Articles tagged with Breast Cancer Cells
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Research reveals that obesity suppresses the epithelial defense against cancer, allowing malignant cells to remain and develop tumors. Aspirin treatment enhances this defense mechanism, suggesting a potential role in cancer prevention.
Researchers identified age-related differences in breast tissue that contribute to increased risk of developing breast cancer in older women. The study found that accumulation of multipotent progenitor cells leads to defective luminal cells, which may be related to the increased susceptibility to breast cancer with age.
Researchers discovered that pre-existing chemoresistant genotypes in tumors can adapt to become fully resistant to chemotherapy, leading to poor overall survival. The study's findings may lead to diagnostic opportunities for detecting resistant clones in TNBC patients before treatment.
Researchers at Michigan Technological University developed a sugar-transporting biosensor to detect and differentiate cancer cells. The fluorescent probe targets the fructose transporter GLUT5, revealing metabolic nuances of different cancer stages.
Researchers identify PFKFB4 enzyme as potent driver of breast cancer, offering new treatment possibilities. The study found that targeting this enzyme or SRC-3 can almost completely eliminate breast cancer recurrence and metastasis.
Researchers found that ionizing radiation softens extracellular matrix stiffness, reducing cancer growth and migration. This could lead to improved fractionated radiation therapy and targeted drug delivery.
Researchers found that cancer cells have extra and longer centrioles, disrupting cell division, in aggressive breast and colon cancers. This discovery may aid in classifying tumors for prognosis and predicting treatment response.
Researchers discover microRNA molecule miR-940 that alters bone structure in late-stage prostate cancer. The molecule promotes osteoblastic lesions, which can cause severe pain and structural weakness.
Researchers at Harvard Medical School and Brigham and Women's Hospital identified hundreds of cancer-driving genes with unique sensitivities in various tissues. The study suggests that tissue type plays a crucial role in cancer genetics and may impact the effectiveness of treatments.
A newly designed chimera could simultaneously decrease the expression of three growth factors that are over-expressed in some cancers, leading to cancer cell death. The molecule has potent anti-tumor activity and is non-toxic, simple to produce, and cost-effective compared to traditional treatment strategies.
Two new studies show that women with 'triple negative' or HER2 positive breast cancers who respond well to chemotherapy before surgery have a very low risk of having cancer cells in their lymph nodes. Chemotherapy can safely reduce or avoid lymph node surgery for these patients, potentially reducing long-term side effects.
New research finds a positive link between BMI and DNA damage in BRCA mutation carriers. Obesity is associated with higher levels of gamma-H2AX foci, indicating increased DNA damage.
Researchers at Lund University have developed a new drug that transforms aggressive breast cancer into hormone-sensitive luminal breast cancers, making them responsive to conventional hormone therapy.
Researchers found a 'stop sign' protein that prevents healthy cells from sorting material, leading to unregulated growth in cancerous cells. This discovery opens the door to designing drugs that block PIP-stop formation by kinase enzymes, targeting difficult-to-treat cancers.
Loss of protein PHLDA1 is sufficient for development of drug resistance to targeted therapy in endometrial and HER2-positive breast cancer cells. Rescuing PHLDA1 expression re-sensitises cancer cells to RTK inhibitor.
Researchers at UT Dallas have isolated cancer stem cells using a two-step process, marking a significant step toward developing new drugs that can target these cells. The technique uses ligands that selectively bind to breast cancer stem cells, allowing for their isolation from standard breast cancer cells.
Researchers found that increased tissue stiffness leads to tumor aggressiveness and drug resistance in breast cancer cells. The study suggests that developing drugs that can prevent stiffness may stop the spread of cancer.
Induced pluripotent stem cells have strong immunogenic properties that provoke a systemic, cancer-specific immune response. The study suggests iPS cells may one day be used as a patient-specific cancer vaccine, potentially preventing tumor development months or years later.
A stem cell vaccine created from induced pluripotent stem cells (iPSCs) has been shown to elicit strong immune responses in lab mice, effectively eliminating breast, lung, and skin cancers. The vaccine also prevented relapses in animals with removed tumors.
A team of researchers developed a fluorescent sensor, TiY, that selectively stains tumor initiating cells (TICs) in various cancer tissues. The sensor can distinguish TICs from non-TICs and inhibit sphere formation, leading to suppressed tumor growth in mice xenograft models.
Researchers at Washington University School of Medicine have developed a novel technique using nanoparticles and light to target and kill metastatic cancer cells. The technique, which harnesses the power of chemotherapy drugs and radiation, shows promise in treating multiple myeloma and aggressive breast cancer.
Researchers at Southern Methodist University have discovered three drug-like compounds that successfully reverse chemotherapy failure in three of the most commonly aggressive cancers. The compounds were tested on micro-tumors and showed effectiveness against specific cancers, giving hope for developing new drugs to fight cancer.
A new study from The Scripps Research Institute found that dietary xenoestrogens like zearalenone and genistein can reverse the effects of palbociclib/letrozole combination therapy for breast cancer. Exposure to these compounds may significantly reduce the effectiveness of anti-estrogen treatments.
Researchers have engineered probiotics that can target and kill colorectal cancer cells using a substance found in broccoli. The mixture killed over 95% of colorectal cancer cells in a dish and reduced tumour numbers by 75% in mice with colorectal cancer.
Researchers found that activating REV-ERB proteins can starve cancer cells by blocking nutrient production, while normal cells are not affected. The discovery sheds light on a new uncharacterized way to treat cancer with limited toxicity.
University of Alberta researchers found that the RYBP protein prevents DNA repair in cancer cells, including breast cancer. This discovery could lead to precision medicine by tailoring treatment to individual patients' DNA.
A new single-cell sequencing tool, TSCS, has provided a clearer understanding of how ductal carcinoma in situ (DCIS) progresses to invasive ductal carcinoma (IDC). Genome evolution occurs in the ducts before cancer clones can be disseminated, and most mutations evolve within the ducts prior to invasion.
New research reveals how alcohol causes permanent genetic damage to blood stem cells, leading to cancer. The study found that acetaldehyde breaks and damages DNA within these cells, altering chromosome sequences and increasing the risk of certain cancers.
Researchers found that macrophages, which reside in healthy breast tissue, help early breast cancer cells leave the breast for other parts of the body. The study identified how macrophages and early cancer cells form a 'microenvironment of early dissemination' that can be targeted to prevent metastasis.
A team of researchers identified a crucial region in Numb that binds and inhibits Mdm2, stabilizing p53 levels. This interaction is key to understanding the regulation of p53 in breast cancers, which tend to retain a functional p53 gene.
Researchers discovered a mechanism to regulate switching between breast cancer-associated genes, using G-quadruplex structures. The study provides new insights into alternative splicing and could lead to the development of novel therapeutic strategies for controlling cancer growth.
The study reveals a novel mechanism by which cancer cells become dependent on methionine, an essential amino acid. Researchers propose using existing drugs like sulfasalazine to trigger this dependency and induce cancer cell death.
Researchers have discovered that interferon-β can impair the migration and formation of tumors in triple-negative breast cancer cells, suggesting a potential new treatment option for patients. Elevated interferon-β levels in breast tissue correlate with extended patient survival and lower cancer recurrence rates.
Researchers have identified a potential therapeutic target for aggressive breast cancer cells lacking estrogen receptor alpha, but expressing estrogen receptor beta. Estrogen or estrogen-like chemicals can slow tumor growth and even cause regression in these cells, which could lead to new treatment options.
A metallopeptide has been synthesized to target and disrupt mitochondrial function in breast cancer stem cells, inducing apoptosis. The peptide effectively delivers ROS and impairs mitochondrial metabolism.
A new drug approach targets breast cancer's stem-like cells, slowing their spread before metastasis occurs. Researchers found co-expression of integrin αvβ3 and Slug identifies these cells in up to 20% of primary breast cancers.
A study published in PLOS ONE found that metformin can prevent the development of multidrug-resistant breast cancer and reverse it after its onset. The research suggests that metformin has potential as a treatment option for aggressive breast cancer, warranting further investigation.
A new treatment approach for ovarian cancer has shown promising results in a mouse model. Combining drugs that reactivate dormant genes with those that activate the immune system led to greater tumor reduction and longer survival rates compared to single-drug treatments.
A new study found that breast cancer proteins can have altered functions in tumor cells due to changes in protein interaction networks. This shift affects the number of genes performing each function, not their expression levels. The study predicts patient survival and cancer subtype based on these functional shifts.
UT Southwestern scientists have developed a method to map protein changes that occur in different subtypes of breast cancer cells in response to DNA damage from new chemotherapy drugs. This could lead to a test to predict an individual patient's response to a particular drug, potentially revolutionizing personalized medicine.
Researchers found that blocking a key protein frees oxygen to damage iron-dependent proteins in lung and breast cancer cells, slowing their growth. The NFS1 protein is crucial for cancer cell survival in high-oxygen environments, but its inhibition may offer a new treatment option.
A joint effort by breast cancer researchers and bioinformaticians has provided new insights into breast development, revealing previously unrecognized cell types. The study used single-cell RNA-sequencing to identify a dramatic shift in gene expression around puberty.
A team of researchers at UC San Diego discovered a specific gene module that predicts patient life expectancy and metastasis across nine cancer types. The study found that a constrained environment triggers the formation of blood vessel-like structures in tumor cells, leading to aggressive behavior.
Researchers have identified a possible way to reengage a tumor suppressor protein, Growth Differentiation Factor 11, in triple-negative breast cancer cells. This could lead to the development of novel medications that can stop the aggressive form of cancer by intervening in its progression.
A University of Guelph professor has identified a protein called cadherin-22 as crucial in the spread of cancer cells. The discovery could lead to new treatments by hindering the protein's function, reducing adhesion and invasion rates by up to 90%.
A protein called tyrosine kinase 6 (PTK6) has been identified as a potential therapeutic target for estrogen receptor positive (ER+) breast cancer. PTK6 promotes cancer cell survival and growth in ER+ breast cancer cells, making it a promising avenue for developing new treatments.
Researchers at Queen Mary University of London used CRISPR-dCas9 epigenetic editing to cause healthy breast cells to undergo 'hyperproliferation', a key early stage of tumour initiation. The findings could lead to the development of new biomarkers for earlier diagnosis and novel therapies.
Researchers at Scripps Research Institute have discovered a compound that irreversibly stops the growth of certain aggressive, treatment-resistant tumor cells. The compound, FiVe1, blocks cell division by binding to a structural protein, vimentin, produced abundantly in mesenchymal-type cells.
The alisertib and TAK-228 combination shows promise in treating solid tumors, particularly triple-negative breast cancer. In a phase 1 clinical trial, the treatment was generally well-tolerated, with patients experiencing fatigue and decreased neutrophil count as common side effects.
Researchers have identified 27 novel tumour suppressor genes that may prevent cancer formation, using a powerful statistical model on over 2000 tumours across 12 human cancer types. This discovery could pave the way for targeted cancer therapies and deepen our understanding of cancer genomics.
A new class of antibody-drug conjugates, dubbed dual variable domain antibodies (DVD-ADCs), have been developed using a versatile double-decker technology. These pharmaceuticals selectively deliver drugs to cancer cells without harming healthy cells and tissues.
Researchers argue that identifying molecular subtypes of different cells within tumors can improve breast cancer treatment. They advocate for more accurate diagnostic tests to capture irregularities between tumor cells, which are often treated as a whole.
Researchers at the University of Wisconsin-Madison have identified a critical step in how cancer cells shift their metabolism, leading them down a cancerous path. By inhibiting a specific protein modification, the study reveals a potential therapeutic target to reverse several hallmarks of cancer.
Researchers at MIT have developed a synthetic gene circuit that can trigger the immune system to target cancer cells. The circuit is designed to detect two specific cancer markers and only activates a therapeutic response when both are present, offering new pathways for cancer immunotherapy.
Breast cancer cells recycle ammonia, a waste byproduct of cell metabolism, and use it as a source of nitrogen to fuel tumor growth. Repressing ammonia metabolism stunts tumor growth in mice.
For-Robin's monoclonal antibody JAA-F11 successfully targets and kills human breast cancer cells in human tumors grafted into mice, effectively treating triple-negative breast cancer. The company is now focusing on fundraising and preparing for human clinical trials to bring its product from the bench to the bedside.
The Translational Genomics Research Institute has developed novel processing methods for single-cell RNA sequencing, enabling researchers to identify genetic sources of diseases and tailor treatments. This breakthrough is crucial for understanding cancer and improving patient care.
Scientists studying cone snail venom aim to develop new medicines by understanding how the poison works. Researchers have discovered that cone snail toxins can overlap between the immune and central nervous systems in humans, potentially leading to breakthroughs in treatments for neurological diseases like Alzheimer's.
Researchers at UCLA have developed a new method called quantitative deformability cytometry (q-DC) to rapidly determine a single cell's stiffness and size. This technique allows for standardized measurements of single cells and could lead to improved cancer treatments by tracking patient progress and predicting drug effectiveness.
University of Minnesota researchers report a novel encapsulation approach to identify and maintain dormant cancer cells in a quiescent state. This method involves immobilizing cells within a rigid silica-PEG matrix, which prevents movement and proliferation, allowing for differential response between cancer cell lines.