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The research, which was conducted on mice, demonstrates how these tiny nanomachines are propelled by urea present in urine and precisely target the tumor, attacking it with a radioisotope carried on their surface.

Bladder cancer has one of the highest incidence rates in the world and ranks as the fourth most common tumor in men. Despite its relatively low mortality rate, nearly half of bladder tumors resurface within 5 years, requiring ongoing patient monitoring. Frequent hospital visits and the need for repeat treatments contribute to making this type of cancer one of the most expensive to cure.

While current treatments involving direct drug administration into the bladder show good survival rates, their therapeutic efficacy remains low. A promising alternative involves the use of nanoparticles capable of delivering therapeutic agents directly to the tumor. In particular, nanorobots—nanoparticles endowed with the ability to self-propel within the body—are noteworthy.

Recent research highlights the dual role of VEGF-C-producing macrophages in breast tumors, potentially guiding metastasis to less harmful areas, opening new avenues for targeted cancer therapies.

A new study from Karolinska Institutet published in Cell reports shows that tumor-associated macrophages, which are white blood cells that are found in breast tumors, can both help and hinder the spread of cancer cells to other organs. The researchers found that macrophages that produce a substance called VEGF-C reduce the spread of breast cancer to the lungs but increase the spread to the lymph nodes. This may have implications for the prognosis and treatment of breast cancer.

Understanding breast cancer and the role of tams.

Research indicates enhanced mental function in individuals who maintain an active lifestyle and engage in social interactions, alongside managing blood pressure and diabetes effectively.

As federal approval for more Alzheimer’s disease medications progresses, a recent study conducted by UC San Francisco and Kaiser Permanente Washington reveals that tailored health and lifestyle modifications can postpone or prevent memory deterioration in older adults at increased risk.

The two-year study compared cognitive scores, risk factors, and quality of life among 172 participants, of whom half had received personalized coaching to improve their health and lifestyle in areas believed to raise the risk of Alzheimer’s, such as uncontrolled diabetes and physical inactivity. These participants were found to experience a modest boost in cognitive testing, amounting to a 74% improvement over the non-intervention group.

face_with_colon_three Year 2021


Nicotinamide adenine dinucleotide (NAD+) is an important molecule that functions as a co-enzyme in numerous metabolic processes. Generated both through de novo synthesis and via salvage pathways, NAD+ is the substrate for a variety of NAD+-consuming enzymes. Among them is CD38, a cell surface ecto-enzyme widely expressed on different types of cells and endowed with the function of cADP-ribose synthases/NAD+ glycohydrolase. Surface CD38 expression is increased in different hematological and solid tumors, where it cooperates with other ecto-enzymes to produce the immunosuppressive molecule adenosine (ADO). Few studies have explored the correlation of NAD+ levels with T-cell mediated anti-tumor response in preclinical models. We therefore discuss these novel findings, examining the possible contribution of NAD+ depletion, along with ADO production, in the immunosuppressive activities of CD38 in the context of human tumors. Lastly, we discuss the use of pharmacological inhibitors of CD38 and supplementation of different NAD+ precursors to increase NAD+ levels and to boost T cell responses. Such molecules may be employed as adjuvant therapies, in combination with standard treatments, for cancer patients.

Nicotinamide adenine dinucleotide (NAD+) and its reduced/phosphorylated forms (NADH, NADP+ and NADPH) are key molecules in cellular metabolism and energy production, acting as hybrid-accepting and hybrid-donating co-enzymes in different biological reactions. NAD+ and NADH are then inter-converted by hybrid transfer and not consumed. NAD+ can be generated de novo starting from tryptophan, which is converted to N-formylkynurenine by indoleamine dioxygenase or tryptophan dioxygenase. Other enzymes are involved in converting N-formylkynurenine to nicotinic acid mononucleotide (NaMN), which is adenylated by adenyl-transferases to generate nicotinic acid adenine dinucleotide (NaAD), finally converted to NAD+ by NAD+ synthetase. NAD+ can also be obtained through different salvage pathways, starting from nicotinic acid (Na) which is converted to NaMN by Na phosphoribosyltransferase (Naprt) or starting from nicotinamide (Nam) and nicotinamide riboside (NR).

Northwestern Medicine investigators have identified a previously unknown regulator of tumor immune evasion, which may help improve the efficacy of current and future anti-tumor immunotherapies, according to recent findings published in the Journal of Clinical Investigation.

“The study provides a molecular insight into understanding why some cannot be treated by the checkpoint blockade antitumor therapy, but others can,” said Deyu Fang, Ph.D., the Hosmer Allen Johnson Professor of Pathology and senior author of the study.

Antitumor immunotherapy is a type of treatment that helps the immune system in fighting cancer and includes a range of therapy types, such as . Immune checkpoints help prevent the immune system from being too strong and eradicating other , including .