Articles tagged with Cancer Genetics
A USC study in Nature Genetics finds genes silenced by Polycomb proteins are more likely to be methylated in cancers, supporting a stem cell origin of cancer. The research also shows that epigenetic alterations precede genetic events in cancer development.
A study published in Nature found that mice lacking a critical gene for repairing damaged DNA grow old rapidly and exhibit physical and genetic changes similar to those of normal-aged mice. The researchers discovered a new type of human progeria, a rare inherited disease characterized by accelerated aging.
Researchers with Bank On A Cure identified genetic pathways associated with venous thromboembolisms in patients treated with thalidomide for multiple myeloma. These findings may lead to screenings and tailored interventions to prevent blood clots, as well as the development of new treatments.
The study presents positive interim results of using ALDESORT to isolate cord blood stem cells, showing improved overall survival at 90.9% compared to a historical control group. The infusion of cells enriched with ALDESORT appears to improve the speed and efficacy of cord blood transplantations.
Scientists have identified nine new genetic mutations in cancer cells that make patients more likely to respond to bortezomib, a common multiple myeloma treatment. These findings may help physicians tailor treatment to individual patients, increasing the effectiveness of the drug.
A new genetic theory suggests that certain offspring characteristics can only be explained by genetic cooperation between maternal and paternal genes. This challenges the prevailing view of a parental power struggle, instead proposing that positive interactions between mothers and their offspring drive imprinting patterns.
A new study aims to uncover the causes of the testicular cancer increase among 15-35 year old Caucasian men. The research will examine environmental hormone disruptors and genetic susceptibility as potential risk factors.
The Ludwig Fund has given a record-breaking $120 million to support cancer research at six top US institutions. The fund will provide annual research grants of approximately $2 million per center in perpetuity.
A systematic review found no consistent evidence linking dietary folate intake to breast cancer risk. The review also did not find a significant association between a common genetic variation in the MTHFR gene and breast cancer risk.
The Ludwig Institute has expended over $1.1 billion in cancer research since its inception, and the new gift will ensure annual research funds of approximately $2 million per center. The six US institutions will collaborate on a powerful force in cancer research.
Scientists discover plant-derived triterpenoids and rexinoid LG100268 significantly reduce tumor growth in mice, offering potential future chemoprevention methods. The compounds inhibit inflammation and induce apoptosis in human lung cancer cells, presenting a promising avenue for preventing lung cancer.
Inhibiting cyclin D1, a gene present in excessive amounts in half of breast cancers, improves cell-killing effects of radiation. Flavopiridol was found to add to ionizing radiation's effects without toxicity, using zebrafish models.
Researchers developed a novel method to produce small chemicals from symbiotic bacteria found in sea squirts, which have anticancer properties. The ability to manipulate these chemicals using genetic pathways opens possibilities for developing new cancer and HIV treatments.
A study found that obese smokers have a 3.5 to 5 times increased risk of death compared to those of normal weight who never smoke. The study also revealed that being a current smoker is a stronger risk factor for cancer death than obesity.
A study pooled data from over 20 groups conducting breast cancer research, identifying 16 single nucleotide polymorphisms (SNPs) that may be linked to breast cancer risk. The authors found that five SNPs showed borderline statistical significance and could contribute to breast cancer incidence.
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.
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.
A new prediction model, MMRpro, assesses a person's probability of carrying a particular defect in mismatch repair genes, which predisposes families to colorectal cancer. The study found that MMRpro outperformed existing assessment tools in identifying mutation carriers and predicting colon cancer 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 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 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 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.
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 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.
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.