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 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.
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.
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.
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 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.
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.
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 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.
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.
Researchers at CHEO have identified a series of genes that magnify the impact of oncolytic viruses, allowing for up to 10,000 times more potent killing of tumor cells. By short-circuiting these rescue systems, tumor cells can be triggered to commit suicide, preserving healthy cells.
A team of researchers at UC Santa Barbara has developed a novel technique using laser spectroscopy and silver nanoparticles to discriminate between cancerous and non-cancerous cells. The technology can help identify unique tumor cells that may spread to other parts of the body, improving diagnosis and treatment outcomes.
A new treatment for alveolar rhabdomyosarcoma has been discovered by IDIBELL researchers, using 2-deoxyglucose to inhibit glucose metabolism and cause cell death in tumor cells. The molecule is similar to those used in PET imaging techniques and shows low toxicity at high doses.
Researchers have successfully delivered chemotherapy to cancer cells inside tiny microparticles, reducing ovarian cancer tumours by 65 times more than traditional methods. The 'Trojan Horse' approach uses a special protein called CD95 to hijack cancer cells and deliver the chemotherapy cargo.
Researchers have discovered how p53 binds to Hsp90, revealing new insights into cancer development and potential therapeutic targets. The study found that p53 binds to both the middle and C-terminal domains of Hsp90, with negatively charged amino acids playing a crucial role in stabilizing the bond.
Researchers confirm vitamin D's role in slowing down colon cancer cell growth and proliferation. The study found that a lack of vitamin D increases the aggressiveness of colon cancer, highlighting its potential as an anti-tumor agent.
Researchers at Penn State College of Medicine have discovered a potential new cancer therapy that inhibits two key enzymes in mouse tumor cells, making them more sensitive to chemotherapy. The drug SLM3, which targets GSK-3ß and CDK1, has shown promising results in lab mice.
Researchers at St. Jude Children's Research Hospital identified a hybrid cell as the origin of childhood eye tumor retinoblastoma, which has been linked to multiple developmental pathways being turned on simultaneously. The study also found that blocking certain chemicals reduced growth in human retinoblastoma cells, providing a potent...
Researchers at the University of Pennsylvania have successfully treated advanced chronic lymphocytic leukemia (CLL) patients with genetically engineered 'serial killer' T cells. The treatment involves removing and reprogramming patient cells to target specific proteins, resulting in sustained remissions and reduced side effects.
Researchers identified genetic changes that led to the loss of E2A, a crucial gene regulator. The loss enables tumor cells to grow rapidly and uncontrolledly, contributing to the aggressive behavior of Sézary syndrome.
Scientists at USC have proven that oncogenes can convert normal cells into stem-like cells, leading to a new approach in treating diseases with stem cell therapy. The study successfully converted human skin cells into brain cells by suppressing p53, suggesting it determines cell fate rather than only cancer outcome.
A recent stem cell study has found that the protein molecule E-cadherin, which plays a key role in cancer, also regulates up to 25% of genes within cells. This unexpected discovery could lead to new cancer treatments by understanding why some cancer cells are difficult to eradicate.
The Damon Runyon Cancer Research Foundation has awarded prestigious fellowships to 18 outstanding postdoctoral scientists, providing them with independent funding to pursue novel ideas in cancer research. The fellowships will support research into various aspects of cancer, including gene expression, cell growth, and tumor development.
Researchers at Dana-Farber Cancer Institute have discovered a new approach to make more types of tumors susceptible to PARP inhibitor treatment. By blocking the cell-cycle protein CDK1, which supports BRCA1 repair function, cancer cells become vulnerable to DNA-damage agents and ultimately die.
A Duke University Medical Center research team has discovered new proteins in blood cells of patients with advanced prostate cancer and metastatic breast cancer. These proteins are associated with embryonic development and may help doctors gauge the progression or response to treatment more accurately.
A new study has identified PI3Kinase gamma as a crucial protein in tumor growth and inflammation. Disrupting this enzyme prevents tumor cells from attracting immune cells, slowing down tumor development and metastasis.
A team of scientists has created a new 3D tumor model that can grow in a realistic and easily accessible substrate, speeding up cancer drug discovery. The model's 3D nature provides a more accurate representation of how tumors grow in the body, reducing the likelihood of promising drugs failing during animal testing.
Researchers at Einstein College of Medicine identified a key player in breast cancer spread, CCL2, which recruits immune cells to facilitate tumor growth. By blocking CCL2 signaling, they found potential for halting or slowing metastatic disease.
Researchers at Instituto Gulbenkian de Ciência found that the actin-capping protein regulates the Hippo complex, leading to abnormal growth and tumour formation. The study provides insights into understanding proliferation gene activation in cancer research.
Researchers at Stanford University School of Medicine have separated two distinct ways in which the p53 protein works, with implications for developing treatments that mitigate radiotherapy and chemotherapy side effects. The study reveals that disabling one part of the protein could allow healthy cells to survive DNA damage without pro...
MIT scientists have designed a new type of nanoparticle that can target nearly any type of tumor by utilizing the acidic environment shared by most cancers. The particles are designed to break down in the slightly more acidic environment near a tumor, revealing another layer that can penetrate individual cells.
Researchers have developed a new technique that allows cancer-fighting cells to survive in patients' bloodstreams for over a year, without the need for toxic treatments. The study showed promising results, with one patient remaining cancer-free two years after treatment.