Articles tagged with Cancer Genetics
Researchers developed an online questionnaire to predict an individual's chances of harboring mutations in genes linked to colon cancer. The tool is based on a five-year study of nearly 2,000 patients and can help healthcare providers identify at-risk patients for early screening.
Two studies developed clinical models, PREMM1,2 and MMRpro, to predict the presence of mutations in MLH1 and MSH2 genes associated with Lynch syndrome. The models accurately estimated genetic risk for colorectal cancer, providing a timely tool for identifying and counseling families at risk.
The Jess and Mildred Fisher Center for Familial Cancer will expand clinical and research programs at Lombardi Comprehensive Cancer Center, providing automated cancer risk assessment and genetic predisposition research. The center also endows the Cecilia F. Rudman Arts and Humanities Program Fund, enhancing arts therapy and patient care.
A study by University College London researchers found that canine transmissible venereal tumour (CTVT) originated in a single wolf over 1,000 years ago and has since spread globally. The tumour cells are transmitted between dogs during sex, challenging current thinking about cancer.
The study found that YAP amplification transforms mammary epithelial cells, opening a novel cell growth controlling pathway. The research links the YAP gene to breast and other kinds of cancers, highlighting its potential as a cancer-causing gene.
Researchers have identified a genetic defect causing some people to feel full despite eating, providing hope for new anti-obesity treatments. The study pinpointed the melanocortin-4 receptor's role in regulating hunger and found potential therapeutic compounds.
Researchers discovered that different genes may be responsible for causing autism in boys than in girls, with varying degrees of severity. The study also found evidence for multiple genetic subtypes of autism, including male versus female and early versus late onset forms.
DNA damage resets the cellular circadian clock, suggesting a link between circadian timing and cancer. The study implies that the biological clock has a protective dimension in addition to its pacemaker functions.
Researchers at Columbia University Irving Medical Center have discovered that a cancer-causing protein can promote growth of axons in damaged spinal cord and brain cells. This discovery could lead to new therapies for treating neurological diseases.
Research reveals that women genetically predisposed to breast cancer may be more susceptible to low-dose ionizing radiation, such as chest X-rays. Women with BRCA1/2 mutations who reported ever having a chest X-ray were found to be 54% more likely to develop breast cancer than those who had never undergone the procedure.
A USC study found that the environment plays a big role in women starting to smoke, while genetics are a stronger influence for men. The study suggests that societal interventions can help prevent smoking initiation and highlight the importance of peer influence and social networks.
Researchers have developed a new test to detect rare genetic mutations in families at risk of passing on hereditary cancers like FAP. The innovative test allows for precise detection of mutations, enabling couples to make informed decisions about their pregnancies.
The HBZ protein is crucial for persistent infection of HTLV-1 in an animal host. Researchers discovered that a drug targeting this protein could disrupt viral replication and provide a new therapy for infected individuals.
Researchers have discovered a connection between a protein that prevents cancer in humans and lifespan in nematode worms, suggesting that this protein may determine how long we live. The 'checkpoint proteins' also appear to play a role in cell division and could be used to develop new strategies for treating neurodegenerative diseases.
Research using transgenic mice found that lower levels of selenoproteins accelerate prostate cancer development, highlighting the importance of selenium-containing proteins in preventing cancer. Further research is needed to understand how selenium supplements can maximize benefits.
A study published in Carcinogenesis reveals that sulforaphane, a compound in broccoli and cauliflower, can inhibit the development of hereditary colon cancer by inducing apoptosis and inhibiting tumor proliferation. The researchers found that mice fed with an SFN-supplemented diet developed significantly fewer and smaller tumors.
A new study by Fox Chase Cancer Center reveals specific defects in RNA translation underlie a progressive disease called dyskeratosis congenita, linked to anemia, immune deficiency, cancer, and premature aging. The research highlights the importance of proteomic analysis and potential therapeutic targets for developing treatments.
Researchers found a molecular mechanism that regulates careless DNA polymerases, preventing excessive mutations and cancer risk. The p53 and p21 proteins act as supervisors, controlling the careless enzymes' activities.
A new technique called Virtual Histology allows for faster and more accurate analysis of mouse embryos, enabling researchers to focus on abnormalities in development and improve treatment of childhood cancers. This breakthrough may also help improve the safety of household products.
The study found that the protein MBD2 mediates DNA methylation to silence specific genes. This could lead to more targeted approaches to reactivate genes and treat diseases such as sickle-cell anemia and beta-thalassemia, with less risk of unintended side effects.
Researchers at Duke University Medical Center are studying the interaction between genes and environment in promoting cancer. Environmental scientists have identified new culprits in the cancer equation, including chemicals that can damage or mutate genes, and epigenetic alterations that occur without changing a gene's fundamental code.
A study published in Nature Genetics found that precancerous tumors with diverse cell populations are more likely to evolve into cancer. The research suggests that genetic diversity could serve as a biomarker for cancer risk, and may help doctors assess the success of cancer prevention therapies.
Dr. Olopade receives AACR-Minorities in Cancer Research-Jane Cooke Wright Lectureship for her pre-eminent research on breast cancer prevention and detection. Her work has led to strategies for identifying novel BRCA-1 mutations in African-American families.
Scientists Jun-Yi Leu and Andrew Murray evolved yeast populations in the lab to study early stages of speciation. After 36 generations, the evolving population became five times more likely to mate with other evolved cells, suggesting genetic mutations altered mating timing and promoted reproductive isolation.
The Generation Scotland project is a multi-million pound initiative that will follow the health of 50,000 Scots family members over the next generation. The study aims to explore the causes of common diseases and identify those at high risk of developing genetic conditions.
A new lentiviral vector combines multiple gene manipulation techniques to efficiently regulate gene expression in cells. This versatile tool has potential applications in studying human genetic diseases, cancer research, and tissue engineering.
The Vilcek Foundation honors Dr. Massagué's work on controlling cell behavior and its connection to cancer development. The prize recognizes his contributions to the field of cancer biology and genetics.
Researchers found that specific single-nucleotide polymorphisms (SNPs) in the IGF1 gene were linked to an increased risk of prostate cancer, accounting for 10% of cases. The study's findings suggest a biologic effect across different ethnic groups.
A team of scientists has found that artificially increasing the activity of the p53 protein in laboratory mice with a hereditary predisposition for cancer significantly reduces tumor development. The study suggests that giving p53 just enough slack in its leash could help patients avoid developing cancer.
A Mayo Clinic study found that women with a genetic change in the CYP2D6 enzyme are at higher risk of breast cancer relapse when treated with tamoxifen. This genetic variation can also reduce the development of hot flashes, a common side effect of tamoxifen treatment.
UC Davis researchers have discovered a genetic switch, Ku86, involved in cells' response to radiation therapy. The switch, when turned off, enhances the effectiveness of radiation therapy with less toxicity than current radiosensitizing drugs.
A recent study published in The Lancet found that consuming cruciferous vegetables may protect against lung cancer, particularly for individuals with inactive forms of specific genes. The research revealed a 33% protective effect in those with an inactive GSTM1 gene and a 37% effect in those with an inactive GSTT1 gene.
A study found that relatives of women with bilateral breast cancer and a normal CHEK2 gene are at a 23.8% risk by age 80, while those with the faulty variant have a 58.8% risk. Testing for the CHEK2*1100delC mutation in women with family history could be useful for predicting personal risks.
Researchers found a unique molecular signature of fused genes in most prostate cancer tissue samples but not in benign tissue. The discovery could lead to a diagnostic test that detects the fused genes or their protein products, making it more accurate than current screening tests.
A new mouse model has been developed to study secondary malignant neoplasms (SMNs) induced by chemotherapy and radiation in humans. The Nf1 mutant mice model mimics human SMNs, including leukemia, sarcoma, and breast cancers, providing a tractable system for mechanistic studies and testing preventive strategies.
Researchers are studying disease at molecular levels to develop personalized medicine, leveraging the analytical skills of engineers in discovery and understanding biological systems. The goal is to create a quantitative-plus-molecular equation that enables intelligent computing tools to aid diagnosis and treatment planning.
Researchers have discovered that the IGF-1 receptor controls 50% of body size in a non-redundant way, suggesting its potential as a target for cancer treatment. Targeting the IGF-1 receptor may lead to cell death and growth regulation in cancer cells.
A recent study found that 50-94% of colorectal tumors have DNA gene changes, which could indicate a molecular defect. The study also found normal colon mucosa up to 10cm away from the tumor had similar gene changes.
A study of 199 families with multiple cases of breast cancer found that women from these families do not have an increased risk of ovarian cancer. Despite this, the genetic mechanism for up to half of hereditary breast cancer remains unknown, prompting ongoing research at Memorial Sloan Kettering Cancer Center.
Researchers found that cells without genetic predisposition have a lower mutation rate in PIG-A gene, ranging from 1 in 3 million to 1 in 300,000. A new test for the mutation rate could identify individuals at high cancer risk and help prevent or treat it.
Researchers at Oregon State University have made significant breakthroughs in cancer research using zebrafish, a small tropical fish. Studies have proven that zebrafish can be used to test high numbers of possible drug therapies and may lead to new cancer therapies.
Researchers at NIA discover new gene FANCM linked to Fanconi anemia and increased cancer risk. The gene plays crucial role in DNA repair machinery, offering potential targets for treatment.
Acetaldehyde's interaction with polyamines may explain the link between alcohol and certain cancers. Researchers found that polyamines can stimulate the conversion of acetaldehyde into a mutagenic DNA base, increasing cancer risk.
Researchers have developed a new gene identification method using the Sleeping Beauty transposon technology, which inserts itself into or between genes and can activate or inactivate their function. This method allows for more efficient and accurate identification of cancer-causing genes compared to traditional methods.
Researchers used high-resolution DNA scanning to identify regions of chromosomes with genetic errors in lung cancer cells. The study found five new areas with copy-number changes, including deleted and over-copied genes, which could lead to targeted therapies.
Researchers found that the unstructured regions of protein Ets-1 play a crucial role in controlling gene expression, acting like a dimmer switch rather than an on-off switch. The study reveals that phosphorylation affects protein activity by decreasing internal motion and altering gene binding.
A new study found that phenotypic and functional qualities of T cells are associated with the ability to regress large tumors. Naïve and early effector T cells were more effective for tumor treatment than more differentiated T cells. This discovery is important for developing improved adoptive immunotherapy approaches.
Researchers found that early-life exposure to diethylstilbestrol (DES) can increase the incidence of uterine tumors in rats with a genetic predisposition. The study suggests that environmental exposures during development can interact with a preexisting genetic susceptibility to increase disease risk.
A study published in PNAS found that prenatal exposure to diethylstilbestrol (DES) can permanently alter tissue in rats, making them more susceptible to hormone-dependent tumors. The researchers believe this phenomenon could explain why some people with inherited tumor suppressor gene defects develop cancer while others do not.
Scientists have discovered a key genetic mutation that causes a dramatic increase in testicular cancer incidence in mice, suggesting new avenues for understanding the disease's genetic control. The mutation affects RNA editing, which may be used to diagnose at-risk individuals or develop targeted therapeutics.
Researchers found a potential link between testicular cancer and male infertility, suggesting that genetic mutations during fetal development may play a role. The study provides insights into the origins of human testicular cancer, which is a leading cause of cancer in men between 15-39 years old.
Researchers identified chromosome 11q deletion as a significant predictor of high-risk neuroblastoma, with 66% overall survival rate. The deletion removes tumor suppressor gene protective effect, allowing tumor growth.
Researchers have created a mouse model that develops a human-like lymphoma, allowing for testing of new therapies and expansion of cancer research. The study's findings confirm that the BCL6 gene plays a key role in tumor development.
A study comparing human and chimpanzee genomes identified genes involved in sensory perception and spermatogenesis, as well as a strong link between immune defense and positive selection. The authors suggest that an evolutionary arms race may have driven the development of tumor-suppressor and apoptosis genes.
A new $8.9 million research program will utilize powerful computing resources to study the systems regulating cell growth and division, potentially leading to new cancer treatments. Dr. Stuart Kauffman, a renowned theoretical biologist, will lead the program at the University of Calgary.
Researchers found a modest increase in colorectal cancer incidence in families without MMR deficiency, but no increased risk for other malignancies. These findings allow clinicians to provide more accurate and lower-risk information to affected families.
Children with childhood soft tissue sarcomas have a six-fold increased risk of developing a second cancer, with absolute risks estimated at approximately 3% by age 20. The risk is highest within the first five years post-treatment, particularly for females and those treated with radiation or chemotherapy.
Researchers developed a genetic blueprint that predicts response to two chemotherapy drugs and/or radiation therapy in esophageal cancer patients. The study found six gene variants associated with improved survival rates, with certain combinations more effective than others.
A portfolio of 173 genes is differentially expressed in patients with hereditary nonpolyposis colon cancer (HNPCC) treated with celecoxib, suggesting the drug may suppress colon polyp formation and early colon cancer.
The study found that sulindac induced expression of the p21 gene, which suppressed tumor formation even in mice missing key tumor suppressor genes and fed a high-fat diet. The researchers suggest that p21 activation through sulindac offers protection against both genetic and dietary factors contributing to cancer development.