A new study finds that pancreatic cells display an adaptive response to repeated inflammation that initially protects against tissue damage but can promote tumor formation in the presence of mutant KRAS.
Engineers developed a way to grow tiny replicas of the pancreas, using either healthy or cancerous pancreatic cells. Their models could help researchers develop and test potential drugs for pancreatic cancer.
Pumping iron: Inhibition of key pathway promotes iron-dependent cell death in pancreatic cancer cells
A cell culture study maps mechanisms underlying a new potential strategy for killing pancreatic cancer cells through a type of cell death known as ferroptosis.
A team of researchers has developed an immunotherapy strategy that can eliminate pancreatic tumors in mice. The new therapy, a combination of three drugs that boost the body’s immune defenses against tumors, is expected to enter clinical trials later this year.
Pancreatic cancer cells typically rely on a mutant version of the KRAS protein to proliferate. These cancer cells can also survive losing KRAS by activating alternative growth pathways. Scientists discovered a new interaction between mutant KRAS and a protein complex called RSK1/NF1 that may be the source of this adaptive resistance.
Tackling the scar tissue that shields pancreatic tumors from effective drug access is a promising advance in a notoriously hard-to-treat cancer.
More than two-thirds of pancreatic cancer patients harboring genetic mutations saw their tumor stop growing or shrink substantially after being switched from intensive chemotherapy to the PARP inhibitor rucaparib as a maintenance therapy.
Giving early-stage pancreatic cancer patients a CD40 immune-stimulating drug helped jumpstart a T cell attack to the notoriously stubborn tumor microenvironment before surgery and other treatments, according to a new study.
Researchers describe how pancreatic cancer cells use an alternative method to find necessary nutrients, defying current therapies, to help them grow and spread.
Scientists have demonstrated that blocking ‘cell drinking,’ or macropinocytosis, in the thick tissue surrounding a pancreatic tumor slowed tumor growth–providing more evidence that macropinocytosis is a driver of pancreatic cancer growth and is an important therapeutic target.
Researchers demonstrated that a new tumor-penetrating therapy could enhance the effects of chemotherapy, reduce the spread of pancreatic cancer and increase survival in animal models.
Researchers have called on European policymakers to make adequate resources available to tackle pancreatic cancer, a disease that is almost invariably fatal and where little progress has been made over the past 40 years. The latest predictions for cancer deaths in the EU and UK for 2021 show that pancreatic death rates are predicted to remain approximately stable for men, but continue to rise in women in most EU countries.
The drug is effective at treating pancreatic cancer and prolonging survival in mice, according to a new study. A second study shows the drug is also effective against triple-negative breast cancer, a fast-growing and hard-to-treat type of breast cancer that carries a poor prognosis. Clinical trials are set to begin in 2021.
The results of a pre-clinical study suggest how a compound derived from the thunder god vine — an herb used in China for centuries to treat joint pain, swelling and fever — is able to kill cancer cells and potentially improve clinical outcomes for patients with pancreatic cancer.
Researchers say they’ve identified a way to disrupt a process that promotes the growth of pancreatic cancers — one of the most difficult and deadly cancers to treat.
Researchers have discovered that a protein thought to only be involved in the development of neurons in the brain also plays a major role in the development and growth of pancreatic cancer. Their findings demonstrate for the first time how the protein, called Netrin-G1, helps pancreatic cancer cells survive by protecting them from the immune system and supplying them with nutrients.
Innovative research has shed light on the mysterious role of long non-coding RNAs in the development of pancreatic cancer and suggests potential new targets for precision cancer therapies.
A new analysis highlights the diversity of immune response in pancreatic cancer, and points toward the need for treatments tailored to individual patients.
Scientists have shown that pancreatic cancer metastasis — when tumor cells gain the deadly ability to migrate to new parts of the body — can be suppressed by inhibiting a protein called Slug that regulates cell movement. The study also revealed two druggable targets that interact with Slug and hold promise as treatments that may stop the spread of pancreatic cancer.
New research provides guidance on clinical decision-making in regards to treating pancreatic cancer patients during the COVID-19 pandemic.
Activating the G protein-coupled estrogen receptor (GPER) — a receptor found on the surface of many normal and cancer tissues — has been shown to stop pancreatic cancer from growing, but may also make tumors more visible to the immune system and thus more susceptible to modern immunotherapy. Researchers observed the effects of GPER activation in human and mouse pancreatic cancer models.
Scientists have uncovered the formation of tuft cells during pancreatitis and the surprising role of these cells in immunity, using mouse models of pancreatitis. The findings could lead to the development of new biomarkers to test for pancreatitis and pancreatic cancer.
In a new study of mice, researchers have found that an experimental drug that breaks down the amino acid cysteine slows pancreatic tumor growth by causing ferroptosis, an unusual form of cell death.
UK scientists have identified a new way to kill pancreatic cancer cells by ‘pulling the plug’ on the energy generator that fuels calcium pumps on their cell surface. The study reports how switching off the cancer’s energy supply causes the pancreatic cancer cells to become ‘poisoned’ by an irreversible build-up of calcium.
A new study reveals the mechanism that helps pancreatic cancer cells avoid starvation within dense tumors by hijacking a process that pulls nutrients in from their surroundings.