Articles tagged with Tumor Suppressors
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Researchers discovered that high levels of protein BATF2 drive tumor immune suppression in head and neck cancer. Glutamine in the tumor microenvironment silences BATF2, affecting the STING signaling pathway and overall immune response.
Researchers at NTU Singapore and Oxford University have discovered a mechanism by which cells identify and repair highly toxic DNA damage, known as DPCs, that cause cancer, neurodegeneration, and premature ageing. The study reveals how SPRTN, a key repair enzyme, selectively targets DPC lesions, increasing its activity 67-fold.
A novel nanocarrier system utilizing metal-polyphenols enables precise intracellular delivery of therapeutic antibodies into cancer cells. This technology overcomes endosomal entrapment, resulting in suppressed tumor growth and enhanced anti-cancer activity.
Researchers identified C5aR1 as a novel prognostic biomarker and potential therapeutic target for treating metastatic skin cancer. Elevated C5aR1 presence suggests increased metastasis risk and poor survival in patients with cutaneous squamous cell carcinoma.
A new study reveals how a deficient ELP1 gene predisposes children to SHH-medulloblastoma, a subtype of malignant pediatric brain tumor. Researchers identified an MDM2-targeted therapy that reawakens the anticancer protein p53, potentially extending survival in model systems.
Researchers at the University of Gothenburg discovered that the influenza A virus exploits a protein called AGO2 to regulate gene activity and weaken the immune system. An existing drug, arsenic trioxide, showed promise in increasing interferon production and reducing viral loads.
Senescent cells can cause chronic inflammation through the secretion of inflammatory molecules, leading to age-related diseases. The study found that a cellular circuit controlling DNA repair can suppress this inflammation, offering potential ways to promote healthier aging.
Researchers have discovered several novel downstream p53 targets that could lead to improved cancer therapies. The study highlights the critical role of p53 in preventing cancer and identifies two new genes, ALDH3A1 and NECTIN4, as potential targets for cancer treatment.
Research reveals LKB1's dual function in cancer, acting as both a tumor suppressor and promoter. Its activity regulates downstream pathways that can enhance or inhibit tumor progression. Targeting LKB1 signaling offers potential therapeutic interventions.
A genetic fault long believed to drive oesophageal cancer development may actually play a protective role early in the disease, according to new research. The study found that defects in CDKN2A were more common in people with Barrett's oesophagus who never progressed to cancer.
Researchers at the University of Konstanz have discovered that different mutations of the tumour suppressor p53 affect pancreatic carcinomas differently. The study found that two variants of p53 selectively control distinct metabolic pathways, providing new insights into cancer development.
Researchers discovered that p14<sup>ARF</sup> activates tumor suppression by forming gel-like assemblies in the nucleolus, disrupting ribosome production and cell toxicity. This process contributes to cancer cell death, providing a new mechanism for tumor suppression.
Researchers found a link between non-functional p53 genes and the regenerative cell state in ulcerative colitis, leading to cancer progression. A new diagnostic test could identify aberrant cells earlier using molecular tools.
Research highlights molecular chaperones' role in maintaining tumor suppressor stability and functional integrity. This understanding is crucial for developing targeted therapies for multiple cancers.
Researchers discover PG3 activates p21, PUMA, and DR5 in cancer cells through ATF4 and ISR, independent of p53. The study provides insights into a novel mechanism by which PG3 induces cell death.
Researchers have uncovered a critical mechanism by which mutant p53 protein converts other proteins into cancer-promoting agents, driving tumor growth. Heparin, a widely used anticoagulant, can inhibit the formation of these harmful aggregates, providing a potential therapeutic approach.
Researchers at the University of Bologna have identified a specific location and genomic context where DNA breaks occur due to topoisomerase I inhibition. This discovery could lead to new cancer treatments by inducing DNA damage and genomic instability in cancer cells.
Researchers at NYU Abu Dhabi have discovered that the tumor suppressor protein Par-4 can cause a unique type of cell death called ferroptosis in human glioblastoma cells, while sparing healthy cells. This new understanding has the potential to inform the development of novel treatments for various hard-to-treat cancers and neurodegener...
A team of researchers from NUS has developed a novel method to stimulate muscle cells using magnetic therapy, which produces and releases proteins with anticancer properties. The study demonstrates that this non-invasive approach can prevent cancer cell growth and invasion, similar to exercise.
Researchers from Japan have discovered a novel targeted molecular therapy using microRNA-451a to suppress the progression of gemcitabine-resistant biliary tract cancers. The study found that miR-451a significantly diminished cell proliferation, induced cell death, and reduced chemoresistance in cancer cells.
Researchers have made a breakthrough in understanding the genetic changes that occur during tumor migration, and discovered a drug that can obstruct this process. A new clinical trial at the University of Rochester's Wilmot Cancer Institute will test the effectiveness of the experimental drug NP137.
Researchers used base editors to introduce specific combinations of activating and inactivating mutations into healthy organoids, creating realistic models for various types of cancer. This allows for further investigation into the development and treatment of cancer, with potential applications including testing new drugs.
A study published in Cancer Research identifies a novel mechanism by which liver cancer develops, involving the aberrant activation of the Wnt signaling pathway and the gene GREB1. The research reveals that GREB1 is responsible for integrating conflicting cellular states of differentiation and proliferation, leading to tumor promotion.
Researchers investigated the roles of STAT3α and STAT3β in aggressive breast cancer and found that differential silencing of these isoforms leads to changes in STAT3 activation. This study emphasizes the importance of distinguishing between STAT3 isoforms for accurate cancer diagnosis and therapy.
Scientists have identified a new emergency brake mechanism that prevents bladder cells from becoming cancerous, even when cancer-promoting genes are active. This discovery could lead to new therapeutic targets for bladder cancer treatment.
A new study reveals that HOXA5 binds to protein IκB-α, boosting its cancer-suppressing properties and reducing the development of breast cancers. The presence of HOXA5 suppresses malignancy in breast epithelial cells by blunting NF-κB action.
Researchers found that HOXA5 binds to IκB-α, boosting its cancer-suppressing properties and inhibiting NF-kappa B's transcription of cancer-causing genes. This helps prevent breast cancer formation by 'putting brakes' on an inflammatory pathway.
Researchers found that overexpressing matriptase reduced myeloma cell proliferation and inhibited migration. Matriptase also blocked Src kinase activation, supporting its potential as a tumor suppressor in multiple myeloma. The study provides new insights into the role of matriptase in hematological malignancies.
A study published in Cancer Research found that constitutively activated p53 in hepatocytes of chronic liver disease patients creates a microenvironment supportive of tumor formation from hepatic progenitor cells. This novel mechanism challenges the traditional role of p53 as a cancer suppressor.
Researchers at Karolinska Institutet have found a way to stabilize the cancer-suppressing protein p53 by adding a spider silk protein, creating a more potent variant. This discovery has potential as an approach for cancer therapy.
Researchers at Osaka University have made a breakthrough in understanding the molecular mechanisms behind Intrahepatic cholangiocarcinoma (ICC), a deadly form of liver cancer. By identifying TRAF3 and NIK as key players, they have uncovered potential therapeutic targets for novel ICC treatment.
Researchers have found that telomere shortening protects against cancer in humans. The study used CRISPR gene-editing technology to analyze mutant cells with long telomeres and found that they were at greater risk of developing breast, colorectal, melanoma, and thyroid cancers.
The study investigates the cooperative effects of targeted deletions of tumor suppressors Rb1, Trp53, Men1, and Pten in neuroendocrine tumors in mice. The authors demonstrate that pRB has the strongest cooperative function with PTEN in suppressing Pit NETs and Menin and TRP53 in suppressing Pan NETs.
Researchers identified 15 potent tumor suppressor genes that, when mutated, triggered rapid growth of HNSCC in mice. These genes include ADAM10 and AJUBA, which are also mutated in human HNSCC. The study reveals the identity of rare driver mutations in tumor-suppressing genes using a mouse-based CRISPR screen.
Researchers analyzed TP53 mutations in human leukemia, finding that most missense variants exert a 'dominant-negative' effect reducing wild-type p53's cancer-suppressing activity. The study challenges previous hypotheses suggesting new oncogenic functions from these mutations.
Research at Technical University of Munich shows that molecular chaperones Hsp70 and Hsp40, as well as Hsp90, control the function of p53 by influencing its three-dimensional structure. This helps prevent cancer cells from growing.
Researchers developed an mRNA-based nanotherapeutic to reintroduce functional copies of PTEN into cancer cells, restoring tumor suppressor function and killing cancer cells. The therapy showed significant suppression of tumor growth and progression in mouse models of prostate cancer.
A protein-coding gene called hnRNP K has been identified as a potential target for treating acute myeloid leukemia. The study found that expression of hnRNP K is significantly reduced in AML patients who carry a specific genetic deletion, suggesting it acts as a tumor suppressor.
Researchers at Indiana University School of Medicine identified a novel pathway that enables solid tumor cancer cells to grow. The protein Mdm2 plays an active role in making p53 ineffective, providing a new target for therapeutic approaches.
Researchers at Brigham Young University have discovered a potential target for tumor suppression, Programmed Cell Death Protein 5 (PDCD5), which may help prevent cancer cell growth by blocking the production of tubulin. The study provides new insights into how PDCD5 functions and offers a promising direction for future research.
Researchers found that loss of RPL5 or RPL11 prevents cell cycle arrest but impairs proliferation due to reduced ribosome content and translation capacity. This discovery highlights a new mechanism for controlling cell growth, relying on the essential role of these ribosomal proteins in biogenesis.
A study found that DCIS patients with combined RB and PTEN loss are at high risk of progressing to invasive breast cancer. Women lacking both genes are over 5 times more likely to develop invasive breast cancer.
Researchers at Salk Institute discovered adenovirus proteins that hijack cell machinery, including growth and replication. E4-ORF3 protein assembles into polymers that capture tumor suppressors and silence genes, providing a new avenue for cancer therapies.
A new study identifies SIRT2 as a key tumor suppressor linked to gender-specific tumor development in mice. The research suggests the existence of a rare family of tumor suppressors, and its findings have implications for understanding the biological processes underlying cancer and aging.
Research findings challenge traditional views on cancer treatment, revealing Cop1's role in tumor suppression rather than promotion. The study suggests that inhibiting Cop1 could stimulate cell proliferation in cancer cells.
A study at Baylor College of Medicine found that eliminating tumor suppressor C/EBP alpha is key to cancer development in the aging liver. Another protein, gankyrin, is elevated first, leading to degradation of C/EBP alpha and allowing uncontrolled growth.
Cold Spring Harbor Laboratory scientists uncover a large cache of genes that act as built-in barriers against cancer, including over 10 new tumor suppressor genes. The study reveals that even partial loss of function in these genes can accelerate tumor growth.
A study by researchers at the Salk Institute has found that tumor suppressor p53 plays a crucial role in controlling somatic cell reprogramming. The study showed that p53 activation prevents cells from reverting back to a less specialized state, which could have implications for cancer development and pluripotent stem cell technology.
A new protein called Trim24 marks the tumor suppressor p53 for destruction by attaching targeting molecules, leading to increased p53 expression and programmed cell death in cancer cells. The discovery provides a potential therapeutic approach to restoring p53 and killing tumor cells.
A team of researchers at Cold Spring Harbor Laboratory has discovered 13 new tumor-suppressor genes in liver cancer, which can help improve diagnosis and treatment. The study used a powerful genetic screen to validate the functional contributions of these genes in living animals.
Researchers at Beth Israel Deaconess Medical Center discovered that PTEN tumor suppression is maintained through a nuclear localization pathway. The study found that the loss of PML and HAUSP can force PTEN out of the nucleus, preventing its ability to act as a tumor suppressor.
Researchers at USC have identified a specific tumor suppressor called UVRAG, which regulates membrane traffic routes for cellular cleaning and recycling. The study found that UVRAG facilitates autophagosome formation and maturation, and is connected to endocytic trafficking.
Researchers at CSHL confirm DLC1 as a tumor suppressor gene that, when deleted or inactivated, leads to liver cancer. The team also identifies RhoA as a key signaling intermediary required for tumor formation, paving the way for new therapeutic targets.
Researchers have discovered that p27 can act as both a CDK-dependent tumor suppressor and a CDK-independent oncogene. This finding has significant implications for understanding cancer growth and developing drugs to target p27 dysfunction.
Researchers at University of Virginia Health System discovered microRNAs can suppress HMGA2 overexpression, a key feature of many tumors. This finding suggests microRNAs may have a role in preventing or curing diet-induced obesity-related diseases.
Researchers found that microRNA let-7 binds to HMGA2 mRNA transcript, suppressing its expression and preventing tumorigenesis. This establishes HMGA2 as a target of let-7, highlighting the potential role of microRNAs in cancer prevention.
Researchers at the University of Pennsylvania School of Medicine discovered how KSHV subverts a normal cell process to promote tumor growth. By tricking tumor suppressors VHL and p53 into being destroyed, KSHV allows cancer cells to grow unchecked.
A University of Southern California-led research group used X-ray crystallography to study the struggle between LTag, a cancer-causing protein, and p53, a key tumor suppressor. The study found that LTag inhibits p53's role by tying up six molecules, but p53 fights back by preventing virus replication.
A team of scientists led by Dr. Xiaojiang Chen have uncovered the molecular mechanism behind how a viral oncoprotein inactivates p53. The study reveals that the viral protein binds to p53, causing a conformational change that prevents it from binding to DNA and thus abolishes its tumor-suppressing function.
Dr. Hammarskjold's team reveals WT1(+KTS) promotes translation by facilitating mRNA transport and stability, highlighting links between transcription and post-transcriptional gene regulation. The study's findings suggest a crucial role for alternative splicing in regulating genes like WT1 during normal development and disease.