Articles tagged with Breast Cancer Cells
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Breast cancer cells spread to surrounding lymph nodes through invasion into lymph vessels. Johns Hopkins researchers discover protein HIF-1 triggers this process by stimulating the growth of new blood vessels and activating genes involved in lymph vessel formation.
Researchers explored the effectiveness of resveratrol in preventing head and neck cancer in Fanconi anemia patients, a rare genetic disorder affecting DNA repair. The study found that resveratrol may eliminate cancer cells in these patients by making them sensitive to certain drugs.
Researchers at Moffitt Cancer Center discovered a mechanism by which cancer cells hijack histone regulation to promote growth and survival. Lower levels of histone protein H2B aid in suppressing core histone gene transcription, leading to unchecked cell growth.
Researchers identified two oncogenes, FAM83A and B, that allow breast cancer cells to survive tyrosine kinase inhibitor treatment. Increased expression of FAM83A enhances proliferation and invasion, while decreased expression delays tumor growth and renders cancer cells sensitive to TKIs.
Researchers have identified two related oncogenes, FAM83A and B, which enable breast cancer cells to survive treatment with EGFR TKIs. Expression of these genes in human tumors is correlated with decreased overall survival.
A study published in Oncogene found that progestins regulate miRNA-29, a molecule that helps breast cancer cells revert to a stem-like state marked by proteins CD44 and CK5. This phenomenon makes breast cancers more resistant to treatments targeting hormone dependence.
A study by Lawson Research Institute suggests that breast cancer stem cells have a preference for specific organs, such as the lung and brain, when spreading to other sites. Researchers hope to uncover the underlying factors driving this phenomenon and potentially develop new strategies to target these aggressive cells.
New human-derived breast cancer models retain heterogeneity, allowing researchers to test drugs more accurately. These models can help identify unique features in individual tumors, enabling targeted treatment.
Researchers found that HSF1 activates a transcriptional program distinct from heat shock, driving the development of aggressive cancer phenotypes in breast, lung, and colon cancers. The findings suggest HSF1 as a potential therapeutic target for treating multiple cancer types.
A new study has found a significant increase in rare de novo genetic mutations in individuals with testicular cancer, suggesting these mutations may be indicative of conditions that result in reduced fertility. The researchers propose that the paradigm of a de novo germline disease etiology may be less applicable to late-onset cancers.
Researchers at the Ludwig Institute for Cancer Research have discovered a molecular switch, ASPP2, that regulates autophagy and senescence in cells. Reduced levels of ASPP2 can lead to unchecked cell proliferation, promoting tumor growth.
Researchers have identified RhoC as a key driver of breast cancer stem cell metastasis. High levels of RhoC are associated with worse patient survival rates. Targeting this molecule may lead to more effective treatments for certain types of cancer, potentially managing cancer stem cells and invasive behaviors.
A new Weizmann Institute-led study identifies a potential molecular mechanism behind the link between cancer and faulty stem cell differentiation. The researchers discovered that the tagging of DNA pieces with ubiquitin is crucial for proper stem cell differentiation, and disruptions in this process can lead to cancer.
A study by University of Michigan researchers found that an inflammatory pathway involving Interleukin-6 drives resistance to Herceptin in HER2-positive breast cancers. Blocking this pathway with a drug improved the treatment's effectiveness, and also prevented cancer stem cells from forming.
Researchers at Vanderbilt University Medical Center found that stress activates the sympathetic nervous system, which promotes breast cancer cell colonization of bone. Beta-blockers, such as propranolol, can prevent this process by inhibiting sympathetic nervous system signals.
Researchers discovered a protein, IGFBP3, that helps stop cancer cell proliferation and found other proteins working together with it. This finding could lead to a therapeutic strategy to reprogram cancer cells into permanent dormancy.
A study published in Journal of Biological Chemistry found that prostate cancer cells lacking the protein SPDEF are unable to establish colonies at possible sites of metastasis, highlighting a potential biomarker for untreated cancers. Researchers hope to regulate SPDEF expression to prevent cancer cell metastasis.
Presentations at the Genetics Society of America's Model Organism to Human Biology meeting revealed key findings on cancer genomic pathways. Researchers identified mediators of metastasis and potential drug targets in model organisms such as zebrafish, fruit flies, and roundworms.
A BUSM in vitro study discovered a potent combination therapy for breast cancer, including triple-negative and hormone-refractory cases. The treatment re-expressed imprinted tumor suppressor genes, inhibiting cancer cell growth and promoting death.
A study by University of California - San Diego researchers blocks the NOTCH1 signaling pathway in cancer cells, reducing their ability to replicate and self-renew. The findings suggest that therapies targeting this pathway could be effective in treating various types of cancer stem cells.
Researchers at Georgetown University Medical Center discovered that glucose-regulated protein 78 (GRP78) is a major determinant of resistance to anti-estrogen therapy. Inhibiting GRP78 may provide a solution for tens of thousands of women who develop resistance to these drugs.
Researchers at UC San Diego have identified a new signal transduction pathway in alternative RNA splicing, which could lead to novel cancer drugs. The SRPK kinase plays a central role in regulating VEGF and controlling tumor growth.
Researchers at Cincinnati Children's Hospital Medical Center have developed a new candidate drug, Rhosin, that inhibits breast cancer cell growth and promotes the growth of nerve cells. The drug targets RhoA, a key component of a cell signaling protein complex involved in various cancers and neurologic disorders.
A recent study has identified the RLIP76 protein as a key contributor to pancreatic cancer cell resistance to chemotherapy and radiation. Depleting levels of this protein was found to kill human pancreatic cancer cells in culture and shrink established tumors in mice, making it a potential new treatment target.
Researchers have discovered a new indicator for breast cancer relapse, directly associated with the activation of NF-kB signaling in tumour cells. The absence of the 14-3-3 protein sigma is not itself a prognosis factor, but its lack enables chronic NF-kB activity linked to tumour progression.
Researchers identified a simplified fruit fly gene that splits into two complex human genes playing roles in cancer and birth defects. This split made studying the genes easier, providing unique insights into massive human MLL2 and MLL3 genes.
Researchers discovered that NOG enables breast cancer cells to invade bone and establish tumors by increasing osteoclast activity and keeping cells in a stem-cell-like state. This gene plays a key role in the complex process of metastasis, increasing breast cancer's potential for spreading to the bone environment.
A preclinical study found that normal p53, a tumor suppressor gene, makes breast cancer chemotherapy with doxorubicin less effective. Senescent cells produced by non-mutated p53 fueled the relapse of tumors. The research challenges the existing paradigm and is another step closer to personalized cancer medicine.
Researchers discovered that ADAM28 inhibits VWF-mediated apoptosis in cancer cells, leading to increased lung metastases. Inhibition of ADAM28 expression or activity significantly reduced lung metastases and increased cancer cell apoptosis.
Researchers have identified changes in adult stem cells and tumor suppressors that contribute to age-related breast cancer vulnerability. The 'HMEC Aging Resource' provides a valuable resource for studying cellular aging, allowing researchers to explore potential preventative measures.
Researchers develop new antibodies that bind to MUC1 protein on cancer cells, depositing toxins directly into diseased cells. This method has shown higher efficacy than existing treatments and may be available for more cancer varieties in the future.
Breast cancer researchers found that two related receptors, LRP5 and LRP6, must work together to maintain normal activity in mammary stem cells. A new signaling pathway may be involved, which could lead to new directions for cancer-drug manufacturers.
Researchers found that Skp2 E3 ligase promotes Herceptin resistance in breast cancer by activating the Akt kinase, which also regulates glucose metabolism. The study suggests that blocking Skp2 could inhibit glycolysis and provide a new approach to cancer treatment.
A study led by Fred Hutchinson Cancer Center researchers found a novel approach to inhibit cancer cells using an inexpensive 'orphan drug', originally developed for sleep disorders. The compound, CSNK 1 epsilon, kills cancer cells while sparing normal tissue, offering new hope for treating Myc-driven cancers.
Researchers from NUS have discovered how a drug-lead compound named BPTES can deprive cancer cells of energy and stop them from growing into a tumour. Building on these findings, they also derived positive results for a novel dual-drug treatment regime that kills kidney and breast cancer cells more effectively.
A new study published in Breast Cancer Research found that panobinostat selectively targets and destroys triple negative breast cancer cells. The HDAC inhibitor also reduces tumor growth in mice and partially reverses the morphological changes in cells to a more epithelial type.
A team of researchers at the Wellcome Trust Sanger Institute sequenced the genomes of 21 breast cancers, revealing new mutation processes that drive their development. The study found that these mutations accumulate over time, creating a complex landscape of genetic changes in the cancer cells.
Researchers at the University of Missouri discovered that apigenin slows breast cancer cell growth by inducing cell death, inhibiting proliferation, and reducing gene expression. Apigenin-treated mice showed smaller tumors and restricted nutrient flow to cancer cells.
Researchers identified a cell surface protein ganglioside GD2 that flags breast cancer stem cells as potent tumor-generating cells. A small molecule drug triptolide inhibits GD3 synthase, essential to GD2 production, and stymies cancer growth in preclinical tests.
Breast cancer cells that develop resistance to tamoxifen therapy increase production of metadherin, a protein associated with recurrence. Reintroducing microRNA 375 restores sensitivity to the drug, suggesting its role in malignancy and resistance development.
Researchers at the University of Georgia found that long-term lack of oxygen in cells may be a key driver of cancer growth. Cancer cells switch to glycolysis for energy production, leading to a vicious cycle of increased hunger and growth.
A study by Fred Hutchinson Cancer Center found that women with low levels of fetal cells have a 70% lower risk of breast cancer, while those with high levels have a four-fold increased risk for colon cancer. The biological reasons behind this contradictory effect are unknown and require further investigation.
Researchers have made significant breakthroughs in understanding the biological differences between individual breast cancers, highlighting the importance of biomarkers in identifying new targets for therapy. Studies also explored the mechanisms behind endocrine resistance and proposed a new approach to predicting response to treatment.
A new study conducted at Elizabeth Wende Breast Care in Rochester, NY found that women aged 40-49 with no family history of breast cancer are still at a high risk of developing invasive disease. The study included 211 women who underwent screening mammography and found that 64% had invasive disease.
Scientists at UCSF used a pioneering imaging technique to study the interaction between breast cancer and the immune system in mice. They found that activated immune cells are headed off at the pass by healthy cells forming a 'thin red line' around tumors.
The study found that overactivation of RANK signalling pathway promotes tumour stem cells, increasing tumour growth and metastasis in human breast epithelial cells. High levels of RANK protein are associated with poor prognosis tumours and basal type tumours.
A recent study by Maggie Louie reveals that prolonged exposure to cadmium can cause breast cancer cells to become more aggressive and develop malignant characteristics. The researchers found that even small concentrations of cadmium at chronic exposures can contribute to the progression of breast cancer.
A study found a potential link between alcohol consumption and breast cancer, suggesting that the protein CYP2E1 plays a direct role in explaining the long-established risk factor. Women who naturally express higher levels of CYP2E1 and consume alcohol may be at a greater risk for developing breast cancer.
Researchers discover Perp, a protein involved in cellular 'glue', plays dual role in preventing breast cancer. Abnormal levels of Perp linked to enhanced inflammatory response and tumor development.
Researchers at IBN discover engineered human stem cells can target and inhibit tumor growth, prolonging survival in mice with breast tumors. This finding paves the way for innovative stem cell-based therapies, offering a promising alternative to conventional cancer treatment.
New research from Lund University identifies a potential cancer treatment by targeting a protein involved in cell division. The study found that blocking this protein could kill cancer cells while sparing healthy ones.
A recent study published in PNAS contradicts the prevailing belief that basal-like cells are responsible for invasive tumors. Luminal-like cells, previously thought to lack stem cell properties, have been found to be highly tumorigenic and capable of generating larger tumors than their basal-like counterparts.
Researchers at Fox Chase Cancer Center have developed a new cell and animal model of inflammatory breast cancer, which may provide a better understanding of the disease and help with developing effective interventions. The model recapitulates aggressive metastasis and cancer stem cell activity associated with poor outcomes in patients.
A new study identified a key mechanism driving breast cancer invasion and linked it to ErbB2 amplification and cathepsin expression. This research offers insights into the molecular basis of ErbB2-induced malignancy and potential therapeutic targets for treatment-resistant forms.
A study published in Journal of Biological Chemistry reveals that protein survivin can prevent normal cell death when located outside the nucleus, but not inside. Researchers suggest measuring overall levels and locations of proteins like HDAC6 could provide new leads for investigating breast cancer.
Researchers have developed a breast implant with a 'bed-of-nails' surface at the nanoscale that reduces cancer cell growth and promotes healthy endothelial breast cells. The implant's unique surface features deter cancerous cells from dwelling and thriving, offering a promising alternative to traditional treatments.
Researchers at Johns Hopkins Kimmel Cancer Center discovered that low doses of epigenetic-targeted drugs azacitidine and decitabine can re-activate genes that stop cancer growth. The study found antitumor responses in breast, lung, and colon cancers, with effects caused by alteration of the epigenetic environment of DNA.
A study found that many women diagnosed with ductal carcinoma in situ (DCIS) felt confused and conflicted about their diagnosis, receiving conflicting messages from medical staff. The research highlights the need for clear communication and tailored support to help women understand this complex breast condition.
Researchers have identified obscurins as tumor suppressor genes in the breast, which are lost or mutated when cancer develops. This discovery holds promise for developing new tools to assess breast cancer risk and diagnose it at an early stage.
Researchers at Rensselaer Polytechnic Institute found a previously unknown link between breast cancer cells and the stroma. Cadherin-23, a new molecule, helps connect cancerous tumor cells to healthy tissue, facilitating invasive growth.