Articles tagged with Cancer Proliferation Genes
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Researchers show that the transcription factor E2F-1 activates both p53 and p73, playing a crucial role in cell death. This finding raises the possibility of using activators of E2F-1 to tip the balance towards apoptosis, potentially leading to new cancer therapies.
Researchers at HHMI discover XRCC4, a new type of genomic caretaker that helps repair double-stranded DNA breaks. In mice without p53, XRCC4-deficient mice survive embryonic development and show normal behavior.
Researchers have identified a protein, Chk2, that activates the tumor suppressor gene p53 to prevent damaged DNA from causing cancer. In Chk2-deficient cells, the brakes on proliferation are released, allowing cancerous cell growth.
Researchers discovered that the PTTG1 gene is highly expressed in colorectal tumors, pre-cancerous polyps, and invasive cancer. The gene appears to play an early role in cancer development, acting as a marker for malignant activity.
Researchers created a DNA microarray called Lymphochip to analyze gene expression in normal and malignant cells, revealing two distinct forms of DLBCL with different clinical outcomes. The study improved diagnosis and treatment of these lymphomas by providing a detailed molecular portrait of the disease.
A University of Pittsburgh-led research team discovered that the gene for gastrin-releasing peptide receptor is more active in women than men, leading to increased cell proliferation and lung cancer growth. Nicotine from cigarettes also stimulates this gene expression, explaining why women are at a higher risk of developing lung cancer...
The researchers created mouse models with benign and malignant NF1-related tumors to study the disease. The studies revealed that neurofibroma tumors invariably include cells lacking the NF1 gene, and that anti-Ras drugs might be useful in treating NF1.
Researchers at Thomas Jefferson University found that a tumor suppressor gene, Rb2/p130, can halt rapid cell growth and prevent smooth muscle cells from building up in arteries. This gene may be used as an adjunct to angioplasty to treat clogged coronary arteries and reduce the risk of restenosis.
Researchers at Vanderbilt University Medical Center have identified a key gene in acute leukemia, suggesting potential new treatments. The study found that the inv(16) translocation collaborates with AML-1 to turn genes off, even when they should be on.
Researchers at Duke University discovered that cancer gene c-Abl triggers the internal framework of cells, building nerve cells and aiding movement. Altering levels of growth factors and Src protein revealed c-Abl's normal function.
Researchers found that losing function of one copy of the PTEN tumor suppressor gene can lead to chronic fatal conditions, including cancer and autoimmune diseases. The study showed that this disruption allows white blood cells to accumulate unchecked and attack their own organs.
Researchers at Whitehead Institute successfully transformed normal human cells into cancer cells, shedding light on the complex process of tumor development. The new cell lines offer a unique window into the biochemical and physiologic changes that occur during cancer formation.
Researchers at UT Southwestern Medical Center found that fluctuations in the hormone Insl3 influence testicular descent in mice, a finding they believe applies to human cryptorchidism. The study also revealed that Insl3 regulates gubernaculum development, leading to underdevelopment and sterility in mice with no Insl3 activity.
A team of scientists, led by Deborah J. Good, has identified a gene called SIL that governs the formation of the left-right body axis during embryonic development. The gene is believed to be crucial in the correct placement of organs such as the heart within the developing organism.
Researchers at UNC-CH discovered three genes crucial to cell survival and protein disposal. The proteins ROC1, ROC2, and APC11 are involved in the ubiquitin ligase enzyme that marks proteins for degradation. Disruption of this mechanism may promote cancer development by driving cells to proliferate uncontrollably.
Researchers at Yale University have successfully inserted a human cancer-suppressing gene into fruit flies, demonstrating a direct link between human and fly tumor suppressor genes. The study reveals that the insects can provide important new insights into human cancers.
Researchers at Johns Hopkins University have linked specific gene mutations to the growth of fatal brain tumors in flies, mirroring human cancer progression. The study's findings suggest that a key signaling pathway may be responsible for tumor growth, offering potential new avenues for cancer treatment.
Researchers have discovered a molecular circuit breaker that prevents uncontrolled cell growth, which could increase the effectiveness of conventional anti-cancer therapy. The protein ARF works as a fuse or circuit breaker, monitoring cell signals and preventing over-stimulation.
Mutations in the beta-catenin gene are frequent in hepatocellular carcinoma, a type of liver cancer. The study found that about 50% of tumors in transgenic mice contained these mutations, and 26% of human liver cancer samples also had similar genetic alterations.
Researchers at Jefferson University have identified a crucial mechanism of the tumor-suppressor protein Fhit, which plays a significant role in preventing cancer development. By understanding how Fhit works, scientists may be able to find ways to interfere with cancer growth and potentially develop new treatments.
Researchers found that when H. pylori attaches to stomach cells with a specific molecule called Leb, it triggers an immune response that can lead to ulcers, inflammation, and increased risk of stomach cancer. The study provides a genetically well-defined model for studying bacterial attachment and its role in disease.
Researchers have discovered a gene called ARF that attaches to and disables the MDM2 protein, helping to protect the body against cancer. This natural mechanism may be manipulated to treat cancer more effectively or detect it earlier.
Researchers at Ohio State University have identified a new category of tumor suppressor genes associated with Peutz-Jeghers syndrome, a rare inherited disorder. The study found that the PJS gene produces a protein kinase enzyme, which is not produced in cancer-causing scenarios.
Researchers at UNC Chapel Hill School of Medicine found that NF-kappa B, a natural protein, teams up with a cancer gene to prevent cell death in tumor cells. The team suggests using new drugs or therapies to turn off or neutralize NF-kappa B to control certain tumors.
A study by Weizmann researchers suggests that a cell-suicide gene called DAP-kinase can prevent metastasis in cancer. The gene's proper functioning is essential for cells to die during different stages of metastasis, and its loss or malfunction can lead to unwanted cell proliferation and tumor development.
Researchers at Thomas Jefferson University found that two missing cancer-suppressor genes play a crucial role in female development, leading to catastrophic cell death. The study suggests that the combination of missing genes is lethal to female mouse embryos, offering new insights into cancer mechanisms and potential therapeutic strat...
Researchers from the University of Wisconsin-Madison have discovered a critical step in cell communication that promotes bone formation, limb growth, and tissue development. The study reveals how the MAD protein regulates gene transcription in response to specific signals.
Researchers at UT Southwestern Medical Center have identified three genes controlling early heart formation, which may lead to new treatments for congenital and adult heart disease. The study found that the absence of these genes can result in cardiac anomalies, highlighting the potential for targeted therapies.
A team from the University of Rochester Cancer Center has identified the protein PP1c that activates the retinoblastoma (RB) gene, a key tumor suppressor. This finding offers a new avenue for controlling cancer cell growth and potentially treating various types of cancer.
Researchers at the University of Maryland School Medicine discovered that mature B cells can re-activate V(D)J recombination, allowing them to produce different antibodies and adapt to new antigens. This finding may help scientists better understand and control the immune system's response to infections.
Researchers have identified a second gene associated with hereditary multiple exostoses, a rare bone disorder characterized by the proliferation of benign tumors. The discovery provides insight into the disease's causes and potential tumor suppressor function.
Researchers identify a molecular 'safety key' that normally regulates cell growth, and discovering how it can be disrupted to trigger cancer. The team found a protein called Abi-2 that fits into the normal enzyme cABL, keeping it turned off, and proposes a new way to treat cancers by targeting this molecular pathway.