Articles tagged with Breast Cancer Cells
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Researchers have identified a critical link in the signaling pathway that enables cancer cells to establish tumors in distant parts of the body. A new drug targeting this molecule may help prevent cancer from spreading, offering hope for improved treatment options.
Scientists at Max Planck Institute for Heart and Lung Research found that blocking Plexin B1 can prevent the formation of breast cancer metastases in mice. The study suggests a new potential approach to improving prognosis for patients with aggressive breast cancer.
Scientists at University of California, San Diego have identified ROR1 as a protein expressed by breast cancer cells but not normal adult tissues. Silencing its expression impairs tumor growth and survival, making it a potential therapeutic target for future anti-cancer drugs.
Researchers find that loss of STAT1 protein leads to increased breast cancer development in mice, as the immune system loses ability to control tumors. This discovery suggests that STAT1 may play a crucial role in preventing unwanted cell division and tumor growth.
Researchers at Oregon State University have discovered two epigenetic mechanisms by which sulforaphane prevents cancer: HDAC inhibition and DNA methylation. These mechanisms work together to maintain proper cell function and prevent cancer.
Scientists at Scripps Research Institute have uncovered a self-sustaining signaling circuit in breast cells that leads to cancer. This circuit is triggered by the activation of MEK/ERK and IKK/NF-kB pathways, which maintain the malignant state of tumor cells.
A study published in American Journal of Pathology reveals that trefoil factor 3 (TFF3) protein, which protects the epithelial surface in normal breast tissue, also promotes tumor invasion and metastasis in breast cancer. Higher TFF3 expression is associated with a more aggressive phenotype.
Researchers found that breast cancers can hijack an embryonic program to promote tumor growth and survival. A new study details how this 'on-off' switch is flipped by a protein called SIX1, which allows doctors to delete the pathway when it promotes tumors.
IKBKE is induced by tobacco carcinogens and mediates tobacco action in promoting lung cancer cell survival. Knocking down IKBKE sensitizes cells to chemotherapy, suggesting a therapeutic role for targeting this pathway.
Researchers found striking similarities between genetic signatures of human breast cancer and those of stem cells in mouse embryos, revealing a new way to predict and personalize cancer therapies. The discovery could lead to the development of targeted treatments for aggressive forms of triple-negative breast cancer.
Researchers have identified a key switch that releases zinc into cells, which could be used to block cancer development and halt tumor growth. Zinc levels are controlled by protein molecules called zinc transporters, and understanding how these transporters release zinc has important implications for disease treatment.
Researchers have developed a new approach to detect cancer cells in the bloodstream, allowing for real-time assessment and control of disease spread. The method could help predict response and resistance to therapies, enabling more effective treatment decisions.
Scientists at Berkeley Lab have discovered a rotational motion called CAMo that plays a critical role in the formation of spherical acini structures in breast cells. Without CAMo, cells lose their structure and become randomly motile, leading to malignancy.
A possible receptor for the key breast cancer regulator Tumor Differentiating Factor (TDF) has been identified by researchers at Clarkson University. The receptor, labeled TDF-R, is found exclusively in breast cancer cells and shows specificity, suggesting its potential as a target for new therapies.
Research finds that ISG15 pathway disrupts cytoskeletal architecture in breast cancer cells, promoting cell migration and invasion. The study suggests that targeting the ISG15 pathway could provide a therapeutic advantage for patients with metastatic tumors.
Researchers used Cell-CT technology to examine cells in 3D, revealing subtle cellular details inaccessible by conventional microscopy. The study found that cancerous cells had distinct nuclear shapes and sizes, which can be used as biosignatures for disease staging and diagnosis.
A Concordia-led research team found that Lithocholic acid (LCA) selectively kills cancer cells while sparing healthy ones. LCA targets cancer cell sensors, triggering mitochondrial self-destruction and bringing the cell down.
LSUHSC researchers found that the ISG15 pathway triggers a cellular defense system that disrupts normal cytoskeletal function and increases cancer cell metastasis. This discovery provides a novel therapeutic target for future drug discovery and has important implications in other cancers.
A Wayne State University researcher is studying the signaling process that triggers breast cancer transformation. The objective of his three-year study is to evaluate the potential roles of two small proteins in breast cancer progression.
Researchers at Ohio State University found that normal cells in tumors can enhance cancer cell growth after losing a tumor suppressor gene called Pten. The study suggests interrupting signals between normal cells and cancer cells as a new approach to treating breast cancer.
Research reveals that cancer cells use a positive feedback loop involving c-MYC and SIRT1 to drive continuous cell division and tumor growth. This mechanism undermines normal cell regulation, leading to uncontrolled proliferation and treatment resistance in certain types of cancer.
A Vanderbilt University team has created a new method to optically assess the response of cancer cells to a specific drug, using light to visualize metabolic pathways. The technique could enable real-time monitoring of tumor response and help doctors make timely treatment decisions.
Researchers have discovered a microRNA, miR-520, that suppresses NFkappaB and TGF-b signaling pathways in breast cancer cells. This finding suggests that miR-520 may act as a tumor suppressor and could lead to new treatment options for ER-negative breast cancer.
Researchers have developed a vaccine that successfully attacks breast cancer in mice, with implications for treating ovarian, colorectal and pancreatic cancer. The vaccine targets MUC1, a protein found on over 90% of human breast and pancreatic cancer cases.
Scientists at Johns Hopkins have found that PARP inhibitors can block the ability of pre-leukemic cells to repair broken DNA, leading to their self-destruction. The treatment has shown promise in clinical trials for patients with aggressive myeloproliferative disorders.
Scientists developed a vaccine that reduces tumors by 80% in mouse models of breast and pancreatic cancer. The vaccine uses a unique carbohydrate signature to train the immune system to target cancer cells.
Dana-Farber Cancer Institute researchers have identified a mechanism that triggers inflammation in the liver and transforms normal cells into cancerous ones. They demonstrated that a particular micro-RNA, miR-124, can be harnessed to treat or prevent liver cancer.
Researchers have discovered a new target for treating aggressive cancers driven by the Myc oncogene, which can be targeted by inhibiting enzymes that are unique to cancer cells. The study identified SAE2 as a potential candidate gene that slows growth rates of human breast cancer cells when depleted.
Researchers at Thomas Jefferson University identified breast cancer cell mitochondria as a key target for therapy, showing that off-patent generic drug Metformin can prevent tumor growth and chemotherapy resistance. The study's findings suggest that targeting mitochondrial metabolism could be exploited in personalized cancer medicine.
Researchers at the University of Texas Health Science Center have identified potent compounds in the bat plant that can selectively kill cancer cells. The taccalonolides stabilize microtubules in cancer cells without affecting healthy cells.
Researchers identified a key interaction between BRCA1 and RHAMM proteins regulating epithelial cell polarity, found altered in some breast cancer patients. The discovery provides new insights into the molecular mechanisms driving breast cancer development.
A Stanford team developed a machine-learning-based method called Computational Pathologist (C-Path) to analyze breast cancer microscopic images, outperforming human evaluations. The model assesses 6,642 cellular factors and identifies structural features that matter in predicting patient survival.
Researchers found that inhibiting Notch signalling converts triple-negative breast cancer cells into hormone-receptor positive cells, making them dependent on estrogen. This technique has potential for combination therapy, where a Notch inhibitor is used to make all cancer cells hormone-sensitive.
Researchers found that a defect in the TERE1 gene, associated with Schnyder's corneal dystrophy, also contributes to invasive bladder cancer progression. The study showed that TERE1 inhibits bladder cancer cell growth and regulates cholesterol levels in cells.
A team of scientists at Tufts University is developing ultra-sensitive techniques to detect breast cancer earlier and treat it with greater precision. They aim to create a simple blood test for screening and diagnose the disease more accurately.
Researchers at VTT Technical Research Centre of Finland discovered a single cell protein that inhibits both cell migration and growth in aggressive breast cancer cells. This finding suggests an interconnected regulation of uncontrollable growth and metastasis, potentially leading to new medicine development.
Researchers at NYU Langone Health have identified the CK1 protein as a key player in cancer cell development. Inhibiting this enzyme may provide a new approach to treating cancer cells, particularly those with malfunctioning mTOR signaling pathways.
Researchers have discovered a small molecule, microRNA-101, that can block autophagy in cancer cells, making them more sensitive to treatment with the anti-hormone Tamoxifen. This breakthrough has significant clinical relevance for treating breast cancer.
A U-M study has identified the p38-gamma molecule as a key regulator of aggressive breast cancer cell movement. By understanding how this molecule influences cell motion, researchers hope to develop targeted therapies that can improve treatment outcomes.
Researchers discovered that PTK6 protein, which regulates cell growth in normal tissue, activates proliferation of damaged cells in cancerous breast tissue. Mice lacking PTK6 gene were highly resistant to carcinogen-induced colon tumors.
Researchers discovered that resveratrol blocks the growth of breast cancer cells by reducing estrogen receptor levels. This finding has significant implications for treating women with breast cancer whose tumors develop resistance to hormonal therapy. Resveratrol may serve as a potential tool to combat hormone-resistant breast cancer.
Researchers found a way to shut down pumps on breast cancer cells' surface that reject chemotherapy drugs, allowing the drugs to penetrate and kill the cells. Activating heat-shock protein Hsp27 forces the pump-action protein P-gp to decrease, making the cells more sensitive to chemotherapy drug Doxorubicin.
Researchers found that Adeno-associated virus type 2 (AAV2) targets all different grades of breast cancer by activating death pathways. The virus causes 100% of cancer cell destruction within seven days, with majority of cell death proteins activated on the fifth day.
Researchers identified the cellular origin of a rare form of breast cancer, metaplastic carcinomas, which originate from basal epithelial cell types. The study used mouse models and cancer-causing genes introduced into healthy breast cells to understand the cellular beginnings of cancer.
Researchers discovered that precancerous cells in high-risk African-American women consume high amounts of glucose and have activated insulin signaling pathways. Conditions like obesity and gestational diabetes can stimulate these cells, but exercise, weight loss, and metformin may help prevent aggressive breast cancer.
Researchers have identified a neurotransmitter released in response to stress that stimulates the growth and migration of breast cancer cells. The study found that this neurotransmitter, norepinephrine, and its receptor NPY play a key role in the progression of breast cancer.
A new study establishes a link between alcohol metabolism and DNA damage that may be related to breast and liver cancers. Acetaldehyde, a metabolite of alcohol, was found to cause DNA damage and trigger a response in human cells.
A study by University of Texas Medical Branch researchers found that protein UNC-45A is linked to increased cell proliferation in breast cancer specimens and cell lines. High levels of UNC-45A also drive enhanced myosin and actin activity, leading to increased rates of cell proliferation and migration.
A protein discovered by Dr. Suresh Alahari's laboratory can inhibit breast cancer cell growth and reduce tumor progression. The research found that Nischarin, a novel protein regulating breast cancer cell migration, acts as a tumor suppressor in breast cancer.
A study published in Food and Chemical Toxicology found that a soy-based natural S-equol supplement did not increase the risk of estrogen-sensitive breast cancer. The supplement, SE5-OH containing Natural S-equol, was previously shown to reduce menopause symptoms in postmenopausal women.
Researchers developed a gene therapy that targets breast cancer stem cells, eliminating them and increasing chemotherapy effectiveness. The therapy, VISA-claudin4-BikDD, was shown to reduce tumor volume by 75% and extend survival in mice.
Researchers have discovered a way to starve breast cancer cells by blocking their efficient amino acid delivery system. This approach could provide new treatment options for patients resistant to standard therapies.
Researchers discovered that measles virus can target tumors through the PVRL4 receptor, a marker found on lung, breast, colon, and ovarian cancer cells. This approach could be used to fight various types of cancer, with ongoing experiments testing its effectiveness in mouse tumor models.
Scientists found that high levels of insulin-like growth factor 1 receptor (IGF1R) expression are required for leukemia-initiating cell activity in T-cell acute lymphoblastic leukemia (T-ALL). Blocking IGF1R using inhibitors or reducing its expression significantly impaired leukemia stem cells' self-renewal capacity.
Researchers at the University of Houston discovered the potential for estrogen hormone compounds to prevent colon cancer by activating estrogen receptors. They also identified a key gene involved in breast cancer tumor cell growth, opening new opportunities for targeted therapeutics.
Researchers at the Broad Institute and Whitehead Institute found that cancer cells can interconvert between different types, existing in phenotypic 'states' that can change over time. This decentralized model challenges the traditional view of cancer stem cells as a hierarchical society.
Researchers at Georgetown University Medical Center have identified a mutant gene STAG2 that is commonly mutated in human cancers and causes aneuploidy, an abnormal number of chromosomes. The study found that 20% of brain, skin, and bone cancer samples lacked the STAG2 protein, leading to increased risk of cancer.
Abnormalities in breast cancer stem cells found in some cancers can lead to tumor development and recurrence, according to a recent study published by OHSU Knight Cancer Institute researchers. The study suggests that these mutated cells are resistant to chemotherapy and radiation, allowing the disease to recur.
A study in mice found that a genetic variation in the CDKAL1 gene leads to misreading of insulin-producing genes, causing decreased insulin production and impaired cell function. Meanwhile, researchers discovered that breast cancer cells evade the antitumor activity of NK cells by modifying their environment.
Researchers found that NSAIDs inhibit COX-2, reducing tumor growth and metastasis. However, the safety of these drugs during pregnancy remains uncertain due to the complex changes occurring in the body after childbirth.