The discovery of a specific gene, SDR42E1, has revolutionized our understanding of vitamin D’s role in human health. This essential nutrient is not only crucial for bone growth and immune function but also serves as a precursor to the hormone calcitriol. Now, researchers have successfully used CRISPR/Cas9 gene editing to uncover the secrets behind SDR42E1’s vital function.

Led by Dr. Georges Nemer, a professor at Hamad Bin Khalifa University in Qatar, and his team, this groundbreaking study published in Frontiers in Endocrinology reveals that SDR42E1 is instrumental in taking up vitamin D from the gut and further metabolizing it. This breakthrough has far-reaching implications for precision medicine, particularly in cancer therapy.

The researchers’ inspiration came from earlier research that linked a mutation in the SDR42E1 gene on chromosome 16 to vitamin D deficiency. By transforming the active form of SDR42E1 into its inactive form using CRISPR/Cas9 gene editing, the team observed a significant decrease in cancer cell viability, with a 53% plummet in the HCT116 line’s survival rate.

The study’s first author, Dr. Nagham Nafiz Hendi from Middle East University in Amman, Jordan, notes that these results open new avenues for precision oncology. However, further validation and long-term development are necessary before this technology can be translated into clinical practice.

Moreover, the researchers discovered that SDR42E1 plays a crucial role in cell signaling and cholesterol metabolism, suggesting its potential to selectively target cancer cells while sparing healthy ones. This finding has sparked excitement among scientists, who envision various applications of this technology, including targeting vitamin D-related diseases like cancer, kidney disease, autoimmune disorders, and metabolic conditions.

However, caution is warranted when exploring broader applications, as the long-term effects of SDR42E1 on vitamin D balance remain to be fully understood. As researchers continue to unravel the mysteries of this gene, one thing is clear: this breakthrough has the potential to revolutionize our understanding of vitamin D’s role in human health and unlock new avenues for precision medicine.

The article highlights a disturbing trend in the United States – cancer deaths linked to obesity have tripled over the past two decades. A study presented at the Endocrine Society’s annual meeting in San Francisco examined more than 33,000 deaths from obesity-associated cancers and revealed sharp increases in cancer deaths, particularly among women, older adults, Native Americans, and Black Americans.

“Obesity is a significant risk factor for multiple cancers, contributing to significant mortality,” said lead researcher Faizan Ahmed. “This research underscores the need for targeted public health strategies such as early screening and improved access to care, especially in high-risk rural and underserved areas.”

The study used mortality data from the Centers for Disease Control and Prevention (CDC) to analyze U.S. deaths from obesity-associated cancers between 1999 and 2020. The results showed age-adjusted mortality rates increased from 3.73 to 13.52 per million over two decades, with steep increases among certain groups.

Obesity is a complex disease resulting from multiple genetic, physiological, hormonal, environmental, and developmental factors. It raises the risk of developing serious chronic conditions such as high blood pressure, high cholesterol, prediabetes, type 2 diabetes, heart disease, and chronic and end-stage kidney disease.

In addition to certain types of cancer, obesity is associated with a higher risk of developing 13 types of cancer, according to the CDC. These cancers make up 40% of all cancers diagnosed in the United States each year.

The regions with the highest rates of obesity-related cancer deaths were identified as follows:

* The Midwest had the highest rate.
* Vermont, Minnesota, and Oklahoma had the highest state-level rates.
* Utah, Alabama, and Virginia had the lowest state-level rates.

This research emphasizes the need for targeted public health strategies to combat the growing epidemic of obesity-related cancer deaths. Early screening and improved access to care are crucial in reducing mortality rates among high-risk groups.

The UC Davis Comprehensive Cancer Center has made a groundbreaking discovery that may explain why certain immune cells in humans are less effective at fighting solid tumors compared to non-human primates. This finding could lead to more powerful cancer treatments.

Researchers have uncovered an evolutionary change that makes the Fas Ligand (FasL) protein, essential for triggering programmed cell death and killing cancer cells, vulnerable to being disabled by plasmin in humans. This genetic mutation is unique to humans and not found in non-human primates, such as chimpanzees.

“The evolutionary mutation in FasL may have contributed to the larger brain size in humans,” said Jogender Tushir-Singh, senior author for the study and an associate professor in the Department of Medical Microbiology and Immunology. “But in the context of cancer, it was an unfavorable tradeoff because the mutation gives certain tumors a way to disarm parts of our immune system.”

The team discovered that a single evolutionary amino acid change – serine instead of proline at position 153 – makes FasL more susceptible to being cut and inactivated by plasmin. Plasmin is often elevated in aggressive solid tumors, such as triple negative breast cancer, colon cancer, and ovarian cancer.

This means that even when human immune cells are activated and ready to attack the tumor cells, one of their key death weapons – FasL – can be neutralized by the tumor environment, reducing the effectiveness of immunotherapies. The findings may help explain why CAR-T and T-cell-based therapies often fall short in solid tumors.

Blood cancers often do not rely on plasmin to metastasize, whereas tumors like ovarian cancer heavily rely on plasmin to spread the cancer.

Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. This finding may open new doors for improving cancer immunotherapy.

By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumors.

“Humans have a significantly higher rate of cancer than chimpanzees and other primates,” said Tushir-Singh. “There is a lot that we do not know and can still learn from primates and apply to improve human cancer immunotherapies.”