Articles tagged with Tumor Suppressor Genes
Defering bilateral salpingo-oophorectomy beyond age 50 increases risk of ovarian cancer in BRCA carriers. The residual risk of ovarian cancer for older women in good health is considered high enough to warrant preventive surgery.
Researchers have uncovered how BAP1 functions at the molecular level and present a novel therapeutic strategy to slow cancer progression. BAP1's role in DNA repair pathways and its potential as a biomarker for personalized treatment are also explored.
The study reveals that low levels of CTDNEP1 drive early and deadly pancreatic tumors, highlighting its role as a tumor suppressor. Tumors with low CTDNEP1 expression showed stronger metabolic activity and immune evasion.
Researchers at MD Anderson Cancer Center have found that inhibiting GFER, a mitochondrial enzyme, in combination with immune checkpoint blockade improves antitumor response in preclinical models. This two-pronged approach holds promise for patients with pancreatic cancer.
Researchers have identified CDX1 and CDX2 as key molecules that counteract β-catenin and suppress stemness in colon cancer. Deletion or overexpression of these proteins increased tumor aggressiveness and expression of cancer stemness-related genes, suggesting a potential therapeutic target.
A new study introduces a multi-omics-based molecular classification of gastrointestinal stromal tumors, categorizing them into four distinct subtypes. The findings identify key genetic signatures and tumor suppressor genes that influence treatment response, providing a roadmap for personalized therapy strategies.
A team of researchers from Xi'an Jiaotong-Liverpool University has engineered a short sequence of artificial DNA to target the mutant protein p53-R175H, linked to lung, colorectal, and breast cancers. The new molecule, dp53m, inhibits cancer cell growth and increases sensitivity to chemotherapy agent cisplatin.
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 developed a new class of drugs targeting PRMT5 enzyme, exploiting genetic vulnerability in tumor suppressor genes. Early clinical trials show promising results for patients with specific types of cancer, including melanoma and mesothelioma.
Scientists at the University of Colorado Anschutz Medical Campus identified protein FAM193A as a key component of a mechanism suppressing tumor growth. The discovery offers new potential for cancer therapies targeting p53, a frequently mutated gene in human cancers.
Researchers have identified three novel pathogenic variants of the ATR gene as predisposing to male breast cancer. These variants were found in a cohort of individuals with early onset and familial breast cancers, using a combination of exome sequencing and functional investigations. The study suggests that extended genetic analysis ca...
A research team led by Ivano Amelio found that the protein p53 acts as a key to maintaining genomic stability, preventing cancer-promoting mutations. Without p53, cells become more aggressive and prone to acquire genomic instability.
Researchers found that APC gene mutations in colon cancer patients disrupt T lymphocyte migration to tumors, making it harder for the immune system to combat cancer. The study provides new insights into the mechanisms of antitumor immune defense.
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 St. Jude Children's Research Hospital found that the tumor suppressor gene PTEN controls rhabdomyosarcoma cell identity and that enhancing PAX7 expression can maintain tumor cell existence, providing a potential treatment target for rhabdomyosarcoma.
Researchers discover that tumor suppressor genes can prevent the immune system from spotting and destroying malignant cells in mice. The study reveals a surprising new action for many of these defective genes, which trigger mechanisms that prevent the immune system's T-cells from targeting tumors.
A new study published in eLife suggests that activating the protein ISGF3 could be a novel therapeutic strategy for patients with clear cell renal cancer. ISGF3 regulates key tumor suppressor genes and acts as a brake on tumor growth, which can be disabled by loss of secondary tumor suppressors.
Researchers at Osaka University discovered how specific genes regulate B cell cycling in germinal centers. They found that Foxo1 promotes B cell proliferation, but its activation is associated with lymphomas. Reviving BATF levels recovered the proliferation of Foxo1-deficient B cells.
A newly discovered tumor suppressor gene, RASA2, has been found to affect melanoma survival. Restoring its function in melanoma cells caused them to stop growing and die.
A new study identifies TET1 as a master regulator in cancer progression by silencing tumor suppressor genes. Adding TET1 back to cancer cells reactivates these genes, reducing abnormal proliferation.
Researchers found that NPM-ALK silences the tumor suppressor gene IL-2Rγ in cancer cells, leading to cell death. The discovery presents a potential new target for treating lymphoma and other types of cancer.
A new study reveals that even slight reductions in PTEN expression can significantly increase cancer susceptibility in specific tissues, implying that environmental factors like diet and carcinogens may drive tumor development. This finding has implications for the development of diagnostic tests targeted to these gene alterations.
Researchers developed a method to distinguish driver mutations from passenger mutations in cancer genomes by analyzing deletions at known tumour suppressor genes and fragile sites. The study found at least one in nine genes can be removed without killing human cells.
Researchers have identified SCARA5 as a candidate tumor suppressor gene in human hepatocellular carcinoma (HCC), a form of liver cancer. Genetic and epigenetic silencing of SCARA5 is linked to aggressive disease, including tumor invasion into blood vessels.
The study reveals how a single event can trigger the collapse of molecular fences, leading to the inactivation of tumor suppressor genes and the initiation of tumorigenesis. The researchers discovered that the loss of PARlation marks on CTCF protein allows it to fail to regulate critical genes, including p16 and RASSF1A.
Scientists have identified p16 as a gene that accelerates cellular aging, while p19 slows it down. The study sheds light on the development of aging-related characteristics such as loss of muscle mass and cataracts.
A new study has identified a potential tumor suppressor gene related to Chinese colorectal cancer patients, located on the long arm of chromosome 1 (1q31.1-32.1). The researchers found a minimal region of frequent deletion in this area, which they believe may be responsible for the development of colorectal cancer in Chinese patients.
A recent study published in Cancer revealed that African-American women are four times more likely than white women to show significant alterations in the tumor suppressor gene p53. This finding suggests a greater burden of poor prognostic factors among African-American women, highlighting a potential link between genetic mutation and ...
Researchers identified Dmp1 as a critical tumor suppressor gene that promotes tumorigenesis when mutated, providing new insights into cancer development. The study found that even one defective copy of the Dmp1 gene is sufficient to drive lymphoma progression in cells with normal p53 status.
A University of Iowa research team discovered that DNA methylation can contribute to oral cancer by silencing tumor suppressor genes. The study found that aberrant cytosine methylation patterns were present in oral cancer cells but not in normal human cells, suggesting a potential mechanism for cancer progression.