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Aquaporins in cancer stem cells targeted to prevent gastric cancer recurrence

Scientists have long suspected that a small population of cells survives treatment and regenerates the tumor. These “cancer stem cells” are thought to resist conventional therapies, allowing the disease to return even after the visible tumor has been removed.

Previous attempts to identify gastric cancer stem cells using other protein markers, such as CD44 or CD133, yielded inconsistent results. These markers often appeared on healthy cells as well or did not fully account for tumor behaviour.

The team discovered that AQP5 reliably marks the cancer stem cells in gastric tumors. Aquaporins are proteins that form channels in cell membranes to control the movement of water into and out of cells. While AQP5 was previously known to mark stem cells in healthy gastric tissue, this study shows it also identifies the specific cells responsible for driving tumor growth, spread, and recurrence.

Importantly, AQP5 does more than simply mark these cells; it actively contributes to their aggressive behavior.

The researchers found that cells with AQP5 were capable of forming new tumors, while cells without AQP5 rarely did so. Most significantly, when they used a targeted method to eliminate only the AQP5-expressing cells, tumors stopped growing or shrank entirely and did not recur. This held true even for cancers that had spread to other organs.


Scientists have identified the specific cells responsible for gastric cancer’s tendency to return after treatment. The study also demonstrated that eliminating these cells stops tumors from growing, even in advanced disease that has spread to other organs.

A Distinct New Type of Diabetes Is Officially Recognized

This year, the International Diabetes Federation (IDF) officially recognized a fifth form of diabetes, after decades of controversy. It’s now urging other health authorities, like the World Health Organization (WHO), to follow suit.

Type 5 diabetes is rarely discussed or researched, and yet it is thought to impact up to 25 million people worldwide, especially those in low-and middle-income nations where access to medical care is limited.

It was first described in 1955 in Jamaica, then forgotten about for many years. Even once it was acknowledged by the WHO in the 1980s, the diagnosis created controversy.

Abdominal obesity and muscle loss increase the risk of death by 83% after age 50, study finds

A study by researchers at the Federal University of São Carlos (UFSCar) in Brazil, in partnership with University College London (UCL) in the United Kingdom, concluded that the combination of abdominal fat and muscle loss increases the risk of death by 83%, compared to people without these conditions.

This combination is so dangerous that it identifies an even greater problem: sarcopenic obesity. This condition is characterized by loss of muscle mass while gaining fat throughout the body. It is a difficult condition to diagnose, and it is related to loss of autonomy and a worsening quality of life in older adults. It is also known as frailty syndrome and is associated with an increased risk of falls and other comorbidities.

“In addition to assessing the risk of death associated with abdominal obesity and low muscle mass, we were able to prove that simple methods can be used to detect sarcopenic obesity. This is important because the lack of consensus on diagnostic criteria for this disease makes it difficult to detect and treat,” says Tiago da Silva Alexandre, a professor in the Department of Gerontology at UFSCar and one of the authors of the study.

Study Sheds New Light on Tanning Bed Melanoma Risks

Frequent tanning bed users may have up to an eight times greater risk for melanoma than people considered at high risk for melanoma who don’t use tanning beds, according to a new study that also showed how tanning beds alter melanoma-linked DNA on the molecular level and damage areas of skin not usually exposed to the sun.


A case-control cohort study of patients considered at high risk for melanoma finds that tanning bed users have higher rates of melanoma and disease with significantly more mutations.

Vascular Lamb1 guides the migration of retinal microglial precursors via Itga6-Rac1 signaling

Zhan et al. show that blood vessels serve as a migratory scaffold directing retinal microglial precursor infiltration into the developing retina. Vascular Lamb1 signaling orchestrates this precise migration, indicating a key mechanism guiding retinal microglial colonization during development.

Lipofuscin accumulation in aging and neurodegeneration: a potential “timebomb” overlooked in Alzheimer’s disease

Lipofuscin, a marker of aging, is the accumulation of autofluorescent granules within microglia and postmitotic cells such as neurons. Lipofuscin has traditionally been regarded as an inert byproduct of cellular degradation. However, recent findings suggest that lipofuscin may play a role in modulating age-related neurodegenerative processes, and several questions remain unanswered. For instance, why do lipofuscin granules accumulate preferentially in aged neurons and microglia? What happens to these pigments upon neuronal demise? Particularly in neurodegenerative diseases like Alzheimer’s disease (AD), why does amyloid β (Aβ) deposition usually begin in late adulthood or during aging? Why do lipofuscin and amyloid plaques appear preferentially in grey matter and rarely in white matter? In this review, we argue that lipofuscin should be revisited not as a simple biomarker of aging, but as a potential modulator of neurodegenerative diseases. We synthesize emerging evidence linking lipofuscin to lysosomal dysfunction, oxidative stress, lipid peroxidation and disease onset—mechanisms critically implicated in neurodegeneration. We also explore the potential interactions of lipofuscin with Aβ and their spatial location, and summarize evidence showing that lipofuscin may influence disease progression via feedback loops affecting cellular clearance and inflammation. Finally, we propose future research directions toward better understanding of the mechanisms of lipofuscin accumulation and improved lysosomal waste clearance in aging.

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