. The finding provides crucial insight into why cancer cells develop incorrectly during division.
Researchers at University of Pennsylvania implicated defects in mitochondria as a key factor in cancerous cell transition. Disrupting mitochondrial components led normal cells to adopt cancerous characteristics, including increased glucose consumption and invasive behavior.
Researchers will investigate the function of MED1 and its pathways in cancer stem cell formation of HER2-driven tumors, with the goal of intervening for possible cancer therapy. They aim to develop new therapies targeting MED1 and HER2 for patients with HER2 and estrogen receptor positive breast cancer.
Researchers have made a breakthrough in understanding how deactivation of a key protein leads to breast cancer metastasis. The new high-speed atomic force microscopy (AFM) technique allows for the first time to image live breast cancer cells, providing insights into the physical properties and dynamics of these cells.
Researchers have discovered a new species of tRNA-derived small RNAs, called SHOT-RNAs, that contribute to cell proliferation in hormone-dependent breast and prostate cancers. These findings suggest a new role for tRNAs and potential therapeutic applications for the treatment of these cancers.
Researchers at the University of Toronto have developed a new device that can track chemical signals within cells, allowing for faster and more accurate detection of cancerous growth. The device uses digital microfluidics to deliver rapid sequences of chemicals, enabling scientists to study cell responses in unprecedented detail.
Researchers found that stress hormones, including glucocorticoids used to treat chemotherapy side effects, can stimulate growth of breast cancer cells resistant to anti-estrogen therapy. However, adding prolactin may prevent this expansion, offering a potential countermeasure.
The study found that Fam20C phosphorylates more than 100 different secreted proteins, directing numerous cellular processes. This discovery has significant implications for understanding cancer cell metastasis and developing new therapeutic targets.
A recent study by MD Anderson researchers identified DAPK1 as a novel therapeutic target for breast and other cancers with TP53 mutations. High levels of DAPK1 are associated with poor prognosis and increased cancer growth in these tumors.
Researchers at Helmholtz Munich developed an assay to rebuild mammary gland tissue architecture using human breast epithelial cells. The mini-mammary glands exhibit properties similar to those of aggressive breast cancer cells, suggesting a link between normal breast stem cell function and tumor progression.
A lab study found that daily aspirin was effective at blocking breast tumor growth. Aspirin appears to affect cancer stem cells, preventing them from reproducing. Experts recommend consulting a doctor before starting a daily aspirin regimen due to potential risks and side effects.
Researchers at the University of Edinburgh discovered a trigger that allows breast cancer cells to spread to the lungs. Blocking these signals in mice significantly reduces secondary tumor formation. The study's findings may lead to new treatments to stop breast cancer progression.
Researchers discovered that TLR4 can function as a growth suppressor in wild-type TP53 cells but promotes growth in TP53 mutant cells. This balance affects survival rates and treatment outcomes.
A study published in Nature Communications reveals that a specific type of non-coding RNA, known as Eleanors, plays a key role in the development of endocrine therapy resistance in ER-positive breast cancer cells. Resveratrol was found to repress these RNAs, inhibiting the proliferation of resistant cancer cells.
Researchers found that HER2-positive breast cancer cells become addicted to the ERAD pathway, allowing them to survive chemotherapy. Inhibiting this pathway and promoting JNK activation selectively kills these cancer cells. The study proposes a new strategy for cancer treatment by maximizing cell stress.
Researchers developed a new micro-device that separates and analyzes highly mobile cancer cells, which are believed to be the more aggressive cells responsible for metastasis. The study aims to gain an understanding of what makes some cancer cells able to spread to other areas of the body.
Researchers at Johns Hopkins Medicine have designed a molecule called RK-33 to target the enzyme DDX3, which is overexpressed in over 90% of lung cancer samples. The therapy has shown promising results in mice, with the ability to lower radiation doses while increasing its effectiveness.
Researchers developed a microfluidic chip to capture CTC clusters from whole blood, revealing their prevalence and potential role in metastasis. The Cluster-Chip captured 30-40% of patients' CTC clusters, offering new insights into cancer biology and potentially leading to breakthroughs in cancer research.
Research published in JAMA Oncology finds that smoking induces epigenetic changes in cheek cells, which can also be seen in non-smoking related cancers. This discovery provides a potential tool for early detection of breast and gynaecological cancers.
Researchers have identified novel non-platinum-based molecules effective against cervical, breast, ovarian, and lung cancers without harming healthy cells. These discoveries could lead to the development of safer anti-cancer treatments with a unique molecular mechanism.
Researchers from the University of Waterloo discovered a new family of nonplatinum-based halogenated molecules that selectively target cancer cells while protecting healthy cells. These molecules generate reactive radicals that kill cancer cells, and increase the protective molecule glutathione in healthy cells.
Researchers have discovered a crucial gene, DNMT1, that maintains breast and cancer stem cells. High levels of DNMT1 expression are associated with increased risk of breast cancer, particularly in women over 30. Restoration of the opposing ISL1 gene significantly reduces stem cell populations and cancer growth.
Researchers found that overexpression of cyclin E slows down DNA replication and introduces harmful mutations in cells. The study discovered specific regions of chromosomes frequently failed to complete replication, leading to genetic instability and potential cancer development.
Researchers at Rockefeller University found that short stretches of genetic material called tRNA fragments can reduce the growth and spread of breast cancer cells. These fragments bind to a key player in the life cycle of cancer cells, known as an oncogene, reducing its ability to promote cell division and metastasis.
Scientists from Houston Methodist report that porous silicon microparticles can potentiate anti-tumor immunity by enhancing cross-presentation and inducing a type I interferon response. This approach shows promise for treating HER2+ breast cancer patients, with potential applications for other types of cancers.
A Mayo Clinic-led research team has identified a molecular switch in the HER2 protein that sets off a cascade of events leading to cancer. Disrupting this site can stem the growth of breast cancer cells more effectively than current treatments.
A new library of authenticated canine cancer cell lines, FACC-29, has been established to aid in research and drug development. The panel includes 29 cell lines from various cancers, allowing researchers to test new treatments and predict responses.
Researchers have tested an experimental immune system drug, MPDL3280A, in a preliminary human study and found it to be generally safe and well-tolerated. The therapy aims to restore the immune system's ability to recognize and attack cancer cells, with promising results in controlling disease in some patients.
Breast cancer cells can survive detachment from the extracellular matrix by forming multicellular aggregates, stabilizing EGFR protein. Elevated Bim-EL protein in inflammatory breast cancer cells blocks anoikis through complex with Beclin-1 and LC8.
Researchers at Cold Spring Harbor Laboratory have identified a previously unknown signaling pathway in HER2-positive breast cancer cells. The pathway involves protein tyrosine phosphatase PTPD2, which regulates abnormal cell growth when the HER2 pathway is activated.
Researchers analyzed over 12,000 proteins in triple-negative breast cancer cells, identifying subtypes and correlations with drug response. The findings suggest that treatments targeting cell spread may be effective against resistant tumors.
A study has identified a molecular signature that drives the growth and survival of triple negative breast cancer cells. The research reveals that high levels of Myc protein and low levels of TXNIP correlate with poor patient outcomes.
A Yale University-led team has compiled sophisticated data on the signaling networks directing highly invasive cancer cells. They found that breast cancer cells prioritize certain cues in the presence of others and can switch their migration mode depending on what they see from the environment.