Articles tagged with Tumor Cells
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Researchers identified 38 prognostic subnetworks of interacting genes that predict cancer progression in chronic lymphocytic leukemia. The study helps define how CLL evolves over time, becoming more aggressive and deadly.
Researchers discovered that tumor cells release chemokine CCL2, which docks onto endothelial cells and activates the CCR2 receptor, making them permeable. This pathway enables tumor cells to migrate and metastasize.
Researchers create high-throughput flow-through optical microscope to classify rare breast cancer cells in blood samples, boasting a throughput of 100,000 cells per second. The technology demonstrates real-time identification of rare cancer cells with a record low false-positive rate.
Researchers develop a new method to isolate and grow cancer cells, which can aid in understanding how cancer spreads and ultimately fighting it. The soft fibrin substrate promotes the growth of tumorigenic cells, making them more efficient at causing tumors.
Researchers showcased the breadth of zebrafish research at an international conference, focusing on cancer and nicotine dependence. A study found that mid-differentiated cells play a key role in tumor growth, challenging traditional views on cancer stem cells. Another study used zebrafish to identify novel candidate genes involved in n...
A recent study found that targeting the JAK1 and JAK2 tyrosine kinase pathways can increase tumor cell susceptibility to natural killer cell-mediated death. Pharmacological inhibition of these pathways was shown to enhance tumor cell killing, making them a promising target for cancer therapy.
Researchers discovered that pancreatic cancer cells produce a protein that tricks the immune system into helping cancer growth. Blocking this protein may lead to effective treatments for pancreatic cancer. The findings suggest restoring the antitumor properties of a patient's immune system could be a therapeutic strategy.
Researchers at NYU School of Medicine have made a key discovery about the progression of pancreatic cancer, revealing how it escapes immune detection. By targeting a protein called GM-CSF, they found that immune cells can be unleashed to attack and halt tumor development.
Researchers at IRB Barcelona have identified specific combinations of errors in cell integrity processes as crucial to initiating tumors. The study reveals that genomic instability alone is not sufficient for tumor development and highlights the need for further investigation into cancer's complex origins.
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.
Scientists have identified the Mitochondrial Pyruvate Carrier (MPC), a universal carrier that transports pyruvate into mitochondria. This discovery could lead to a better understanding of how cancer cells produce energy and potentially develop new treatments.
Researchers at Massachusetts General Hospital identified a tumor-propagating cell required for growth in a pediatric muscle tumor model. Another type of differentiated tumor cell must first colonize new areas to prime an environment for metastatic growth.
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.
Researchers have discovered that children's brain tumors preserve characteristics of the normal cells from which they originate, offering new hope for effective treatments. The study found that tumour malignancy is linked to cellular origin and time of tumour development, improving prospects for targeted therapies.
Researchers have developed a potent new drug called Lys05 that kills tumor cells in mouse models by clogging their recycling system. This approach has shown promise as a single-agent anti-tumor therapy with minimal toxicity to healthy cells.
A new Stanford study reveals that the cells sloughed off from a cancerous tumor into the bloodstream are genetically diverse and may require different treatments. The research found that these cells can express genes that predict their response to therapy, highlighting the need for personalized treatment approaches.
Researchers discovered a population of low-PSA prostate cancer stem cells that are resistant to hormone therapy and chemotherapy. These cells can differentiate into other cancer cell types and have long-term tumor-propagating capacity.
Researchers have identified a molecule, PDE4, that plays a key role in regulating the division of tumor cells and blood vessel growth in lung cancer. By blocking PDE4, they were able to significantly reduce tumor growth in laboratory experiments and mouse models.
Researchers have discovered that NKCC1 protein facilitates the movement of glioblastoma cells, which are notoriously aggressive and deadly. The study also suggests that a cheap FDA-approved drug, bumetanide, could slow cell migration and contain tumor spread.
Researchers have discovered that the NKCC1 protein may hold key to understanding how glioblastoma, the deadliest type of brain cancer, moves and invades healthy brain tissue. Blocking NKCC1 with a cheap FDA-approved drug slows movement of glioblastoma cells, suggesting a potential new approach to treat this aggressive cancer.
Researcher Carlos Martino explores how fluctuations in static and radiofrequency magnetic fields impact biochemical reactions. His work shows that low-level fields can inhibit tumor growth and modulate cellular proliferation, offering potential for a therapy based on weak radiofrequency fields.
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 identify non-classical oncogenes critical for leukemia cell survival and develop a strategy targeting these molecules, potentially reducing toxicity of current treatments. Dual inhibition of PI3K subtypes supports cancer cell death in mice and human tumor cells.
Researchers created transgenic mice with light-emitting lymphatic vessels to study tumor cell dissemination. The technique detects lymph node invasion by tumor cells, providing a unique tool for studying inflammation and metastasis.
Researchers have identified metastasin as a crucial protein that helps stop tumor cells from spreading. By understanding how metastasin binds to motor proteins, scientists can develop drugs to block this interaction and prevent tumor cell proliferation.
A study led by experts at the University of Nottingham has discovered a link between chromosomal abnormalities and survival rates in children with brain cancer. The research identified increased copies of chromosome 1q25 as associated with poorer outcomes, paving the way for a new diagnostic test.
Cancer researchers employed game theory to study the physics of tumor evolution under stress conditions. They found that modifying their framework accounted for heterogeneous stress patterns, leading to emergent cooperative outcomes between cooperator and cheater cells.
Researchers at Winship Cancer Institute developed a technique to remove cancer cells' defenses against radiation by disabling their ability to repair DNA. The experimental method uses RNA molecules that shut down genes needed for DNA repair, making brain and lung cancer cells more sensitive to X-ray radiation.
Brain-tumor cells infected with a cancer-killing virus release CCN1, which initiates an antiviral response that reduces viral replication and limits its cytolytic efficacy. This mechanism may help control viral infections and improve oncolytic viral therapy for glioblastoma.
Research reveals that BRG1 gene mutations render tumor cells unresponsive to hormones like retinoic acid and steroids, leading to continued growth and spreading.
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.
Researchers have created a universal approach to personalized cancer therapy based on T cells, offering a highly adaptable and effective treatment option. The system uses engineered T cells capable of targeting multiple tumor antigens simultaneously or sequentially, significantly extending conventional CAR approaches.
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 new microfluidic device can isolate target cells much faster than existing devices, using a soft membrane with nanoscale pores to guide fluid and bring cells in contact with antibodies. This technology could be used for point-of-care diagnostics and personalized medicine applications, such as cancer diagnosis.
Researchers found that inhibiting telomerase triggers alternative lengthening of telomeres (ALT) in cancer cells, leading to increased expression of PGC-1ß gene. Targeting PGC-1ß weakens mitochondria function and enhances anti-telomerase therapy.
Researchers at MGH Cancer Center have discovered a potential treatment target for KRAS-mutant colon cancer, which may lead to new strategies for treatment-resistant tumors. Targeting TAK1 and BMP pathways may induce tumor cell death, offering hope for patients with KRAS-dependent colon cancers.
Scientists have developed a new method using DNA sequencing to identify cancer cells that can be targeted by the immune system. By analyzing genetic data from cancer cells and normal cells, researchers were able to identify specific mutated genes whose altered proteins trigger immune system attacks.
Researchers at Boston University have created a 3D model that simulates the growth of cancer tumors, suggesting that softening of cancer cells accelerates proliferation and extends lifetime, leading to rapid tumor growth. The study provides a new quantitative approach to understanding tumor development based on mechanical properties.
Researchers at Sanford-Burnham identified a molecular switch, controlled by protein kinase C-epsilon, that enables melanoma cells to resist chemotherapy. High levels of PKC-epsilon in melanoma are associated with poor prognosis and increased tumor-promoting activity.
A team of researchers has identified a potential new therapeutic target for the treatment of glioblastoma multiforme (GBM), a highly aggressive form of brain cancer. They found that protein SULF2 is expressed in primary human GBM tumors and cell lines, and its expression is associated with abnormal activation of signaling pathways down...
Researchers found that Pannexin1 helps closely pack together tumor cells, forming large multicellular tissues. The protein sets off a chain reaction involving ATP and receptors, ultimately remodeling the actin network to increase forces between cells, driving them to bind more tightly.
Researchers studied the role of immune responses in oncolytic adenovirus therapy and found that CD8+ T cells mediate antitumor efficacy. The study proposes a new therapeutic regime combining oncolytic adenovirus with immunotherapy.
Researchers at Scripps Research Institute found that a cell surface protein called CDCP1 protects tumor cells from apoptosis and promotes metastasis. The team identified plasmin as the key enzyme responsible for cleaving CDCP1, which triggers a signaling cascade blocking apoptosis and enabling cancer cells to colonize distant organs.
EMBL Monterotondo researcher Rocio Sotillo has won a $650,000 Howard Hughes Medical Institute award to support her research on cancer and chromosomal errors. She will use the prize to establish an independent research programme and develop new ways to grow lung cancer cells in three-dimensional cultures.
A study published in The Journal of Cell Biology reveals how DGK-alpha, a lipid-converting enzyme, enables invasive cancer cells to recycle integrins, providing better traction on fibronectin fibers. This process is essential for tumor progression and metastasis.
The study highlights the chain reaction required to prevent tumor formation, involving protein kinase ATM and its regulation of p53 and Mdm2. This new understanding may lead to the development of new therapeutic approaches to cancer.
Researchers found a strong link between an inherited TP53 gene mutation and chromothripsis, a condition where chromosomes shatter and reassemble incorrectly. This discovery has significant implications for diagnosis and treatment, as patients with the mutation may be at high risk of developing certain types of cancer.
A study has identified a protein called hepsin that may trigger the spread of breast cancer in certain cases. Hepsin, a protease enzyme, was found to free tumor cells from their native tissue matrix, allowing them to invade other tissues and grow into aggressive tumors.
Researchers have discovered a way to selectively target the glutathione pathway in brain cancer cells, making them more susceptible to chemotherapy. The breakthrough could potentially improve treatment outcomes for the nearly 45,000 people diagnosed with brain cancer each year.
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.
Researchers have discovered a technique to keep normal cells and tumor cells taken from an individual cancer patient alive in the laboratory. This breakthrough could revolutionize personalized cancer medicine and regenerative medicine, enabling oncologists to find the right therapies for patients.
Researchers at IRB Barcelona have discovered a new genetic program that converts epithelial cells into mobile invasive cells, which is common in embryonic development and tumour progression. The GATA6 gene plays a key role in this process, triggering survival factors and degrading the cellular matrix to facilitate cell migration.
Researchers discovered a novel viral oncogenesis mechanism in which KSHV co-opts cellular signaling pathways and modifies the microenvironment for viral replication. The virus induces EndMT, giving rise to infected invasive cells, allowing efficient spread of the virus.
Scientists have identified a gene mutation that underlies the vast majority of cases of Waldenstrom's macroglobulinemia. The mutation causes tumor cells to produce a distorted protein, leading to activation of NF-kB and growth of Waldenstrom's tumor cells.
The seven winning Celldance 2011 videos demonstrate the structure and function of living organisms at a microscopic scale. The award-winning entries feature various cell types, including fibroblasts and tumor cells, showcasing their behavior and interactions.
A study published in the Journal of Experimental Medicine reveals that protein BMP7 signals prostate tumor cells to enter a state of dormancy. Withdrawal of this protein restarts tumor growth, offering potential new therapies to prevent recurrence.
Researchers have created a highly sensitive surface that enables multivalent binding, allowing for the efficient capture of circulating tumor cells from the blood. The combination of nanotechnology and biomimicry demonstrates great potential for detecting rare tumor cells.
A study by MIT cancer biologists reveals that platelets release chemical signals inducing tumor cells to become more invasive and form new tumors. The findings suggest that direct physical contact between platelets and tumor cells is necessary for metastasis, highlighting potential targets for drug development.
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.