Researchers at The Wistar Institute found that older melanoma patients have a better response to immune checkpoint blockade therapy due to decreased regulatory T cells and increased killer CD8 T cells. Combining anti-PD1 and anti-CD25 treatment may improve response rates in younger patients.
Researchers found targeting telomerase and inhibiting mitochondrial function synergistically killed NRAS-mutant melanoma cells, inducing extensive cell death and DNA damage. Combination therapy also improved survival in a mouse model.
A collaborative effort found that CD32 identifies actively infected cells, not latently infected ones. The study challenges recent results suggesting CD32 as a preferential biomarker to identify HIV reservoirs.
Researchers identified a novel therapeutic vulnerability in NRAS mutant melanoma, using a combination of BET and MEK inhibitors. The combination treatment showed potent anti-tumor effects and prolonged survival in mice with melanoma resistant to targeted therapies and immunotherapies.
Researchers found that soluble antibodies from B cells induce accumulation of myeloid-derived suppressor cells, which inhibit antitumor immune response and worsen cancer outcomes. Targeting antibody production may slow down tumor progression.
Researchers at The Wistar Institute have found that HDAC inhibitors can suppress proliferation and induce programmed cell death in ovarian cancer cells with ARID1A gene mutations. This new treatment approach has therapeutic potential, slowing tumor growth and improving survival rates in mouse models.
A study published in Clinical Cancer Research demonstrated the efficacy of targeting aberrantly active telomerase to treat therapy-resistant melanoma. The research found that a modified telomerase substrate impaired telomere dysfunction and induced cell death in melanoma cells, suggesting a potential therapeutic strategy.
A new study found that phosphorylation of IRE1 regulates its RIDD function, which is critical for antibody production in response to immunization. The research provides deeper understanding of the ER stress response and its implications in various human pathological conditions.
A genetic variant of mutant p53 enhanced mitochondrial function, leading to increased tumor cell metabolism and poorer prognosis for breast cancer patients. The study found that this variant was associated with faster migration and higher ability to invade and metastasize in models of lung and bone metastasis.
Researchers have identified a crucial role for myeloid-derived suppressor cells (MDSCs) in regulating inflammation in newborns. These immature immune cells help control the inflammatory response during the first weeks of life, and their accumulation is linked to milk feeding.
Researchers found a novel combination of PARP and BET inhibitors to be effective in treating ovarian cancers without BRCA1 and BRCA2 gene mutations. The combination resulted in enhanced sensitivity of cells to cell death, offering potential applications in broadening treatment options for various malignancies.
New research reveals how accumulation of chemically modified lipids interferes with the function of a protein involved in antitumor immune responses and effective cancer immunotherapy. The findings point to new strategies for improving the response to immunotherapy.
Researchers discovered a novel form of crosstalk among tumor cells and immune cells that inhibits the effectiveness of immunotherapeutic strategies. Combining CSF-1R inhibitors with selective CXCR2 inhibitors shows significant anti-tumor effects, suggesting new approaches to enhance therapeutic efficacy.
Researchers at The Wistar Institute discovered how the genome's three-dimensional architecture changes during the cell cycle. The study found that condensation and de-condensation occur gradually, with larger domains forming during mitosis.
Kavitha Sarma, a researcher at The Wistar Institute, has been awarded the NIH Director's New Innovator Award for her work on epigenetic regulation and chromatin biology in neurodegeneration and cancer. The $1.5 million grant will support her research efforts to identify new therapeutic targets.
A phase 1 clinical trial demonstrated the safety and ability of a new DNA-based Zika vaccine to elicit an immune response against the virus, with 100% of participants developing Zika-specific antibodies. The vaccine also showed promise in preventing infection in immunocompromised mice.
A study at The Wistar Institute has discovered a slowly proliferating and highly invasive melanoma cell subpopulation that can leave the primary tumor and colonize distant sites. These cells express higher levels of the protein SerpinE2, which plays a critical role in melanoma invasion.
This study identifies the role of tumor-infiltrating B cells in promoting melanoma progression and resistance to therapy. The researchers found that depletion of B cells in the tumor microenvironment shows antitumor activity in patients with advanced metastatic melanoma.
Researchers discovered that promoting T cells to use fat as energy instead of glucose increases their antitumor activity and improves T cell function within tumors. This metabolic shift also enhances the efficacy of immune checkpoint blockade therapy.
Researchers at The Wistar Institute have discovered a novel metastasis suppressor pathway orchestrated by the mitochondrial protein SNPH. This pathway promotes tumor cell proliferation in local growth but inhibits invasion and metastasis. By studying SNPH, scientists may uncover new therapeutic approaches to target metastatic cells.
Researchers at The Wistar Institute have established a correlation between the Wnt signaling pathway and a novel class of autophagy inhibitors in melanoma therapy. High levels of Wnt5A expression are linked to increased autophagy activation, making cells less sensitive to autophagy inhibition.
Researchers at The Wistar Institute have developed a gene-based delivery system that instructs the body to generate therapeutic antibodies against cancer cells. This technology has shown promising results in treating prostate cancer by binding to cancer cells and recruiting immune cells, resulting in tumor shrinkage and improved survival.
Researchers at The Wistar Institute have discovered a potential new therapeutic strategy for ovarian clear cell carcinoma, a difficult-to-treat form of ovarian cancer. By targeting the activity of histone deacetylase 6, a protein that suppresses tumor suppressive functions, they were able to increase apoptosis in tumor cells and reduce...
Entinostat inhibits myeloid derived suppressor cells, leading to enhanced antitumor activity when combined with PD-1 blockade. This preclinical study suggests entinostat may provide an effective combination treatment approach for patients with solid tumors.
A novel DNA-based strategy delivers monoclonal antibodies to protect against highly diverse strains of influenza A and B viruses. The approach holds promise as a simple and economical way to overcome current flu vaccination limitations.
Scientists at The Wistar Institute have identified a new function for ADAR1, which protects cells from dying due to stressors like UV radiation by regulating the response to apoptosis. This discovery sheds light on the role of ADAR1 in postnatal development and disease.
African American women who carry a specific genetic variant of the p53 gene may have a nearly 70% increased risk of developing breast cancer before menopause. The study found an association between the polymorphism and breast cancer risk in premenopausal women, highlighting disparities in cancer research.
A novel DNA vaccine approach targets Wilm's tumor gene 1 (WT1), breaking immune tolerance and inducing robust T cell responses. The vaccine shows promise in generating improved immunity to WT1-expressing cancers, with therapeutic effects observed in mice.
Scientists at The Wistar Institute have identified an anti-aging gene that inhibits a protein involved in metastatic progression and resistance to targeted therapies. Activating this gene with an anti-diabetic drug may provide a promising adjuvant therapy for older melanoma patients.
Scientists at The Wistar Institute have identified a novel protein pathway in mitochondria that controls energy production for cell invasion and metastasis across multiple cancer types. This pathway, previously observed in neurons, has strong clinical implications and represents a potential therapeutic target for several types of cancer.
A DNA-based Zika vaccine generated robust antigen-specific antibody and T cell immune responses that protected against infection, brain damage, and death. The vaccine was also neuroprotective, preventing the disease from spreading to the brain in animal models.
Researchers at The Wistar Institute found TRAP1 increases tumor cell proliferation and invasion while providing a potential new therapeutic target for prostate cancer. TRAP1 overexpression combined with PTEN loss led to aggressive invasive prostate cancer in mice.
Scientists at The Wistar Institute discovered how MEK inhibitor trametinib controls tumor progression by reducing immune suppression and allowing anti-tumor T cells to target tumors. This finding provides new insights into the effects of targeted therapies on antitumor immunity.
Researchers at The Wistar Institute have developed a combination therapy that improves chemoresistance in ovarian cancer. BET inhibitors can suppress ALDH activity, making treatment more effective when used with cisplatin. This approach has shown extended survival rates and delayed tumor growth in mice.
Researchers identified HMGB2 as a critical regulator of cytokine and chemokine expression during senescence, which may have detrimental effects on tumor growth. Silencing HMGB2 suppresses the expression of pro-tumorigenic factors, suggesting potential therapeutic strategies to mitigate negative side effects of senescence.
New research from The Wistar Institute found that estrogen signaling is responsible for immunosuppressive effects in the tumor microenvironment across various cancers. This discovery paves the way for combining anti-estrogen therapy with immunotherapeutic treatments to extend survival in patients.
Researchers at The Wistar Institute discovered that BET inhibitors can suppress PD-L1 activity, a major therapeutic target in various tumors. This approach may reduce side effects while enhancing the immune response against cancer.
Two key protein complexes, condensin and cohesin, play critical roles in organizing chromosomes during cell division. A recent study sheds new light on the specific functions of these proteins, which can help pinpoint the origins of genetic diseases like cancer.
Scientists at The Wistar Institute identified a critical pathway driving tumor adaptation in hypoxic conditions, enabling tumor cells to survive and proliferate despite low oxygen levels. This pathway, involving the protein Akt and PDK1, has implications for glioma treatment and potential therapeutic targets.
Researchers have identified a marker for myeloid-derived suppressor cells (MDSCs) that distinguish them from normal neutrophils. Higher numbers of these cells are associated with larger tumor sizes, suggesting the marker could help predict disease severity and outcome.
Researchers at The Wistar Institute have identified a specific receptor-protein expressed on the surface of ovarian tumor cells, offering a highly targeted therapeutic target for immunotherapy. This technology uses chimeric endocrine receptor-expressing T-cells to selectively eliminate cancerous cells with minimal adverse effects.
Researchers at The Wistar Institute have discovered a specific network of proteins present in the mitochondria of cancer cells that enables their ability to proliferate, migrate, and spread. By targeting this pathway, they believe it may be possible to develop new treatments for various types of tumors
Research shows that aged tumor cells in melanoma are more metastatic and resistant to treatment with targeted therapies due to changes in the microenvironment. Antioxidants, such as N-acetylcysteine, may be a better treatment strategy for older patients.
A novel vaccine strategy has been developed to provide both short-term and long-term protection against the Chikungunya virus. The strategy combines a non-viral, vector-based monoclonal antibody delivery method with a DNA-based vaccine approach.
Researchers identified a single variant in the p53 gene that contributes to increased cancer risk in African-Americans. This variant makes cancer resistant to cell death and may lead to poor prognosis and treatment outcomes.
Researchers found that dozens of targeted therapies inhibit T cell activity, which can help fight tumors. However, pairing these drugs with an IL-15 superagonist stimulates T cell activity, preserving cancer-blocking effects. The study suggests a potential way to overcome immunosuppressive effects while maintaining anti-cancer benefits.
Researchers have discovered a new class of drugs that specifically induce apoptosis in B cell malignancies, such as leukemia and lymphoma. The drugs target the STING protein, which plays a critical role in regulating the immune system, and have been shown to be effective in treating chronic lymphocytic leukemia and multiple myeloma.
A study found that a variant of the p53 tumor suppressor gene is linked to obesity and type 2 diabetes, with mice carrying the variant showing increased weight gain and glucose intolerance. The research suggests that the variant may have evolved in colder climates to promote energy storage, but its modern-day implications are negative.
Researchers at The Wistar Institute found that hypoxia in tumors lowers STAT3 activity, allowing myeloid-derived suppressor cells to differentiate into tumor-associated macrophages. A combination of an experimental STAT3 inhibitor and sialidase showed substantial antitumor activity
Researchers identified Gabra3 as a key driver of metastatic breast cancer progression. The gene promotes cell growth and invasion when activated by RNA editing.