Articles tagged with Solid Tumors
Researchers at MD Anderson Cancer Center presented new findings on novel therapeutic approaches, including cell therapy for solid tumors and antibody drug conjugates targeting TROP2. The therapies achieved partial responses in six patients, with an overall response rate of 35.3% and disease control rate of 70.6%.
A new DNA-based test using whole genome sequencing can identify tumour-specific markers to measure cancer levels in children's bodies. This technology has the potential to detect minimal residual disease and change treatment outcomes.
A new study from Penn Medicine demonstrates that RN7SL1, a naturally occurring RNA, can activate the body's own natural T cells to seek out cancer cells that have escaped recognition by CAR T cells. This approach may help improve efforts to treat solid tumors.
Researchers have uncovered a weakness in the key enzyme that solid tumour cancer cells rely on to adapt and survive when oxygen levels are low. Inhibiting this enzyme, called Carbonic Anhydrase IX (CAIX), can effectively stop cancer cell growth.
Researchers at UC San Diego developed a cancer immunotherapy that pairs ultrasound with CAR T-cell therapy to destroy malignant tumors while sparing normal tissue. The therapy significantly slowed down tumor growth in mice and showed minimal on-target, off-tumor side effects.
Researchers have developed a new generation of CAR T cells that safely target and kill solid tumors in mice with mesothelioma, ovarian cancer, and glioblastoma. The 'prime-and-kill' molecular circuits enable specific recognition of tumor antigens on healthy tissues, reducing the risk of side effects.
Researchers at UVA Cancer Center discovered that antibody approaches targeting death receptor-5 could be revived by co-targeting negative biological processes with immune-activating therapy. This combination therapy increased the effectiveness of cancer killer immune cells, shrinking tumors and improving survival in lab mice.
A new study suggests that adding a small molecule to CAR-T cell therapy can boost the effectiveness of immunotherapy against breast cancer and other solid tumors. Researchers found that the addition of cGAMP activated an immune response, leading to enhanced T cell proliferation and tumor growth reduction.
Researchers successfully combined two immunotherapies to target and eliminate difficult-to-treat solid tumors. The combination showed a powerful, synergistic effect, leading to prolonged protective anti-tumor immunity in mice.
Scientists discovered genes with decreased expression in individuals with Down syndrome, which may also protect people from developing solid tumors. These findings could lead to the development of gene-targeted therapies for both people with Down syndrome and the general population.
The Childhood Solid Tumor Network data portal on St. Jude Cloud provides comprehensive data for studying pediatric solid tumors, accelerating discoveries and novel therapies. The portal offers interactive tools for analyzing genomic sequences, epigenetic data, and preclinical pharmacokinetic reports.
SYNB1891, an engineered E. coli Nissle strain producing cyclic di-AMP, demonstrates anti-tumor activity and generates immunological memory in preclinical models of cancer. The therapy is being evaluated in a Phase 1 clinical trial for patients with advanced solid tumors or lymphoma.
A new Cleveland Clinic study evaluates germline genomic profiles in C-AYA patients with solid tumors, revealing a significant proportion carry heritable cancer-predisposing gene variants. The research highlights the need for genetics evaluation and genetic testing to inform management and treatment options.
Researchers at Kazan Federal University have made significant progress in developing CAR T-cell therapy for solid tumors. The treatment uses genetically modified lymphocytes to target and destroy tumor cells, showing promising results in animal models.
Researchers have engineered immune cells to target solid tumors using a new cancer immunotherapies approach. They found that T cells can be reprogrammed to turn on tumor cells when exposed to high concentrations of transforming growth factor beta, a protein that suppresses the activity of T cells in the tumor environment.
Research conducted at the Irvine Lab at MIT's Koch Institute showed that activation of CAR-T cells in lymph nodes leads to massive CAR-T cell expansion and significant functional improvements. The AMP-CAR-T Platform combines CAR-T therapy with Amphiphile immunotherapies to amplify immune responses and combat solid tumors.
Researchers engineer bacteria to target CD47 on cancer cells, inducing local inflammation and boosting T cell activation. The therapy leads to complete tumor regression and reduced metastasis in mouse models.
Shapiro's comprehensive program in early cancer drug development has provided scientific and clinical direction for multiple investigational agents. His work has contributed to the advancement of several approved drugs, including CDK4/6 inhibitors.
A new RNA-Seq assay detects gene fusions in solid tumor cells with high accuracy, identifying 93% of fusions missed by other techniques. The assay also discovers 18 novel fusions, including 11 previously unknown combinations, which may have clinical significance.
Researchers at the University of Cincinnati discovered a potential new target to enhance T cell infiltration in solid tumors. Targeting the KCa3.1 potassium channel can restore CD8+ T cell migration, suggesting a new therapy option for solid tumor treatment.
Researchers found that nearly half of neuroblastoma samples had gene loss or imbalance in DNA damage response-associated molecules located on chromosome 11. PARP inhibitors, commonly used for ovarian cancer treatment, showed promise as a potential therapeutic approach for targeting childhood cancer.
PharmaMar is conducting a Phase I clinical study to identify the optimal dose of PM14 in patients with advanced solid tumors. The trial aims to assess the safety profile and pharmacokinetics of PM14, with approximately 50 patients forecasted to participate.
The Childhood Solid Tumor Network offers a vast collection of pediatric solid tumor samples, drug-sensitivity data, and related information to researchers worldwide. This resource has significantly expanded scientific resources for pediatric solid tumor research, enabling the study of rare cancers like osteosarcoma and retinoblastoma.
Researchers found that downregulation of the interferon receptor IFNAR1 creates an environment where cancer cells can survive and reproduce unchecked. Modifying immunotherapies by stabilizing IFNAR1 may improve treatment outcomes for solid tumor cancers.
PharmaMar is conducting a Phase I study to determine the recommended dose of PM1183 in Japanese patients, with secondary objectives including safety profile and antitumor activity evaluation. The study focuses on patients born in Japan or with Japanese ancestry affected by solid tumors.
Researchers found that genetically modifying oncolytic viruses to express a junction opening (JO) protein significantly enhances their ability to penetrate and kill malignant epithelial cells. This breakthrough could improve cancer therapy for bulkier solid tumors.
Researchers have eradicated solid tumors in laboratory mice using a novel combination of two targeted agents that stimulate an immune response. This approach allows the patient's own tumor to act as a cancer vaccine, differing from traditional methods where the immune system is stimulated by administering a vaccine.
BIND-014, a PSMA-targeted nanoparticle containing docetaxel, demonstrated anti-tumor activity in 28 patients with advanced or metastatic solid tumors. The Phase 1 trial showed encouraging signs of effectiveness, including one complete response and five patients with stable disease.
BIND-014, a targeted docetaxel Accurin candidate, demonstrated encouraging anti-tumor activity and was well-tolerated in 28 heavily-pretreated patients with advanced or metastatic solid tumors. The Phase 1 results established the maximum tolerated dose of 60 mg/m2 and showed signs of stable disease lasting at least four cycles.
Researchers at MGH have identified components responsible for therapy-blocking solid stress and suggest therapeutic strategies. By measuring solid stress in tumor tissues, they found that inhibition of fibroblast growth can reduce solid stress and open up compressed blood vessels, improving treatment outcomes.
Researchers have discovered a compound, ABT-737, that sensitizes hypoxic cancer cells to apoptosis. This compound synergizes with conventional chemotherapeutic agents in tumor-bearing mice, suggesting improved treatment of solid tumors.
Researchers identified signaling molecules linked to B cell actions and solid tumor growth, suggesting a previously used lymphoma treatment may be effective against other solid tumors. The discovery opens up new therapeutic targets and combinations of chemotherapy with immune system-modifying drugs.
Researchers found that solid tumor cells can adapt to chemotherapy and radiation by increasing a regulatory factor called HIF1, which drives oxygen production and growth. Blocking HIF1 may provide a clear mechanism for killing resistant tumor cells.
A report calls for improved monoclonal antibodies against solid tumors, as only 25 percent of approved therapies target these cancers. Researchers suggest manipulating the physical properties of a monoclonal antibody to improve treatment outcomes.
Researchers identify optimal T cell selection and preparation strategies for adoptive immunotherapy approaches to treat tumors. Naive and early effector T cells are more effective than differentiated T cells in causing regression of large, established melanomas.
Researchers at Lund University have discovered that the same genetic mechanism is responsible for developing both leukemia and solid tumors, contrary to previous assumptions. This finding has significant implications for treatment strategies, as it may lead to more effective medicines targeting specific fusion proteins.
The European Society for Medical Oncology survey found that stem cell transplants for breast cancer decreased from 2,629 in 1997 to 330 in 2002. The use of autologous transplants continued to rise for certain types of solid tumours, while allogenic transplants saw a slight increase, particularly for metastatic tumours.