A precursor of cholesterol, previously categorised as harmful, can protect cancer cells from cell death. This finding, published in Nature, opens new doors for cancer research.
Breast cancer is the most common cancer in women. The development of breast cancer often originates from epithelial cells in the mammary gland – the very cells that specialise in milk production during and after pregnancy. A team of researchers from Friedrich Schiller University Jena (Germany), the university in Shenzhen (China) and Jena University Hospital (Germany) has taken a closer look at this specialisation process and deciphered a molecular mechanism that also appears to play an important role in cancer development. It may be possible to develop new diagnostic procedures and treatment methods for breast cancer based on these research findings.
Deceiving cancer to facilitate treatment The effect of the phenotypic plasticity of cancer cells and how to exploit it
Cancer cells are notorious for rapidly changing their phenotype, driving within-host spread and evading treatment. Scientists in Plön used a mathematical model to understand the role of a signal used by cancer cells to control their phenotype. By manipulating these signals, cancer cells can be tricked into a less harmful phenotype that is more responsive to treatments.
A research team at Helmholtz Munich revealed a specific mechanism that is able to promote cell death in cancer cells by pharmacological targeting of a ferroptosis surveillance system.
A team of researchers led by Dr. Marcus Conrad from Helmholtz Munich discovered a novel anti-cancer drug, called icFSP1, which sensitizes cancer cells to ferroptosis.
An interdisciplinary team of researchers at the Otto-von-Guericke University in Magdeburg has gained new insights into how inflammatory mediators of pathogen defense can remotely drive cancer cells into death – an important contribution to improving cancer immunotherapies.
How do the nerve cells in our brain communicate with each other? What processes take place when T cells render cancer cells harmless? Details of the mechanisms at the cellular level remain hidden from view. Now, special reporter proteins developed by a research team led by the Technical University of Munich (TUM) may help unveil these mechanisms.
Resistance to HER2-targeted therapies can be a problem when treating patients with HER2-positive (HER2+) breast cancer. Therefore, the identification of new therapies for this patient group is important. Researchers at the Leibniz Research Centre for Working Environments and Human Factors in Dortmund (IfADo) have already shown that the enzyme EDI3 is associated with changes in the metabolism of cancer cells. Their most recent results reveal that inhibiting EDI3 may be a new therapeutic target in patients with therapy-resistant ER-HER2+ breast cancer.
Researchers at Georg-Speyer-Haus and Goethe University Frankfurt have discovered a new mechanism that explains why only some of the cells in a colon tumour respond to chemotherapy. The research team led by Professor Florian Greten was able to establish that tumour cells dying off during chemotherapy communicate one last time with neighbouring tumour cells to give them instructions on how to resist the therapy. The dying cells re-programme the signalling cascades in the neighbouring tumour cells in such a way that these are no longer vulnerable to chemotherapy. By doing so, the dying cells literally ensure that the tumour survives.
New insights into tumour biology: Cancer cells adopt hitherto unknown state to facilitate metastasis
The ancient Egyptians, as described in the Ebers Papyrus, already knew that palpation –feeling for hardened lumps – can help diagnose breast cancer. Palpation is still an important element in early screening for breast cancer. On the other hand, measurements on individual cancer cells show that they are softer than the healthy epithelial cells from which they stem, which probably makes them better able to metastasise in dense human tissue. An international collaborative project led by the Soft Matter Physics Division at Leipzig University got to the bottom of this apparent paradox and has now published its findings in the renowned journal Nature Physics.
Bacteria promote cancer metastasis by bolstering the strength of host cells against mechanical stress in the bloodstream, promoting cell survival during tumor progression, researchers report.
Searching for ways to extend the survival benefit of targeted therapies, a team led by researchers has identified a potential new tactic to disrupt the repair mechanism that cancer cells use after treatment, blunting their ability to regenerate. The approach could present a new treatment strategy.
With help from the best tweezers in the world a team of researchers has shed new light on a fundamental mechanism in all living cells that helps them explore their surroundings and even invade tissue. Their discovery could have implications for research into cancer, neurological disorders and much else.
The findings of a new study suggest that a ketogenic diet — which is low in carbohydrates and protein, but high in fat — helps to kill pancreatic cancer cells when combined with a triple-drug therapy. In laboratory experiments, the ketogenic diet decreased glucose (sugar) levels in the tumor, suggesting the diet helped starve the cancer. In addition, this diet elevated ketone bodies produced by the liver, which put additional stress on the cancer cells.
Metastases in cancer are often caused by a few abnormal cells. These behave more aggressively than the other cancer cells in a tumor. Researchers are now on a method to detect these cells.
Researchers have genetically engineered a microbial encapsulation system for therapeutic bacteria that can hide them from immune systems, enabling them to reach tumors more effectively and kill cancer cells in mice.
Both nanomedicines and metronomic scheduling — when medications are given at lower, more frequent doses — can correct abnormalities surrounding tumors that help protect cancer cells and foster their growth and spread. Combining nanomedicines and metronomic scheduling may help improve cancer treatment strategies.
Amyloid beta, a protein known to build-up in the brains of Alzheimer’s patients, also helps skin cancer cells thrive when they spread to the brain, a new study finds.
Squeezing through tight spaces makes cancer cells more aggressive and helps them evade cell death, shows a new study.
Researchers found that some cancer cells weave a deactivating signal into a protective coat of armor, immobilizing and excluding T cells that would otherwise kill them. This immune deactivation pathway offers a promising new therapeutic approach for pancreatic, breast, and colorectal cancers.
Nanomaterials have revolutionized the world of cancer therapy, and plant-derived nanoparticles have the added advantage of being cost-effective and easy to mass produce. Researchers have recently developed novel corn-derived bionanoparticles for targeting cancer cells directly, via an immune mechanism. The results are encouraging, and the technique has demonstrated efficacy in treating tumor-bearing laboratory mice. Moreover, no serious adverse effects have been reported in mice so far.
When tumors spread, cancer cells migrate to other parts of the body through the blood or lymphatic vessels. Scientists have now found a new protein that prevents cancer cells from doing so by making them stick more tightly to their surroundings. Their findings could in the future help doctors determine the aggressiveness of a tumor and fine-tune the therapy.
In many mammals including humans, the placenta invades the wall of the uterus during pregnancy in the same way that cancer cells invade surrounding tissues. Using genomic sequences and gene expression information, researchers were able to predict specific signaling proteins that drive the expression of genes that decrease the susceptibility of invasion in human cells. Using a custom fabricated bio chip, the researchers confirmed that these predicted proteins did in fact decrease the invasion of both cancer and placental cells.
Hyaluronic acid, or HA, is a known presence in pancreatic tumors, but a new study shows that hyaluronic acid also acts as food to the cancer cells. These findings provide insight into how pancreatic cancer cells grow and indicate new possibilities to treat them.