Lifeboat Foundation

Myeloid cells are a population of cells classified to denote a specific lineage. “Myeloid” specifically refers to granulocytes and monocytes generated from the bone marrow. Many cells under this term share common progenitors from which they derive including, macrophages, neutrophils, basophils, and eosinophils. In the context of cancer, many of these cells become ‘pro-tumorigenic’. More specifically, they suppress the immune system to allow the tumor to proliferate and progress. Each myeloid cell type is associated with antitumor immune suppression. Myeloid cells suppress antitumor immune activity by blocking T cell activation, aid in angiogenesis (blood vessel formation) to increase metastasis, and producing cytokines or proteins that activate suppressive activity in other cells. Unfortunately, myeloid cells make up a major percentage within the tumor microenvironment, so targeting these cells is crucial. Many researchers are currently working on different ways to target these cell populations.

A recent article in Nature by Dr. Miriam Merad and her team demonstrated how protein signaling drives pro-tumor myeloid cell generation. Merad is a physician scientist, Director of the Precision Immunology Institute at Mount Sinai School of Medicine in New York, and Director of the Mount Sinai Human Immune Monitoring Center (HIMC). While her work focuses on targeting myeloid cells (particularly macrophages) to lower their suppressive phenotype and improve cancer treatment, her current publication identifies specific drivers of immunosuppressive myeloid states, previously undefined.

Merad and her team used advanced single cell sequencing to analyze non-small cell lung cancer (NSCLC) lesions from both humans and mice. Single cell sequencing is commonly used to identified up-and downregulated genes in a variety of cell types. By sequencing the tumor lesions the team discovered that interleukin 4 (IL-4) was a predictive driver of macrophages that infiltrated the tumor. Researchers used various genetically modified mouse models to conclude that the IL-4 receptor is necessary for tumor progression. Interestingly, they concluded that deletion of the IL-4 receptor in the progenitor phase reduced tumor growth compared to IL-4 deletion in mature macrophages which had little effect.

Cervical cancer, which develops in the lower portion of the uterus, known as the cervix, typically grows slowly. Cells in the cervix can change, a process known as dysplasia, and the resulting abnormal cells, if not removed, can develop into cervical cancer.

When cervical cancer occurs, treatment options vary based on many factors, including how far the disease has advanced and the overall health of the patient. Some cervical cancer patients may undergo a simple hysterectomy (also known as a complete or total hysterectomy). A simple hysterectomy removes the uterus and cervix.

The perimetrium, fat and connective tissue around the uterus, connects the uterus to the cervix and other tissues. Some patients with cervical cancer experience “parametrial invasion” (also referred to as parametrial infiltration), during which cervical cancer has spread into the parametrial tissue.

Techsomed’s thermal ablation therapy, a minimally invasive procedure for small tumors, has huge benefits over surgery or chemotherapy for patients and is a world first.

In a collaboration with Houston Methodist Hospital, researchers from the UH Engineering Robotic Swarm Control Laboratory led by Aaron Becker, assistant professor of electrical and computer engineering, are developing a novel treatment for pulmonary embolism (PE) using millimeter-scale corkscrew shaped robots controlled by a magnetic field. PE is the third most common cardiovascular disease, resulting in up to 300,000 deaths annually.

“Using non-invasive miniature magnetic agents could improve patient comfort, reduce the risk of infection and ultimately decrease the cost of medical treatments,” according to Julien Leclerc, a Cullen College research associate specializing in applied electromagnetics. “My goal is to quickly bring this technology into the clinical realm and allow patients to benefit from this treatment method as soon as possible.\.

Researchers at the Max Planck Institute of Psychiatry have investigated how stress hormones affect the early development of brain cells in the cerebral cortex of the fetus. The cortex is the crucial area of the brain for thinking. The team was able to demonstrate causal links between stress hormones and altered brain structure, which relate to higher levels of educational attainment later in life.

The hormone group of glucocorticoids is crucial for the regulation of our metabolism and immune response, but also for the development of organs such as the brain and lungs before birth. The hormones are released in response to stress and can travel from the mother to the fetus. One of the best-known stress hormones is cortisol. Synthetic forms are prescribed, for example, in pregnancies at high risk for preterm delivery in order to help the maturation of the fetal lungs.

“We found that glucocorticoids, when present early in gestation in the first or early second trimester, increase the number of a particular type of brain cells that are formed very early in development (called basal progenitor cells)”, reports Anthi C. Krontira, who led the study published in Neuron. “These are cells that are important for the growth of the cerebral cortex.”

A RIKEN-developed mouse model of an enigmatic lung disease promises to unlock new biological insights and catalyze the development of treatments for millions affected globally. The research is published in Nature Communications.

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease in which scarring of the lungs makes breathing increasingly difficult. The cause is unknown with no cure, and it often leads to eventual death.

About a decade ago, Kazuyo Moro of the RIKEN Center for Integrative Medical Sciences and her colleagues investigated the role that a special population of immune cells, known as group 2 innate lymphoid cells (ILC2s), play in the body’s response to lung infections. As part of that effort, they created mice lacking two key immune-related genes.

The elevated cardiovascular disease risk among people with HIV is even greater than predicted by a standard risk calculator in several groups, including Black people and cisgender women, according to analyses from a large international clinical trial primarily funded by the National institutes of Health and presented at the 2024 Conference on Retroviruses and Opportunistic Infections (CROI) in Denver. The risk of having a first major cardiovascular event was also higher than previously predicted for people from high-income regions and those whose HIV replication was not suppressed below detectable levels.

Researchers examined the incidence of major adverse cardiovascular events in people who did not take pitavastatin or other statins during the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE) trial, a large clinical trial to test whether pitavastatin—a cholesterol-lowering drug known to prevent cardiovascular disease—could prevent major adverse cardiovascular events, such as heart attacks and strokes, in people with HIV. The scientists compared the incidence of cardiovascular events in the trial to the incidence predicted by standard estimates, which use the American College of Cardiology and American Heart Association’s Pooled Cohort Risk Equations (PCE) score.

They found that the rate of cardiovascular events occurring in many groups of people differed from predicted rates, even considering that people with HIV have a higher overall risk of cardiovascular disease than people without HIV, including double the risk of major adverse cardiovascular events. Notably, in high-income regions—as defined by the global burden of disease classification system—including North and South America and Europe, cardiovascular event rates were higher overall, with cisgender women experiencing about two and a half times more events than predicted, and Black participants having more than 50% higher event rates than predicted.

Organoids of multiple different tissue types can be generated from cells collected from amniotic fluid samples, without termination of the pregnancy, according to a study in Nature Medicine.

The generation of primary organoids, from fetal fluid-derived epithelial stem or progenitor cells, offers the possibility of modeling different developing tissues during gestation, even beyond the limits of pregnancy termination.

New method will help scientists study neural networks and neuroplastic changes underlying higher brain functions and disease processes in model animals.