Fast jeder vierte Krebstote hatte einen Hohlorgantumor etwa im Gallengang oder in der Speiseröhre. Ein derartiger Tumor kann meist nicht operativ entfernt werden. Möglich ist nur eine kurzzeitige Öffnung des Hohlorgans mit einem Stent, also einer röhrchenförmigen Prothese. Der Tumor wächst jedoch wieder ein und dringt durch den Stent in das Hohlorgan. Ioana Slabu vom Institut für Angewandte Medizintechnik und Benedict Bauer vom Institut für Textiltechnik haben nun eine neuartige Technologie für die Therapie von Hohlorgan-Tumoren entwickelt, die mit dem zweiten Platz des RWTH Innovation Award 2022 ausgezeichnet wurde

Only one in 100,000 people suffer from a pheochromocytoma, a tumor of the adrenal gland. If the tumor has already metastasized, a radioactive compound can be used to detect malignant cells that have spread to other parts of the body, and to irradiate them from the inside. However, the preparation containing the beta emitter Lutetium-177 can only bind to the tumor if it has sufficient target molecules, which is not always the case. By administering two approved drugs prior to therapy, a research group at the Helmholtz-Zentrum Dresden-Rossendorf (HZDR) has succeeded in increasing the number of target molecules for radionuclide therapy in a mouse model, delaying tumor growth.

Plectonic Biotech, a spin-off of the Technical University of Munich (TUM), has developed a nanoswitch that binds immune cells to tumor cells. The goal is to facilitate the development of immunotherapies that target tumors specifically and have fewer side effects. The German Federal Agency for Disruptive Innovation SPRIND will provide funding for the work of Plectonic Biotech in the coming years.

Proteins that are frequently altered in tumors play a prominent role in cancer research. The protein RFX7, a largely unknown transcription factor, has recently been linked to lymph node cancer. Researchers at the Leibniz Institute on Aging – Fritz Lipmann Institute (FLI) in Jena have now partially elucidated the function of this protein. RFX7 acts as a tumor suppressor and counteracts the development of cancer. Once activated, it induces other tumor suppressors and inhibits important growth regulators. The reactivation of RFX7 could therefore be of substantial interest in future cancer studies.

Non-small cell lung carcinoma is a particularly aggressive type of lung cancer. Tumor cells and tumor DNA (ctDNA) in the blood of patients with the disease can be analyzed by means of liquid biopsy throughout the course of the disease. This information is important in order to be able to target the constantly changing tumor. A study from the University of Bayreuth is the first to show that liquid biopsy significantly improves treatment outcomes in many cases and can be cost-effective in the German care system. The scientists present their research results in the Journal of Cancer Research and Clinical Oncology.

How does cancer arise? How does cellular composition influence tumor malignancy? These questions are profound and challenging to answer, but are crucial to understand the disease and find the right cure. Now, a German-Danish team led by Professor Matthias Mann has developed a ground-breaking technology called ‘Deep Visual Proteomics’. This method provides researchers and clinicians with a protein read-out to understand cancer at single cell-type resolution. The technology was published in the journal Nature Biotechnology and demonstrates its potential in a first application to cancer cells.

A new study suggests that people with cancer and non-O blood types, such as types A, B, and AB, face an increased risk of developing venous thromboembolism (VTE), or blood clots in the veins, three months after their initial diagnosis. Scientists have long strived to understand the risk factors for VTE, the leading cause of preventable hospital deaths in the United States. Existing assessments use factors like tumor or cancer type to detect those at high risk of VTE. Yet, many patients without these diagnoses still develop life-threatening blood clots but go unidentified.

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.

Researchers have found that treatment with miR-634 reduces the resistance of oral squamous cell carcinoma cells to cisplatin, resulting in increased tumor cell killing. An ointment containing miR-634 had a similar effect in mice, suggesting that this simple topical treatment could be used to improve the prognosis of patients with advanced oral cancer.

Researchers have found that treatment with miR-634 reduces the resistance of oral squamous cell carcinoma cells to cisplatin, resulting in increased tumor cell killing. An ointment containing miR-634 had a similar effect in mice, suggesting that this simple topical treatment could be used to improve the prognosis of patients with advanced oral cancer.

Adding an anti-inflammatory medication to immunotherapy and standard chemotherapy drugs may provide long-term suppression of aggressive bladder tumor growth, according to a proof-of-concept study.

Researchers have discovered another way tumor cells transfer genetic material to other cells in their microenvironment, causing cancer to spread.

Treatment for glioma has long relied on MRI imaging to track tumor markers and treatment response. But new findings suggest a new method could provide additional data about tumor markers before changes appear on an MRI, indicating possible strategies to help clinicians address this aggressive form of cancer.

Invading armies need a steady supply of fuel and armaments. That’s just as true when the invaders are cells, such as when tumor cells break away and spread to other parts of the body in a process called metastasis — the most deadly part of cancer. Now, a study in C. elegans worms provides new insight into how invading cells deploy fuel to the front lines of invasion to power their break-through machinery.

A researcher has found, through extensive data analysis, that the youngest patients with brain tumors — those ages birth to 3 months — have about half the five-year survival rate as children ages 1 to 19.

Scientists have developed a genetic screening platform to identify genes that can enhance immune cells to make them more persistent and increase their ability to eradicate tumor cells.

Radiation therapy is one of the cornerstones of cancer therapy. However, some types of tumor respond little or hardly at all to radiation. If it were possible to make tumor cells more sensitive, treatment would be more effective and gentler. Empa and ETH Zurich researchers have now succeeded in using metal oxide nanoparticles as „radiosensitizers“ – and in producing them on an industrial scale.

Metastatic cells form in a primary tumor and then break away from it, migrate to other organs, attach to them and form new tumors. This spread reduces patients‘ chances of recovery. Scientists have discovered some of the mechanisms by which these cells arise. This is due to cells that have narrowly escaped cell death (apoptosis) following a chemotherapeutic treatment. Those cells reprogram themselves to acquire metastatic skills. Thanks to this study, these cells – called PAME by the researchers – now appear as new therapeutic targets.

Phosphatidylinositol 3-kinase, or PI3K for short, is a family of lipid kinases that plays a key role in the human body, performing functions such as cell division, metabolism, and cell growth. While class I PI3Kα is well-researched and an important target for cancer drugs, little is known about class II of this lipid kinase family. Now, researchers from the Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP) have been able to shed light on its structure and function. The results pave the way for the development of new types of antithrombotic drugs. Moreover, it is likely that the inhibition of class II PI3KC2α is able to arrest tumor angiogenesis.

It may be possible to identify the presence of an aggressive brain tumor in children by studying their cerebrospinal fluid, according to new research.

Acute myeloid leukemia, which affects blood and bone marrow cells, is a particularly dangerous form of cancer. More than half of patients under the age of 60 die. This proportion rises to 85% for patients over 60. A team has now identified a previously unknown mechanism that could lead to the development of new therapies. The selective activation of AMPK, a key enzyme in the energy balance of tumor cells, would indeed lead to their death by triggering the cells stress response. Moreover, the scientists have successfully exploited this energy gap in an animal model of the disease: a combination of two drugs — one of which is already on the market — has indeed shown promise. However, their effectiveness has yet to be confirmed on leukaemia stem cells, which have the ability to escape many treatments to restart tumor growth.

A new study adds to a growing body of evidence that organoids — lab-grown collections of cells that mimic a patient’s tumor — are a promising avenue for drug discovery to improve outcomes in patients with cancer, particularly rare cancers for which clinical data on drug effectiveness is often lacking.

Using data from over 100,000 malignant and non-malignant cells from 15 human brain metastases, researchers have revealed two functional archetypes of metastatic cells across 7 different types of brain tumors, each containing both immune and non-immune cell types. Their findings provide a potential roadmap for metastatic tumor formation that could be used to design therapies to improve the treatment of metastasized patients.

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.

A new study demonstrates the ability of the mutant Kras oncogene to use genetic reprogramming to make cells more stem-like and plastic; it resolves the long-standing debate over why Kras is so special in tumor formation. They were also able to identify an effector complex that can be targeted for therapeutic treatment against mutant Kras.