Research on the biology of tumor cells. Covers tumor spread, cell-particle diagnostics, new anti-tumor molecules, and cancer-killing immune cells.
Researchers at Ohio State University have identified a novel lung-cancer tumor-suppressor gene, TCF21, which is silenced through DNA methylation. The study suggests that reactivating this gene may provide a new strategy for treating cancers, and the findings could lead to improved early detection methods for lung cancer.
Researchers at Vanderbilt-Ingram Cancer Center have identified a crucial link between the CXCR4 receptor and the invasion of glioblastoma, a type of aggressive brain tumor. By inhibiting this receptor, experts hope to develop new treatments to prevent cancerous cells from spreading to other organs.
Bcl-3 is activated by DNA damage and required for p53 control of Hdm2 gene expression. Constitutive Bcl-3 expression subverts normal p53 regulation, leading to oncogenic potential.
Tumor cells that border normal tissue exhibit distinct behavior, losing surface proteins and gaining the ability to dissolve matrix surrounding cells. This change signals activation of proteins allowing tumor cells to migrate, posing a risk for metastasis. The discovery highlights the importance of tumor environment in cancer progression.
Researchers found that combining trastuzumab, an antibody targeting HER2 protein, with immune-stimulating agents like IL-12 can activate the immune system to attack tumor cells more effectively. This combination may improve treatment outcomes for breast cancer patients.
Researchers have identified a gene called caspase 8 that plays a crucial role in preventing tumor cells from metastasizing, or spreading to distant sites. By activating this mechanism, the researchers aim to develop targeted therapies to halt the spread of neuroblastoma and possibly other cancers.
Researchers found that cancer cells can signal surrounding tissue cells to alter their molecular composition, promoting tumor growth and proliferation. The study suggests that cell mutations that promote cancer progression may arise in non-cancerous cells, indicating a need for broader anti-tumor therapies.
Columbia University researchers found that stem and progenitor cells are deficient in a quality control checkpoint, leading to chromosomal defects. This deficiency may explain how cancer stem cells arise from normal cells and acquire mutations that increase tumor malignancy.
Researchers found L1 in large quantities exclusively in aggressive colon cancer cells, enabling them to invade and metastasize more effectively. The discovery may have important implications for diagnosing colon cancer and designing new therapies.
Cancer cells hybridize with macrophages to exhibit traits such as migration and blood supply formation. The study provides new insights into metastasis, a process previously attributed to tumor cell fusion.
Researchers developed a treatment that targets glioblastoma cells using epidermal growth factor receptors (EGFR), eliminating tumors in mice implanted with human brain cancer cells. The therapy showed no evidence of recurrence and remained effective for over a year, offering new hope for GBM patients.
Researchers at Duke University Medical Center successfully tested eliminating CD25-expressing regulatory T cells using immunotoxin DAB389IL-2. This strategy improved tumor-specific T cell responses in cancer patients, enhancing vaccine efficacy.
Researchers at UF have discovered a population of stem cells with characteristics of adult and embryonic stem cells in cultures derived from bone tumor biopsies. These findings suggest that osteosarcoma, a common bone malignancy in children, may be linked to primitive stem cells.
Researchers have developed an immune-boosting vaccine that combines with surgery and chemotherapy to treat pancreatic cancer. Early results show improved survival rates, surpassing previous studies, and the team hopes to refine the vaccine's targets through further analysis.
Researchers found that vasostatin, a protein gene incorporated into an adenovirus vector, effectively blocks the formation of new blood vessels and curbs tumour growth in mice with pancreatic cancer. This approach may represent a promising therapeutic option for malignancy with a poor prognosis.
A recent study at Cold Spring Harbor Laboratory found that certain viral infections may cause cancer by fusing cells, leading to aneuploidy and potentially tumor formation. The researchers discovered that specific gene mutations in human cells can make them more susceptible to this process.
Researchers have discovered that sphingosine kinases SphK1 and SphK2 have opposing roles in regulating ceramide biosynthesis, with SphK2 potentially sensitizing cancer cells to chemotherapy. This finding may lead to the development of more effective chemotherapeutic agents targeting specific sphingosine kinase without affecting others.
Researchers have discovered a novel treatment target in the protein EphA2, which plays a major role in the progression of brain tumors. The inactive form of this protein aids in cancer cell survival and spread.
Researchers found that cells with double genomes are more prone to generating tumors in mice, and these tumors show genomic instability similar to many human cancers. Inaccurate chromosome segregation can also lead to the formation of tetraploid cells, which contribute to cancer development.
New research confirms a century-old theory that genetic instability caused by duplicate genomes can lead to tumor formation. The study found that cells with extra chromosomes and centrosomes are more likely to become malignant, making them vulnerable to certain cancer treatments.
A Penn research team found that Snail promotes breast cancer recurrence by inducing changes in tumor cell shape and gene expression. High Snail expression predicts rapid tumor recurrence in women treated for breast cancer.
Researchers at Temple University have found a link between the Rb2/P130 gene and lung cancer, with epigenetic activity causing the gene to be silenced. A simple genetic test could identify cancerous or pre-cancerous conditions using this epigenetic state.
eEF1A2 protein is moderately to highly expressed in two-thirds of breast tumor cells, with significant over-expression in estrogen receptor-positive tumors. The protein's role in breast tumour development remains unclear, but may be related to its function in protein synthesis or cytoskeletal remodelling.
Researchers at Stanford Medicine identified unique patterns of immune cells in breast cancer patients' lymph nodes that predict clinical outcome and can identify tumor spread. The study found that immune changes within these lymph nodes predicted clinical outcome even better than their tumor invasion status.
Researchers have identified a new strategy to turn off the function of CD4+ regulatory T cells, which suppress immune responses to tumors and infectious diseases. This approach could lead to enhanced anti-tumor immunity and boost response to cancer vaccines.
Researchers at Dartmouth's Geisel School of Medicine have discovered that two kinases, CaMKKα and CaMKKβ, can regulate AMPK independent of LKB1, potentially offering new opportunities for cancer treatment. This finding may also contribute to the development of treatments for type 2 diabetes and obesity.
Researchers found that HIF-1 inhibition impacts tumor biology differently depending on the local environment, with proximal cells less affected. This study suggests optimizing HIF-1 blockade to maximize effects on vasculature and minimize effects on distal tumor cells.
Researchers found that tumor cells can stimulate blood vessel growth by activating the MAPK pathway and inducing Notch ligand Jagged1, which promotes formation of new vessels. This interplay between tumor cells and blood vessel cells supports tumor growth and progression.
Researchers discovered that tumor cells physically attach to a protein displayed on the surfaces of endothelial cells, triggering angiogenesis. The finding suggests a new anti-angiogenic strategy by blocking both secreted molecules and cell-to-cell contact.
Researchers found that tumor cells use jagged1 protein to interact with endothelial cells, prompting angiogenesis and tumor growth. This discovery could lead to a two-pronged approach to treat cancer by blocking protein secretion and cell contact.
Resistant tumor cells can be sensitized to ONYX-015 replication by inducing a heat shock response, which could greatly augment the therapy's clinical utility. This study suggests that clinical strategies focusing on tumor-selective replication would favor the use of ONYX-015.
Researchers found that cells with damaged DNA trigger a mechanism to signal natural killer cells, which attack and destroy cancerous cells. The immune system's ability to identify cancer cells is crucial in preventing tumor growth.
Increased expression of claudin-1 has been found in human primary colon carcinomas and metastases. Claudin-1's mislocalization is associated with higher levels of expression and increased metastatic behavior in colon cancer cells.
Researchers have identified a novel type of lung cell that can divide into fresh copies and specialized types, suggesting these cells may contribute to the development of most common lung cancers. The discovery could lead to earlier diagnosis and potentially more effective treatments for lung cancer.
Researchers discovered that EGFR interacts with STAT3 in the cell nucleus, leading to increased expression of inducible nitric oxide synthase (iNOS) and a new transcriptional mechanism in human cancers. This interaction provides a potential target for anticancer therapies against EGFR, STAT3, and iNOS/NO.
Researchers found that a vaccine targeting TRP-2 improves chemotherapy sensitivity in brain tumors. The study showed significant improvements in patient survival and tumor response rates compared to conventional treatments.
Researchers study natural products that may prevent certain cancers. Propolis and turmeric, rich in plant polyphenolic compounds, exhibit potent antitumor activities, protecting mice against radiation-induced inflammation and rats against chemotherapy-induced heart muscle damage.
A study published in the Journal of Clinical Investigation has identified a new protein called SPARC that plays a crucial role in tumor therapy resistance. The researchers found that restoring SPARC expression in resistant cells improved their sensitivity to chemotherapy, suggesting potential therapeutic applications.
A Medical College of Georgia researcher has developed a mouse model to study the immune system's initial response to cancer. The goal is to understand how the body decides which cancer cells to attack and which to ignore, in hopes of developing new treatments that utilize the body's natural defenses.
Researchers have developed a novel delivery system that uses siRNA to silence the growth-promoting gene EWS-FLI1 in tumor cells, effectively inhibiting cell replication by 80%. The nanoparticles are designed to target specific tumor sites and avoid degradation, making them a promising treatment option for Ewing's sarcoma.
A University of Central Florida researcher has discovered a protein called MKRN1 that promotes the destruction of telomerase, an enzyme that enables rapid cell division. The study suggests that MKRN1 could be a critical component in preventing cancer cells from replicating uncontrollably.
Researchers have discovered a new treatment that uses a chemical to prevent PARP repair, making recombination essential for cancer cell growth. This approach shows promise as a potential breakthrough for women with hereditary breast cancer.
Researchers have identified a previously unknown protein called Fra-1 that controls cancer cells' malignant characteristics and spread to healthy tissue. The discovery, made in glioblastoma brain tumors, suggests new treatment possibilities for multiple cancers.
Researchers at The Wistar Institute found that an initiating genetic error can lead to relentless cell division, causing DNA replication stress and breaks. This stress creates conditions for tumor progression and the accumulation of mutant genes, ultimately leading to cancer.
A new cancer test uses the physical strength of each cell to diagnose and stage cancer, reducing the need for biopsies and potentially saving lives. The 'optical stretcher' can detect cancer in as few as 50 cells, allowing for early diagnosis and treatment.
USC researchers found that the BRCA1 gene disrupts interactions between different cell types, leading to ovarian cancer. The gene's indirect action may lead to new treatment options by targeting a biochemical mediator.
Researchers discover ON01910, a non-ATP-competitive small molecule inhibitor of Plk1, arrests cell division in human cancer cells and inhibits a variety of tumors. Clinical studies are currently underway to determine the best way to utilize this potent anticancer agent.
Researchers discovered a compound called STA-21 that blocks a key protein, Stat3, in breast cancer cells. This inhibition leads to the death of cancer cells and may increase effectiveness of chemotherapy while reducing treatment toxicity.
Researchers discover viral DNA sequence in MMTV Env protein that transforms mouse breast cells. The study suggests a potential new mechanism for virus-induced breast cell transformation.
Researchers successfully redirected human immune cells to target and kill cancer cells by introducing a specific gene that allows for high-affinity recognition of tumor-associated p53. This breakthrough approach holds promise for a novel, broad-spectrum immunotherapy for malignant diseases.
Research reveals that cancer cells can become resistant to treatment by acquiring P-glycoprotein from neighboring cells, rendering chemotherapy ineffective. This phenomenon has significant implications for tumor behavior and genomic analysis, highlighting the potential benefits of studying protein transfer between cells in tumors.
Researchers aim to understand the growth and spread of breast cancer by targeting tumor stem cells, which are hypothesized to perpetuate cancer growth. The project may lead to a critical adjunct therapy targeting these cells.
Researchers at University of Pittsburgh Medical Center found that overexpression of protein NuMA can cause changes in a cell associated with tumor formation. By studying the mechanism by which this occurs, the team identified a possible treatment target for some types of cancer.
Scientists have discovered a new gene, Bnip3L, that helps p53 eliminate cancer cells under low-oxygen conditions. Silencing this gene allows tumors to grow more aggressively in hypoxic environments.
Researchers at Cincinnati University and the University of Munich have identified a novel oncogene in papillary thyroid cancer cases among Chernobyl residents. This oncogene resulted from fusion of part of the AKAP9 gene with one end of the BRAF gene, leading to uncontrolled cell division and transformation into malignant tumor cells.
Researchers have identified a subset of tumor cells that resist inhibition of the Hedgehog signaling pathway, leading to cancer recurrence. However, targeting these residual cell populations could lead to effective treatment of basal cell carcinoma.
Researchers have discovered a new gene, 15-PGDH, that acts as an antagonist to control the enzyme COX-2, a major early event in human colon tumors. The study found that 15-PGDH is directly controlled and activated by TGF-beta, and its presence can suppress COX-2 activity, potentially leading to tumor development without it.
A recent study suggests that Akt3 protein is key to melanoma's resistance to chemotherapy, promoting tumor cell survival and development in 43-60% of non-inherited melanomas. Lowering Akt3 activity can reduce tumor-creating potential and make cancer cells more susceptible to signals inducing apoptosis.
Researchers at Scripps Research Institute use a class of compounds known as Src kinase inhibitors to stabilize blood vessels and block tumor cell metastasis. By increasing the protective barrier strength of host blood vessels, the approach prevents cancer cells from exiting the bloodstream, making them vulnerable to immune system attack.
Researchers have developed core/shell nanogels that can target cancer cells using folic acid, a nutrient that cancer cells absorb more than healthy cells. The nanoparticles can be heated to kill cancer cells, but applying targeted heat sources like ultrasound can spare healthy cells.