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"They Found A Virus Hiding In Her DNA": Doctors Shocked As Beta-HPV Drives Aggressive Skin Cancer Until Stem Cell Transplant Saves Her Life
"They Found A Virus Hiding In Her DNA": Doctors Shocked As Beta-HPV Drives Aggressive Skin Cancer Until Stem Cell Transplant Saves Her Life

Sustainability Times

time4 days ago

  • Health
  • Sustainability Times

"They Found A Virus Hiding In Her DNA": Doctors Shocked As Beta-HPV Drives Aggressive Skin Cancer Until Stem Cell Transplant Saves Her Life

IN A NUTSHELL 🔬 Researchers found beta-HPV can integrate into DNA, directly promoting skin cancer growth. can integrate into DNA, directly promoting skin cancer growth. 🧬 The study focused on a 34-year-old woman with recurrent cutaneous squamous cell carcinoma . . 🤝 A collaborative medical approach led to a successful bone marrow stem cell transplant for treatment. for treatment. 💡 The findings suggest new avenues for personalized cancer treatments targeting viral factors in immunocompromised patients. A groundbreaking study has unveiled new insights into the role of the human papillomavirus (HPV) in the development of certain skin cancers. Previously, beta-HPV was considered a minor player in cancer progression, primarily exacerbating UV-induced damage. However, recent findings indicate that this virus can integrate itself into cellular DNA, directly promoting cancer growth. This revelation emerged from a detailed examination of a 34-year-old woman affected by recurrent cutaneous squamous cell carcinoma (cSCC) on her forehead. The discovery that beta-HPV can hijack the body's cells to sustain cancer growth signals a significant shift in our understanding of viral contributions to cancer. Unveiling the Mechanism of Cancer Development The study centered on a young woman who faced persistent cSCC despite undergoing multiple treatments, including surgeries and immunotherapy. Researchers delved into the genetic makeup of her tumors, uncovering that beta-HPV had not only infiltrated her DNA but was also producing viral proteins that facilitated cancer's resilience and growth. This marked the first time beta-HPV was observed integrating into cellular DNA, challenging previous assumptions about its role in cancer. Immunologist Andrea Lisco from the National Institute of Allergy and Infectious Diseases (NIAID) highlighted the broader implications of this finding. It suggests that there could be more cases of aggressive cSCC linked to underlying immune defects, which might be better addressed through treatments targeting the immune system rather than conventional methods. Asteroid Impact 'It's Not Sci-Fi Anymore' Research Led by Carrie Nugent Compares Odds to Lightning, Rabies, and Car Crashes—Public Left Reeling The woman's condition underscored a critical aspect of the study: her inherited immune disorder, specifically an issue with the ZAP70 protein, hampered her T cells' ability to combat HPV. While her immune system could still repair UV-induced DNA damage, the impairment allowed beta-HPV to invade and trigger cancer. Her case illustrates the complex interplay between viruses, immune function, and cancer development. A Collaborative Approach to Treatment Upon identifying the viral integration, the patient received a bone marrow stem cell transplant aimed at replacing her faulty T cells with functional ones. This intervention proved successful, resolving her aggressive skin cancer and other HPV-related issues. Over a three-year follow-up, none of her conditions recurred, highlighting the potential of personalized, targeted treatments. Scientists Warn 'These Ice Quakes Could Shatter' After Detecting Mysterious Deep Tremors In Greenland's Frozen Rivers 'This discovery and successful outcome would not have been possible without the combined expertise of virologists, immunologists, oncologists, and transplant specialists,' Lisco noted. The interdisciplinary effort was crucial in navigating the complexities of the patient's condition and devising an effective treatment strategy. While UV radiation remains a well-known cause of skin cancer, this case underscores that other factors, such as viral infections, can also play a significant role, particularly in individuals with compromised immune systems. The study's findings advocate for a more nuanced understanding of cancer etiology and the development of tailored treatment approaches. 'This Changes Everything': Scientists Unearth Pristine Ancient Forest Frozen For Thousands Of Years In Rocky Mountains Lessons from Related Viral Diseases The success of vaccination programs against alpha-HPV, which is responsible for many cervical and throat cancers, provides a hopeful perspective. These efforts have led to a substantial decline in deaths from such cancers, emphasizing the impact of targeted preventive measures. The parallels between alpha-HPV and beta-HPV suggest that similar strategies could be beneficial in managing virus-associated skin cancers. While the prospect of a universal cure for cancer remains distant, the ongoing advancements in understanding the molecular and viral underpinnings of various cancer types are promising. The new research on beta-HPV contributes to this growing body of knowledge, potentially paving the way for more effective interventions for cSCC and beyond. The Future of Cancer Treatment As research continues to unravel the intricate relationships between viruses, immune function, and cancer, the medical community is prompted to reconsider treatment paradigms. This study highlights the importance of recognizing viral factors in cancer development, especially in immunocompromised individuals. It raises the question of how personalized medicine can be further integrated into standard cancer care. With the findings published in The New England Journal of Medicine, the study opens new avenues for research and treatment. As we advance in our understanding of cancer's multifaceted nature, the question remains: how can we best leverage these insights to improve outcomes for patients with diverse genetic and immunological backgrounds? This article is based on verified sources and supported by editorial technologies. Did you like it? 4.5/5 (26)

Microbiome Changes May Affect Squamous Cell Carcinoma Risk
Microbiome Changes May Affect Squamous Cell Carcinoma Risk

Medscape

time07-08-2025

  • Health
  • Medscape

Microbiome Changes May Affect Squamous Cell Carcinoma Risk

Comparing metagenomic profiles of the skin microbiome in immunosuppressed patients and those at high and low risk for cutaneous squamous cell carcinoma (SCC) revealed distinct expansions in fungal and viral taxa in the first two groups, according to the authors of a recent research letter reporting the results. Such differences one day may help clinicians identify patients at high SCC risk, they added. Shadmehr Demehri, MD, PhD Currently, physicians identify patients at high SCC risk based on whether they have had several prior SCCs. Analyzing skin microbiome changes to identify patients at high SCC risk before they develop several SCCs could revolutionize dermatologic care, senior author and investigator, Shadmehr Demehri, MD, PhD, said in an interview. He is the Arthur and Sandra Irving Endowed Chair in Cancer Immunology and director of the High Risk Skin Cancer Clinic at Massachusetts General Hospital in Boston. Although age, ultraviolet exposure, and immunosuppression are well-known SCC risk factors, Demehri said, the skin microbiome's contribution to SCC risk remains unclear. To explore this issue, he and his coinvestigators conducted comparative metagenomic analyses of skin microbiomes from 30 patients: six with high SCC risk (> 2 prior SCCs), nine with low SCC risk (≤ 2 prior SCCs), and 15 solid organ transplant recipients (SOTRs). The results were published online in July in the Journal of Investigative Dermatology . Using swabs from six bilateral anatomical sites per patient, with air swabs as negative controls, the investigators performed shotgun metagenomic sequencing and differential-abundance analyses to compare relative taxa populations across patient groups. After an analysis of 249 metagenomes, high-risk individuals had the highest mean SCC count (11.8), followed by SOTRs (8.73) and low-risk individuals (0.33). 'Compared with low‐risk SCC subjects,' Demehri added, 'both solid organ transplant recipients and high‐risk SCC subjects showed higher relative abundances of eukaryotes, such as Malassezia restricta and M globosa , and viruses such as Betapapillomavirus .' Moreover, these taxa showed robust differences and strong discriminatory power between patient groups, indicating their potential utility as signatures of elevated SCC risk, he told Medscape Medical News . Which Comes First? Currently, it remains unclear whether the relative expansion of certain skin microbiome components directly drives SCC pathogenesis or reflects underlying immune alterations that raise SCC risk indirectly. And despite the eukaryotic expansions observed in the high-risk and SOTR groups, researchers saw no between-group differences in Malassezia -related conditions such as seborrheic dermatitis. Yet subclinical expansions in Malassezia and viral taxa still may translate into increased SCC risk, Demehri said. Accordingly, he said, dermatologists must not assume that people who develop certain viral and fungal skin diseases are at higher risk for SCC. 'It's more subtle changes, probably in association with other microbiome changes, that seem to be associated with skin cancer risk.' Nonetheless, Demehri said, watching for skin conditions that signify an expanded skin microbiome — such as the appearance of warts in fair-skinned adults — may signal the need to monitor for SCC risk. Commensal Concern Sancy A. Leachman, MD, PhD Sancy A. Leachman, MD, PhD, professor and vice-chair of faculty development in the Department of Dermatology at the University of Utah, Salt Lake City, said that although the study requires replication in larger, prospective cohorts, its findings are provocative for several reasons. She was not involved with the study but was asked to comment. Dermatologists are starting to embrace the skin microbiome concept but rarely beyond bacteria and yeasts, Leachman told Medscape Medical News . 'I don't believe most dermatologists are thinking about papillomaviruses being commensal: present on your skin as a normal part of your microbiome,' she said. The observation that baseline papillomavirus populations can exist on normal-appearing skin without causing pathology is important information, she added. 'What is their purpose there? What's the evolutionary advantage?' A study published in Cancer Cell in January 2025 showed that commensal papillomaviruses can boost immune surveillance and clearing of UV-induced p53-mutant keratinocytes. 'It appears that the commensal papillomavirus population may help to stimulate the immune system in a way that helps the immune response against skin cancer,' Leachman said. Papillomaviruses work primarily through p53. 'So if you've developed an immune reaction against a p53 element of the papillomavirus,' Leachman said, 'there's a possibility that might cross-react with abnormalities of the p53 pathway in squamous cell carcinomas and act like a mini-vaccine against the tumor. And if that's true, could you do that intentionally as a therapeutic or prevention strategy?' Human Papillomavirus (HPV) vaccines have proven highly effective in preventing cervical cancer. However, she said, based on the results of commensal HPVs protecting against SCC, it is unclear whether elimination of commensals by the vaccine could render some women more or less susceptible to SCC later in life. 'If those papillomavirus vaccines cross-react, and you're diminishing the commensal papillomaviruses that are helpful in recognizing squamous cell carcinoma,' she asked, 'are you going to have people who experience an idiosyncratic increase in squamous carcinoma because the HPV vaccine prevents development of a robust commensal population of helpful papillomaviruses? I don't believe anyone has even examined alterations of commensal HPV populations following vaccination.' Functional Immunosuppression One of the study's most tantalizing findings requiring further follow-up, Leachman said, is that the nonimmunosuppressed high-risk group (median age, 78.5 years) was much older than the low-risk group (63.0 years). 'That says there's probably some sort of functional immunosuppression occurring in those high-risk people.' As baby boomers age, Leachman added, the population with immune-system senescence will grow. 'If you can use solid organ transplant recipients as a model for the aging population that is becoming functionally immunosuppressed, that would be very beneficial, to know how to tailor treatments, detection methods, and even potential risk evaluation methods for these people.' Anecdotally, Leachman has identified a group of patients with what she calls systemic 'skin failure' — elderly patients at an extremely high SCC risk who routinely have multiple skin cancers and precancers excised. 'Generally, those people are older and have an apparent functional immunosuppression; in my hands, they seem to respond better to topical imiquimod than topical 5-fluorouracil.' Based on years of clinical observation, she prescribes topical immunotherapy rather than topical chemotherapy depending on patient age and the number and (wart-like) appearance of their SCCs. Microbiome Manipulation? In the interview, Demehri said that although it might be tempting to try and alter the skin microbiome through supplements or topical agents, nothing in the study suggests a cause-and-effect relationship such that modifying the microbiome would directly affect SCC risk. Therefore, he said that along with SCC detection and monitoring, immunosuppression and its role in skin cancer development should receive more emphasis. Presently, Demehri's lab is exploring ways to detect and monitor microbiome changes more feasibly than through costly shotgun sequencing. 'It's not something we can do for every patient all the time to monitor their skin. But there are ways we could extract that information more directly from the skin by swabs and then inform the physician that the patient might be at risk of cancer as well because their microbiome is being altered in ways that are associated with increased risk.' Broad adoption of such techniques, he estimated, is perhaps a few years away. This study was supported partly by the Intramural Research Programs of the National Human Genome Research Institute (NHGRI) and the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) at the National Institutes of Health. Study coauthors were from the Center for Cancer Immunology and the Cutaneous Biology Research Center at Massachusetts General Hospital and Harvard Medical School, Boston, and from the NHGRI and NIAMS. Demehri had filed a patent for the development of T cell-directed anticancer vaccines against commensal viruses. Other authors had no disclosures. Leachman is an investigator or advisor for several companies involved in screening and early diagnosis of melanoma but reported no relevant financial relationships . John Jesitus is a Denver-based freelance medical writer and editor.

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