The human body is made up of trillions of tiny cells, each working together in harmony to keep us alive. At the heart of this complex system are proteins – the building blocks of life that facilitate communication between cells and ensure biological systems function properly. Despite their importance, there’s still much we don’t know about proteins, including how many exist within a human cell.

A team of scientists at the University of Copenhagen has made a groundbreaking discovery that could revolutionize our understanding of protein research. Led by Professor Jesper Velgaard Olsen, the researchers have developed a cutting-edge technology called SC-pSILAC that allows them to analyze and quantify proteins in individual cells with unprecedented depth.

With this new approach, scientists can measure how individual cells produce and break down proteins – a process known as ‘protein turnover’. This technique has significant implications for cancer research, drug development, and personalized medicine. By tracking the abundance of proteins and the rate at which they are turned over in single cells, researchers can gain a deeper understanding of how specific drugs impact protein function.

The SC-pSILAC method is particularly useful when studying cancer cells, which divide rapidly and are typically targeted by chemotherapy. However, some cancer cells do not divide, allowing them to evade chemotherapy. The new method helps identify these treatment-resistant cells, leading to better therapies.

In one notable example, the researchers used SC-pSILAC to examine how the cancer medication bortezomib impacts protein turnover in individual cells. Their findings uncovered specific proteins and previously unknown biological processes influenced by the treatment.

“This method represents a significant leap in protein research,” Professor Olsen says. “We have worked for years to analyze proteins within cells, but only recently has technological progress enabled us to do so at the single-cell level.”

Thanks to this innovation, scientists now have a far more detailed understanding of how proteins operate at the molecular level. The hope is that this knowledge will drive advancements in disease diagnostics and treatment strategies, ultimately improving human health and saving lives.

The article “Unlocking the Secrets of Zombie Cells: New Findings Reveal Distinct Subtypes of Senescent Skin Cells” reveals that senescent skin cells, also known as zombie cells, are not all the same. Researchers from Johns Hopkins University have identified three subtypes of senescent fibroblasts with distinct shapes, biomarkers, and functions.

The study published in Science Advances analyzed skin cell samples from 50 healthy donors between the ages of 20 and 90 who participated in the Baltimore Longitudinal Study. The researchers extracted fibroblasts associated with skin tissue and pushed them toward senescence by damaging their DNA. Using specialized dyes, they captured images of the cells’ shapes and stained elements that are known to indicate senescent cells.

Algorithms developed for this study analyzed the images, measured 87 different physical characteristics for each cell, and sorted the fibroblasts into groups. The researchers found that only one subtype of senescent fibroblast, named C10, was more prevalent in older donors.

The three distinct subtypes of senescent fibroblasts (C10, C7, and C3) responded differently when exposed to existing drug regimens designed to target and kill zombie cells. Dasatinib + Quercetin, a drug being tested in clinical trials, most effectively killed C7 senescent fibroblasts but was limited in killing the age-associated C10 senescent fibroblasts.

The findings show that drugs can target one subtype of senescent skin cells and not the others. With further research, the researchers hope to develop new therapies that preferentially target the senescence subtype that drives inflammation and disease.

This study has implications for cancer treatments and age-associated diseases. Certain therapies are being designed to trigger senescence in cancer cells, but the buildup of senescent cells during treatment can be problematic as those cells may promote inflammation at a time when a patient’s immune system is at its most vulnerable.

The researchers plan to look at senescence subtypes in tissue samples, not just in flasks and petri dishes, to see how those subtypes might be associated with various skin diseases and age-associated diseases. They hope that their technology will eventually be used to help predict which drugs might work well for targeting senescent cells that contribute to specific diseases.

The dream is to provide more information in a clinical setting to help with individual diagnoses and boost health outcomes.

Colorectal cancer was once considered a disease that predominantly affected older adults, but its incidence has been rising alarmingly among young people worldwide. In an effort to explain this modern medical mystery, researchers have identified a potential microbial culprit behind the surge: a bacterial toxin called colibactin.

Produced by certain strains of Escherichia coli that reside in the colon and rectum, colibactin is a toxin capable of altering DNA. The new study analyzed 981 colorectal cancer genomes from patients with both early- and late-onset disease across 11 countries and found that exposure to colibactin in early childhood imprints a distinct genetic signature on the DNA of colon cells – one that may increase the risk of developing colorectal cancer before the age of 50.

The study revealed that colibactin-related mutations were 3.3 times more common in early-onset cases than in those diagnosed after the age of 70 and were particularly prevalent in countries with high incidence of early-onset cases. The researchers demonstrated that colibactin-associated mutations arise early in tumor development, consistent with prior studies showing that such mutations occur within the first 10 years of life.

The findings have sobering implications, as colorectal cancer is projected to become the leading cause of cancer-related death among young adults by 2030. Until now, the reasons behind this surge have remained unknown, and young adults diagnosed with colorectal cancer often have no family history or risk factors.

The study’s lead author emphasized that understanding the role of colibactin in early-onset colorectal cancer is crucial for developing targeted prevention strategies and early detection tests. The researchers are investigating several hypotheses, including how children are exposed to colibactin-producing bacteria, whether certain environments or lifestyle behaviors contribute to its production, and whether probiotics can safely eliminate harmful bacterial strains.

As the study highlights the potential link between environmental exposures in early life and cancer risk, it reshapes our understanding of cancer etiology. The researchers call for sustained investment in this type of research to prevent and treat cancer before it’s too late.