The study, led by researchers at Yale University, has shed new light on the potential link between early-life exposure to air and light pollution and an increased risk of pediatric thyroid cancer. The findings are concerning, especially given how widespread these exposures are.

The research team analyzed data from 736 individuals diagnosed with papillary thyroid cancer before age 20 and 36,800 matched control participants based on birth year. Using advanced geospatial and satellite modeling, the team assessed individual-level exposure to fine particulate matter air pollution (PM2.5) and outdoor artificial light at night (O-ALAN). The results showed that for every 10 micrograms per cubic meter increase in PM2.5 exposure, the odds of developing thyroid cancer rose by 7% overall.

The strongest association between exposure and thyroid cancer was found among teenagers (15-19 years of age) and Hispanic children. Children born in areas with high levels of O-ALAN exposure were 23-25% more likely to develop thyroid cancer. The study’s lead author, Dr. Nicole Deziel, emphasized that these results are concerning and highlight the importance of addressing environmental factors in childhood cancer research.

Thyroid cancer is among the fastest-growing cancers among children and adolescents, yet we know very little about what causes it in this population. This study suggests that early-life exposure to PM2.5 and O-ALAN may play a role in this concerning trend. The impact of papillary thyroid cancer on children can be extensive, with survivors often suffering from aftereffects such as temperature dysregulation, headaches, physical disabilities, and mental fatigue.

Both PM2.5 and O-ALAN are considered environmental carcinogens that have been shown to disrupt the body’s endocrine system, including thyroid function, in animals and adults. The particles associated with PM2.5 pose a threat because they are small enough to enter the bloodstream and can interfere with hormone signaling, including those involved in regulating cancer pathways.

The current research raises important environmental justice concerns. Communities of color and lower-income populations are often disproportionately exposed to both air pollution and light pollution – inequities that may contribute to the higher thyroid cancer burden observed in Hispanic children.

In conclusion, this study highlights the need for more work to replicate and expand on these findings, ideally using improved exposure metrics and longitudinal designs. In the meantime, the results point to the critical importance of addressing environmental factors in childhood cancer research. Reducing exposures to air pollution and managing light pollution could be important steps in protecting children’s health.

The researchers at the Department of Pathology, School of Clinical Medicine at the LKS Faculty of Medicine of the University of Hong Kong (HKUMed) have made significant strides in understanding the earliest stages of stomach cancer, a leading cause of cancer-related deaths worldwide. Through two innovative studies, they have uncovered crucial insights into the early changes in the stomach that contribute to the development of stomach cancer, laying the foundation for improved prevention and early detection.

While the stomach’s acidic environment aids digestion, it can induce cancer-causing mutations in normal stomach tissues as individuals age. However, the timing and mechanisms of these early changes and how they promote the progression to cancer remain largely unknown. The HKUMed researchers provided valuable insights into these processes.

Mapping the Origins of Stomach Cancer

In a collaborative study, researchers from HKUMed, the Wellcome Sanger Institute, and the Broad Institute of MIT and Harvard analyzed genetic mutations in normal stomach lining tissue using advanced genome sequencing. For the first time, they sequenced whole genomes from 238 samples and performed targeted sequencing on an additional 829 samples from individuals with and without stomach cancer in Hong Kong, the US, and the UK.

The study revealed that despite the stomach’s harsh acidic environment, the stomach lining has protective mechanisms that prevent significant mutations. The researchers found that the number of mutations increases with age, with normal stomach glands accumulating approximately 28 mutations annually. In stomach cancer patients, the mutation rate is more than double, especially in the metaplastic glands.

Professor Leung Suet-yi, co-lead author of the research and Chairperson of the Department of Pathology, School of Clinical Medicine, HKUMed, said, “By age 60, nearly 10% of the stomach lining has mutations in known cancer genes, highlighting a gradual accumulation of potential cancer-causing changes over decades. The most surprising finding was that some stomach regions exhibited chromosome abnormalities linked to chronic inflammation.”

Risk Factors and Pre-cancer Model

The researchers identified risk factors for stomach cancer, including smoking, excessive alcohol drinking, a high salt diet, and a Helicobacter pylori infection. Professor Leung elaborated, “Our multinational team found that individuals with long-term stomach inflammation had significantly more mutations or extra chromosomes, indicating the potential role of inflammation in shaping a pre-cancer environment from an early age.”

World’s First Biobank of ‘Intestinal Metaplasia’ Organoid Models

In a related study, researchers from HKUMed and the InnoHK Centre for Oncology and Immunology investigated intestinal metaplasia (IM) in which stomach cells are transformed to resemble intestine cells. This transformation significantly increases the risk of developing stomach cancer, but the process remains poorly understood.

Co-led by Professor Helen Yan Hoi-ning, Assistant Professor in the Department of Pathology at HKUMed, and Professor Suet Yi Leung, the study used organoid culture to make a 3D model of IM. Organoids, tiny versions of organs grown in the lab from a patient’s tissue, provide a realistic model for studying the progression of IM to cancer.

The study revealed that IM organoids contain ‘hybrid’ cells with a mix of both stomach and intestinal characteristics. Typically associated with cancer cells, these traits facilitate tissue spread and make identifying early warning signs crucial. Professor Yan explained, “Using organoid technology, we can identify early changes when stomach cells become pre-cancerous.”

Harnessing Innovation for Early Detection and Prevention

By uncovering the earliest mutations and risk factors associated with stomach cancer and developing a sophisticated pre-cancer model, these studies offer invaluable insights for current prevention and early detection strategies. Professor Leung Suet-yi said, “With a living cell model now available, the potential for drug development to reverse IM becomes increasingly achievable.”

These breakthroughs provide new hope in the fight against stomach cancer, potentially transforming patient outcomes and clinical practices. The findings of these studies have significant implications for the prevention and early detection of stomach cancer, offering new avenues for research and treatment that can improve patient lives worldwide.

The study, led by researchers at NYU Langone Health and its Perlmutter Cancer Center, has made a groundbreaking discovery that could change the way melanoma is diagnosed and treated. The researchers have found that monitoring blood levels of DNA fragments shed by dying tumor cells may accurately predict skin cancer recurrence in stage III melanoma patients.

The study showed that approximately 80% of stage III melanoma patients who had detectable levels of circulating tumor DNA (ctDNA) before they started treatment to suppress their tumors went on to experience recurrence. The researchers also found that the disease returned more than four times faster in this group than in those with no detectable levels of the biomarker, and the higher their levels, the faster cancer returned.

“Our findings suggest that circulating tumor DNA tests could help oncologists identify which melanoma patients are most likely to respond well to therapy,” said study lead author Mahrukh Syeda. “In the future, such assessments may be used routinely in the clinic to help guide treatment decisions.”

The research team also found that nearly all of those with detectable levels of ctDNA at three, six, nine, or 12 months into treatment experienced melanoma recurrence. This suggests that if the gene fragments are not observable prior to therapy but appear later on, this could indicate that the disease might be worsening.

The study’s senior author, David Polsky, notes that in some cases, cancer still recurred even though the patient had received a negative ctDNA test before starting therapy. To address this, the authors next plan to improve the sensitivity of their test and explore whether using the biomarker to make treatment decisions can indeed improve patients’ chances of survival and quality of life.

The study’s findings have significant implications for melanoma patients and could potentially save lives by providing early feedback on treatment progress and cancer growth. The researchers are now planning to further investigate the use of ctDNA tests in clinical settings, which could lead to more targeted and effective treatments for this aggressive form of skin cancer.