Research on the biology of tumor cells. Covers tumor spread, cell-particle diagnostics, new anti-tumor molecules, and cancer-killing immune cells.
Scientists have created a novel type of immune system cell called Induced T to Natural Killer Cells (ITNK cells) that can kill cancer cells in lab tests and mouse models. These reprogrammed killer cells are more efficient at targeting tumour cells than unmodified Natural Killer cells.
Researchers found that high interleukin-10 levels in tumor cells are associated with worse prognosis after autologous melanoma cell vaccine treatment. High IL-10 levels can downregulate the immune response, decreasing the effectiveness of the vaccine.
Researchers found that blocking a receptor thought to mediate cell suicide in normal cells paradoxically stopped tumor growth. The study suggests using a drug that blocks the receptor to treat cancer. Further research will explore how this receptor promotes tumor growth and develop new therapies.
Two teams of researchers identified biomarkers that predict excellent graft function in kidney transplant recipients who stop taking immunosuppressive drugs. A molecular signature indicative of future organ failure was also found. The signatures may help physicians design personalized treatment regimens for kidney transplant recipients.
Melanoma cells can self-renew and induce new tumors, defying the traditional cancer stem cell model. Targeting both bulk tumor cells and slow-growing JARID1B-positive subpopulations is proposed as a dual therapy to combat therapy resistance.
Researchers have developed a powerful new technique for analyzing genome data from single tumor cells. The breakthrough allows scientists to study the biology of tumor development and identify dangerous cells in small samples. By profiling individual cells, researchers can understand genetic changes that occur as cancer progresses.
Researchers at the University of Kentucky Markey Cancer Center have discovered a key molecular mechanism behind breast tumor cell spread. The finding focuses on Snail's interaction with LSD1 enzyme, which regulates DNA structure and shuts down E-cadherin gene expression, leading to metastasis.
Researchers have found that parvoviruses can completely regress malignant brain tumors in rats and human gliomas. The viruses target cancer cells without affecting healthy tissue, making them a potential new approach to treating glioblastoma.
A new study has found that genetically short-circuiting the ability of cancer stem cells to absorb a key nutrient can kill many colon cancer cells. The approach targets tumor cell 'factories' and could potentially reduce recurrence rates of colon cancer. However, further research is needed to ensure the treatment does not harm normal s...
Cancer cells require actin, microtubules, and intermediate filaments to break through the basement membrane and escape. The study found that these components collaborate in a specific order to facilitate metastasis.
Researchers at Fox Chase Cancer Center have isolated an engineered antibody, GS45, that targets the Müllerian Inhibiting Substance Type II Receptor on ovarian cancer cells. This unique target is scarce in normal tissue, reducing the risk of side effects associated with traditional targeted therapies.
Researchers found that the Retinoblastoma protein targets DNA replication genes during cellular senescence, preventing cancer cells from replicating. This mechanism is crucial for tumor suppression, and its disruption can lead to genomic instability and malignant tumors.
Scientists have discovered that residual glioblastoma cells have different properties than those found in the tumor mass, making them more mobile and resistant to treatment. This breakthrough could lead to new therapeutic approaches against this aggressive brain cancer.
Researchers found that stress-activated protein protects fugitive ovarian cancer cells from programmed death, allowing them to escape the primary tumor and metastasize. The study suggests that restoring cancer cells' vulnerability to anoikis could suppress tumor growth and metastasis.
Researchers developed a combinatorial approach using viruses to destroy tumors, which was shown to provide substantial regression and cure of tumors in mice. By targeting tumor blood vessels, this approach could potentially treat a wide range of cancers, offering new hope for cancer treatment.
A new microchip-based device enhances rapid and comprehensive analysis of circulating tumor cells, revealing key biological properties. The improved system allows for better monitoring of prostate cancer treatment responses.
Researchers identify Decapentaplegic protein as key player in cell migration, found in healthy Drosophila melanogaster cells. The protein triggers cell mobility and invasion, benefiting metastasis.
Researchers have discovered that blocking Mcl-1, a protein inhibiting Bak activation, enables TRAIL to activate Bak and kill resistant tumor cells. This strategy has potential for improving the efficacy of anti-cancer treatment.
Scientists at Dana-Farber Cancer Institute have developed a laboratory technique that more closely simulates the real-world conditions in which tumor cells mingle with normal cells, improving the accuracy of anti-cancer drug screenings. This new 'cell-specific in vitro bioluminescence imaging' (CS-BLI) technique can identify compounds ...
A new study suggests that stimulating human lung cancer cells with TLR7 or TLR8 agonists can lead to increased tumor cell survival and resistance to chemotherapy. This approach is being investigated as an adjuvant for anticancer immunotherapies, but caution should be exercised due to these potential risks.
Researchers have identified a potential therapeutic target for brain cancer, the A20 protein, which is highly expressed in glioblastoma stem cells. Decreasing levels of A20 in these cells reduces their growth and induces cell death, increasing survival rates in animal models.
A team of scientists is researching self-cannibalizing cancer cells to develop new therapies. Cancer cells can stop proliferating and consume themselves when stressed, allowing them to survive enormous amounts of stress.
Researchers found that tumor suppressor p53 limits the growth of cells with incorrect numbers of chromosomes and prevents their progression toward cancer. Cells lacking p53 become aneuploid after induced missegregation, indicating that the p53 pathway normally serves to limit the propagation of cells with odd numbers of chromosomes.
Researchers discovered that distinct cancer-causing mutations in neighboring cells can cooperate to promote tumorigenesis. The study found that the genetic cooperation occurs through a signaling pathway that activates cellular proliferation and stress response pathways.
Yale researchers found that cancer-causing mutations can cooperate to promote tumor development even when located in different cells within a tissue. Stress conditions like wounds can trigger cancer formation by activating signaling process JNK.
Researchers at Purdue University have developed nanoprobes that deliver cancer drugs directly to tumor cells, reducing damage to healthy cells. The nanoprobes mimic the natural delivery system of endosomes and can track their distribution within cells.
MIT chemists develop a new platinum compound called mitaplatin that selectively destroys tumor cells while leaving normal cells intact. The compound combines cisplatin and dichloroacetate to target cancer cells' altered mitochondrial properties.
A new study from Cold Spring Harbor Laboratory has found that certain types of aggressive tumors lacking p53 protein can be stopped in their tracks when TAp63, a sister protein, steps in. Researchers were able to shut off tumor growth by increasing TAp63 levels, which induced senescence and prevented cancer cell division.
A new Notre Dame study provides insights into the molecular basis by which tumor cells modulate their surroundings to favor cancer progression. The research identifies a unique population of microvesicles enriched in proteases, which facilitate tissue breakdown and remodeling at distant sites.
Scientists at MIT have discovered that tumors can arise from different types of cells in the pancreas, depending on whether they are injured or inflamed. This finding could lead to new treatments and early diagnosis methods for pancreatic cancer.
A team of researchers has identified a biochemical signaling pathway that protects normal tissues from radiation damage. Blocking this pathway increases tumor death in mouse experiments, offering hope for new cancer therapies.
A new study published in Nature reveals that the loss of a gene called PTEN from surrounding cells can dramatically alter the tumor environment, fostering tumor growth. The findings suggest a new role for PTEN in suppressing cancer development and could lead to entirely new treatments targeting both cancer cells and their surroundings.
Researchers at the University of Florida have found that inflammation in the colon tissue can trigger the transition from a non-cancerous state to cancer. The study suggests that targeting specific immune system hormones may be a key to preventing or inhibiting cancer growth, with potential implications for diagnostic tests and therapy.
Researchers at Yale University have discovered a novel mechanism that stops cancer cells from growing and dividing. The 'on-off switch' mechanism involves a tiny bit of genetic material that regulates the function of tumor-suppressor proteins, preventing cancer cells from proliferating.
Researchers at University of Iowa have modified siRNA to be injectable into the bloodstream, targeting specific genes overexpressed in cancer cells. The new compound triggers tumor regression without affecting normal tissues.
Researchers at Harvard Medical School found that separated cells lose energy-harvesting ability and eventually starve due to metabolic defects. Increasing antioxidant activity restores metabolic function, allowing cells to use alternative energy sources, raising the possibility of early-stage tumor cell survival.
Researchers at Case Western Reserve University School of Medicine have discovered the prion protein as a novel biomarker for pancreatic cancer. The study found that the prion binds to filamin A in human pancreatic cancer cells, disrupting cell organization and signaling, and leading to aggressive tumor growth.
Researchers found that estrogen temperes the killing activity of cytotoxic T cells through the molecule EBAG9. In its absence, CTLs release more tumor-killing enzymes, making them more effective at attacking cancer cells.
Researchers found stem-like cancer cells that share characteristics with healthy stem cells, including unlimited lifespan and migration properties. These cells were localized in the same tissue location as bladder stem cells and showed increased activity in genes related to cell proliferation and metastasis.
Researchers at the University of Kentucky discovered that tumor-suppressor protein Par-4 is secreted by most human and rodent cells and can target large numbers of cancer cells by binding to receptors on the cell surface.
Researchers at Cedars-Sinai Medical Center have isolated stem-like cells from benign pituitary tumors and shown they can generate new tumors in laboratory mice. The study supports the cancer stem cell hypothesis, suggesting similar mechanisms may be involved in malignant and benign tumor formation.
Researchers at Yale University School of Medicine and the University of California Davis have discovered a protein, PRCP, that regulates appetite suppression by breaking down alpha-MSH in mice. Administration of PRCP inhibitors reduced food intake in both normal and obese mice.
Researchers propose a novel two-agent combination therapy that selectively kills tumors while sparing healthy cells. The approach leverages the frequent absence of methylthioadenosine phosphorylase in various lethal cancers, allowing for increased doses and reduced toxic side effects.
Researchers at Dartmouth Medical School have developed a Trojan horse nanoparticles to target ovarian cancer, reprogramming protective cells into killers. The approach triggers an inflammatory immune response, directly killing tumor cells and potentially complementing current therapies.
Researchers discovered that cancer cells and their neighboring cells share similar structural abnormalities on the nanoscale level, validating the 'field effect.' This finding could lead to early detection of cancer through simple blood or tissue tests.
Researchers discovered that certain carbohydrates on normal cells and enzymes like β3GnT1 function as tumor suppressors. Upregulation of β3GnT1 reduced tumor activity and metastasis in breast and prostate cancers. The study provides new insights into the role of complex carbohydrates in cancer.
Researchers at Cedars-Sinai have developed a novel gene therapy that uses immune cells to target glioblastoma multiforme. A specific biomarker, HMGB1, has been identified as an effective tool to monitor tumor response to this treatment.
A recent study published in Science found that the STAT3 protein plays a key role in converting normal cells to cancerous cells by regulating gene expression in both the cell nucleus and mitochondria. This discovery may lead to the development of targeted cancer therapies.
A study published in Science Express demonstrates the first definitive link between mutations in the DICER1 gene and cancer. Children with pleuropulmonary blastoma carried a mutation in one of their two DICER1 gene copies, which may disrupt normal lung development and communication.
Researchers propose that cancer stem cells could provide an important avenue for controlling cancer if targeted by new treatments. The subpopulation of malignant cells may be the root cause of cancer, offering a potential new approach for therapy.
The Damon Runyon Cancer Research Foundation has awarded prestigious fellowships to 17 outstanding postdoctoral scientists conducting innovative cancer research. The fellows will receive $140,000 each to work on projects aimed at improving cancer treatments and diagnostics.
Scientists at the University of Gothenburg have discovered a 'water gate' in yeast cells that regulates water flow, which may lead to new cancer drugs. The discovery has potential applications in human cancer research and could result in inhibitors for human aquaporins.
Scientists have identified a new approach to detect and treat Peutz-Jeghers syndrome, a rare inherited cancer syndrome, by exploiting tumors' weak spot in glucose metabolism. They found that targeting mTOR pathway with rapamycin can stop tumor growth, offering new treatment options.
A single gene, EBNA1, plays a crucial role in the activation of EBV genes responsible for indiscriminate tumor cell growth. The LSUHSC research team discovered that oxidative stress regulates EBNA1's ability to activate these genes, leading to potential therapeutic approaches using existing treatments like Vitamin K.
Scientists have found that replacing microRNAs in liver cancer cells can be lethal, while leaving healthy cells unaffected. The study used a special delivery virus to introduce the microRNA into mice with liver cancer, resulting in rapid death of tumor cells.
Researchers uncover molecular mechanism that enables tumor cells to attract new blood vessels continuously in the brain, even when oxygen is still abundant. The discovery could provide a basis for therapies targeting activated integrin alpha-vbeta3 to inhibit metastatic brain disease.
PTEN is often inactivated in breast cancer, leading to poor patient outcomes. Researchers found that a drug called perifosine specifically targets the breast cancer stem cell population by inhibiting the Akt pathway, reducing tumor-forming cells by up to 90%.
Researchers successfully engineer MSCs to deliver cancer-killing protein TRAIL, destroying tumor cells while sparing normal cells. In mouse models, the genetically modified stem cells reduced breast and lung cancer growth by up to 80%.
The study found that miR-196a promotes the metastasis of tumors by activating oncogenic pathways, leading to increased lung metastases in animal models. Additionally, high levels of miR-196a were associated with poor patient survival in pancreatic cancer patients.
Researchers have developed a four-in-one agent that can detect, target, and disable tumor cells while also making them visible through MRI and microscopic imaging. The agent uses siRNAs to suppress specific genes in cancer cells, providing a new approach to targeted gene suppression in cancer treatment.