BUFFALO, NY- April 23, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 7, entitled, “The coupling between healthspan and lifespan in Caenorhabditis depends on complex interactions between compound intervention and genetic background.”

Aging is characterized by declining health that results in decreased cellular resilience and neuromuscular function. The relationship between lifespan and health, and the influence of genetic background on that relationship, has important implications in the development of pharmacological anti-aging interventions. 

In this new study, researchers Stephen A. Banse, E. Grace Jackson, Christine A. Sedore, Brian Onken, David Hall, Anna Coleman-Hulbert, Phu Huynh, Theo Garrett, Erik Johnson, Girish Harinath, Delaney Inman, Suzhen Guo, Mackenzie Morshead, Jian Xue, Ron Falkowski, Esteban Chen, Christopher Herrera, Allie J. Kirsch, Viviana I. Perez, Max Guo, Gordon J. Lithgow, Monica Driscoll, and Patrick C. Phillips from the University of Oregon, The State University of New Jersey (Rutgers), The Buck Institute for Research on Aging, and National Institute on Aging assessed swimming performance as well as survival under thermal and oxidative stress across a nematode genetic diversity test panel to evaluate health effects for three compounds previously studied in the Caenorhabditis Intervention Testing Program and thought to promote longevity in different ways – NP1 (nitrophenyl piperazine-containing compound 1), propyl gallate, and resveratrol. 

“Overall, we find the relationships among median lifespan, oxidative stress resistance, thermotolerance, and mobility vigor to be complex.” 

The researchers showed that oxidative stress resistance and thermotolerance vary with compound intervention, genetic background, and age. The effects of tested compounds on swimming locomotion, in contrast, are largely species-specific. In this study, thermotolerance, but not oxidative stress or swimming ability, correlates with lifespan. Notably, some compounds exert strong impact on some health measures without an equally strong impact on lifespan. 

“Our results demonstrate the importance of assessing health and lifespan across genetic backgrounds in the effort to identify reproducible anti-aging interventions, with data underscoring how personalized treatments might be required to optimize health benefits.”

DOI - https://doi.org/10.18632/aging.205743

Corresponding authors - Gordon J. Lithgow - glithgow@buckinstitute.org, Monica Driscoll - driscoll@dls.rutgers.edu, and Patrick C. Phillips - pphil@uoregon.edu

About Aging-US

Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

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The Coupling Between Healthspan and Lifespan in Caenorhabditis Depends on…

BUFFALO, NY- May 21, 2024 – A new research #paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 9, entitled, “Germicidal lamps using UV-C radiation may pose health safety issues: a biomolecular analysis of their effects on apoptosis and senescence.”

The battle against the COVID-19 pandemic has spurred a heightened state of vigilance in global healthcare, leading to the proliferation of diverse sanitization methods. Among these approaches, germicidal lamps utilizing ultraviolet (UV) rays, particularly UV-C (wavelength ranging from 280 to 100 nm), have gained prominence for domestic use. 

These light-emitting diode (LED) lamps are designed to sanitize the air, objects, and surfaces. However, the prevailing concern is that these UV lamps are often introduced into the market without adequate accompanying information to ensure their safe utilization. Importantly, exposure to absorbed UV light can potentially trigger adverse biological responses, encompassing cell death and senescence.

In this new study, researchers Nicola Alessio, Alessia Ambrosino, Andrea Boggi, Domenico Aprile, Iole Pinto, Giovanni Galano, Umberto Galderisi, and Giovanni Di Bernardo from the University of Campania Luigi Vanvitelli, Regional Public Health Laboratory in Siena, Italy, ASL Napoli 1 Centro P.S.I. Napoli Est-Barra, and Temple University performed a series of investigations aimed at comprehending the biological repercussions of UV-C radiation exposure from readily available domestic lamps. 

“Our focus centered on epithelial retinal cells, keratinocytes, and fibroblasts, components of the skin and ocular targets frequently exposed to UV irradiation.”

Their findings underscore the potential harm associated with even brief exposure to UV, leading to irreversible and detrimental alterations in both skin cells and retinal cells of the eye. Notably, epithelial retinal cells exhibited heightened sensitivity, marked by substantial apoptosis. In contrast, keratinocytes demonstrated resilience to apoptosis even at elevated UV doses, though they were prone to senescence. Meanwhile, fibroblasts displayed a gradual amplification of both senescence and apoptosis as radiation doses escalated.

“In summary, despite the potential benefits offered by UV-C in deactivating pathogens like SARS-CoV-2, it remains evident that the concurrent risks posed by UV-C to human health cannot be ignored.”

DOI - https://doi.org/10.18632/aging.205787

Corresponding authors - Umberto Galderisi - umberto.galderisi@unicampania.it, and Giovanni Di Bernardo - gianni.dibernardo@unicampania.it

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Keywords - aging, senescence, apoptosis, UV light, public health

About Aging-US

Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.

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Germicidal Lamps Using UV-C Radiation May Pose Health Safety Issues

BUFFALO, NY- October 11, 2024 – A new #editorial was #published in Oncotarget's Volume 15 on October 1, 2024, entitled, “Transplant or no transplant for TP53 mutated AML.”

As highlighted in this editorial, TP53 mutations (mut) occur in 10–15% of acute myeloid leukemia (AML) cases, commonly associated with therapy-related AML (t-AML) and complex cytogenetics (CG). TP53-mut AML is inherently resistant to conventional chemotherapies and continues to show a poor prognosis, even with venetoclax-based therapies. Allogeneic hematopoietic stem cell transplant (allo-HCT) remains a potential curative option, though only 10–15% of patients receive it. In a recent study, allo-HCT was the only variable significantly improving survival, despite only 16% of patients successfully bridging to it.

In their editorial, researchers Talha Badar, Moazzam Shahzad, Ehab Atallah, Mark R. Litzow, and Mohamed A. Kharfan-Dabaja from the Division of Hematology-Oncology and Blood and Marrow Transplantation and Cellular Therapy Program at Mayo Clinic (Jacksonville, Florida) evaluated the outcomes of TP53-mutated AML patients based on data from the Consortium of Myeloid Malignancies and Neoplastic Diseases (COMMAND). The study found a “dismal” survival rate of 8.5 months, with no significant difference among treatment types, and allo-HCT was the only variable associated with improved survival.

The authors also report on the “better long-term outcomes” when allo-HCT was performed during Complete Remission 1 (CR1) in previous observations. They acknowledge the limitations of their retrospective analysis, including selection bias, data heterogeneity from participating institutions, and the lack of complete molecular data prior to allo-HCT that might have influenced the results. Nevertheless, the findings are encouraging and suggest that allo-HCT improves long-term outcomes in this poor prognostic disease, where effective therapies remain limited.

“In summary, this study reported improved survival when allo-HTC was performed in CR1 versus after later lines of therapy.”

DOI -  https://doi.org/10.18632/oncotarget.28652

Correspondence to - Talha Badar - badar.talha@mayo.edu

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Keywords - cancer, AML, TP53 mutation, allogeneic stem cell transplant

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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TP53 mutated AML: Transplant or No Transplant

TP53 Mutated AML: Transplant or No Transplant

BUFFALO, NY- November 5, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 20 on October 17, 2024, entitled, “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.”

Researchers from the Department of Laboratory Medicine and Pathology at the University of Washington have discovered that the Werner syndrome gene (WRN), linked to premature aging, plays a crucial role in maintaining cellular organization and DNA stability. Their study shows that loss of WRN function disrupts essential protein interactions, potentially accelerating aging as cells lose structural integrity.

Werner syndrome is a rare genetic disorder that causes accelerated aging due to mutations in the WRN gene, which disrupts normal cell functions. The WRN gene is typically responsible for essential tasks like DNA repair, replication, and maintaining telomeres—the protective caps on DNA that shorten with age. However, exactly how WRN loss leads to faster aging is still not fully understood.

In this study, researchers Pavlo Lazarchuk, Matthew Manh Nguyen, Crina M. Curca, Maria N. Pavlova, Junko Oshima, and Julia M. Sidorova found that beyond its known roles, the WRN gene is also essential for maintaining a specialized structure in the cell nucleus called constitutive heterochromatin (CH). CH is a densely packed form of DNA that keeps certain parts of the genome stable and “switched off,” protecting against unwanted changes. In cells lacking WRN, the CH structure becomes disorganized, leading to DNA instability and accelerating cellular aging.

Another important finding was that WRN loss affects the nuclear envelope, the membrane surrounding DNA, which houses essential proteins like Lamin B1 and Lamin B receptor (LBR). These proteins anchor constitutive heterochromatin (CH) to the nuclear membrane, helping keep DNA compact and stable. Without WRN, this anchoring weakens, and the cell’s internal structure begins to resemble that of aging cells.

“Our study highlights WRN as a contributor to the integrity of CH and points at the altered levels and distribution of LBR as a mediating mechanism.” 

By identifying WRN’s role in organizing the cell’s interior, this study provides a new perspective on age-related genomic instability, where DNA becomes more prone to damage.

In conclusion, this research highlights the importance of stable cell structures in slowing aging, potentially paving the way for future treatments targeting WRN pathways to protect DNA integrity and combat premature aging. This new insight may also inform therapies for age-related diseases.

DOI - https://doi.org/10.18632/aging.206132

Corresponding Author - Julia M. Sidorova - julias@uw.edu

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Keywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeats

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The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

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Werner Syndrome RECQ Helicase and Heterochromatin Maintenance in Human Cells

BUFFALO, NY- November 19, 2024 – A new #review was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 29, 2024, Volume 16, Issue 20, titled, ”Brain aging and Alzheimer’s disease, a perspective from non-human primates.“

In the review, Ferrer Isidro from the University of Barcelona and Reial Acadèmia de Medicina de Catalunya, explores the differences in brain aging and Alzheimer’s disease between humans and their closest evolutionary relatives, such as chimpanzees, baboons, and macaques. The study highlights that while humans are uniquely susceptible to severe cognitive decline and memory loss caused by Alzheimer’s disease, non-human primates typically experience only mild changes as they age.

Alzheimer’s affects over 50 million people worldwide, making it crucial to understand how aging impacts the brain. This review sheds light on the differences between humans and non-human primates and reveals that while brain aging in primates involves some structural and protein changes, it does not result in the toxic protein deposits that drive Alzheimer’s in humans.

In humans, harmful tau protein deposits, known as tau tangles, appear early in life and spread widely through the brain, which damages cells and contributes to memory loss. In non-human primates, tau tangles are rare and typically confined to small regions. While primates may develop beta-amyloid deposits—fragments derived from amyloid precursor protein—these deposits are less toxic and do not interact with tau tangles to trigger Alzheimer’s-like symptoms. Aging primates experience only mild memory or behavioral changes, avoiding the severe cognitive decline and dementia often seen in humans.

Humans’ unique vulnerability to Alzheimer’s may be linked to traits that emerged through evolution, including larger brains, longer lifespans, and higher cognitive abilities. These adaptations may have come at a cost, making human brains more susceptible to aging-related damage.

This review also suggests that tau tangles play a more critical role in Alzheimer’s progression than previously thought. While traditional treatments focus on targeting beta-amyloid deposits, this research highlights the need to shift attention to tau pathology. The work challenges the widely accepted amyloid cascade hypothesis, which suggests that beta-amyloid is the main driver of Alzheimer’s. Instead, it points to tau tangles as the initial and most damaging change in human brains. This insight could encourage new treatments that focus on preventing or reducing tau deposits.

The findings also emphasize the value of studying non-human primates to understand why their brains are more resistant to severe aging-related damage. By identifying protective mechanisms in primates, researchers may discover new strategies to delay or prevent Alzheimer’s in humans. 

“These observations show that human brain aging differs from brain aging in non-human primates, and humans constitute the exception among primates in terms of severity and extent of brain aging damage.”

In conclusion, this review not only improves our understanding of why humans are uniquely vulnerable to Alzheimer’s disease but also opens new avenues for exploring innovative strategies to combat aging-related brain damage in humans.

DOI - https://doi.org/10.18632/aging.206143

Corresponding author - Ferrer Isidro - 8082ifa@gmail.com

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About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

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Brain Aging and Alzheimer’s: Insights from Non-Human Primates

Would you take a test to find out your cancer risk? At-home genetic testing makes it easy, but experts warn that these tests may create more harm than good.

A New Approach to Genetic Testing

Genetic testing has traditionally been performed under the supervision of healthcare providers, with genetic counseling to help patients navigate their results. This approach ensures that individuals receive proper guidance, reducing the emotional and practical challenges of interpreting complex genetic information.

In September 2023, the United States Food and Drug Administration (FDA) approved a new test called the Invitae Common Hereditary Cancers Panel. This test checks for changes in 48 genes linked to hereditary cancers, including breast, ovarian, and Lynch syndrome-related cancers. What makes it different is that it can be ordered online and taken at home with no doctor required.

While the convenience of these tests is appealing, health experts have raised serious concerns. An editorial titled “Pitfalls and Perils from FDA-Approved Germ-line Cancer Predisposition Tests,” authored by Dr. Wafik S. El-Deiry, Editor-in-Chief of Oncotarget, and Dr. Eli Y. Adashi, both from Brown University, highlights the potential risks of using these tests without professional guidance.

Full blog - https://www.oncotarget.org/2025/01/03/the-hidden-risks-of-at-home-genetic-cancer-tests/

Paper DOI - https://doi.org/10.18632/oncotarget.28677

Correspondence to - Wafik S. El-Deiry - wafik@brown.edu

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Keywords - cancer, cancer predisposition, germline, marketing authorization, hereditary cancer, direct to consumer

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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The Hidden Risks of At-Home Genetic Cancer Tests

BUFFALO, NY – February 14, 2025 – A new #review was #published in Oncotarget, Volume 16, on February 12, 2025, titled “SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.”

Authors Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, and Antonin Marchais from the Gustave Roussy Cancer Campus analyzed recent studies on a gene called SETDB1, which may play a key role in osteosarcoma, a type of bone cancer that mostly affects teenagers and young adults. Their review highlights how SETDB1 helps cancer cells grow, resist treatment, and avoid the immune system. Because of this, blocking SETDB1 could be a promising new way to treat osteosarcoma.

Osteosarcoma is a fast-growing bone cancer that is usually treated with surgery and chemotherapy. However, if the cancer spreads or returns, treatment options are very limited. Scientists are searching for new ways to stop this disease, and recent studies have found that osteosarcoma cells often have extra copies of the SETDB1 gene. This seems to make the cancer more aggressive and harder to treat.

“Whole exome sequencing of osteosarcoma samples from both diagnosis and relapses has highlighted several factors, including SETDB1, that are amplified in the most aggressive forms of the disease.”

SETDB1 is involved in epigenetics, meaning it affects how genes are turned on and off without changing the DNA itself. The review explains that SETDB1 helps tumors hide from the immune system, making it difficult for the body to fight the cancer naturally. The researchers believe that blocking SETDB1 could help the immune system recognize and attack osteosarcoma cells. Some experimental drugs that target SETDB1 are already being tested in the lab.

The review also describes how SETDB1 influences key cancer pathways, such as Wnt signaling, which helps cancer cells grow, and epithelial-mesenchymal transition (EMT), a process that allows cancer to spread. The authors suggest that combining SETDB1-blocking drugs with immunotherapy or radiation could be an effective new strategy for treating osteosarcoma.

Another key finding is that SETDB1 may help cancer cells become resistant to chemotherapy, making treatment less effective. This means that drugs targeting SETDB1 could not only slow cancer growth but also make existing treatments work better.

While more research is needed, this review brings attention to SETDB1 as a potential treatment target. Scientists hope that a deeper understanding of SETDB1 will lead to new therapies that improve survival rates for osteosarcoma patients.

DOI - https://doi.org/10.18632/oncotarget.28688

Correspondence to - Antonin Marchais - antonin.marchais@gustaveroussy.fr, and Maria Eugenia Marques Da Costa - jenny.marquescosta@gustaveroussy.fr

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About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

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SETDB1 Amplification Identified as a Potential Target for New Osteosarcoma Treatment

BUFFALO, NY – July 14, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 25, 2025, titled “Hypoxia induced lipid droplet accumulation promotes resistance to ferroptosis in prostate cancer.”

In this study, researchers led by Shailender S. Chauhan and Noel A. Warfel from the University of Arizona discovered that prostate cancer cells survive treatment by storing fats in tiny cellular compartments when oxygen levels are low. This process makes the cancer cells less vulnerable to a type of cell death known as ferroptosis. The findings provide new insight into why prostate tumors often resist therapies and suggest potential strategies to improve treatment outcomes.

This study focused on ferroptosis, a form of programmed cell death that relies on iron and lipid oxidation to destroy cancer cells. Researchers tested prostate cancer cells under normal and low oxygen conditions and found that hypoxia, or reduced oxygen levels, allowed cancer cells to build up lipid droplets (LD). These structures act as storage units for fats, shielding cancer cells from oxidative damage and preventing ferroptosis from occurring.

The researchers found that this adaptation of prostate cancer cells made them less sensitive to ferroptosis-inducing drugs like Erastin and RSL3, even when these drugs were combined for a stronger effect. The team also reported that hypoxia caused significant changes in lipid metabolism, decreasing the availability of specific fatty acids that normally promote ferroptosis. 

“Transcriptomic analysis revealed that hypoxia significantly reduced the expression of genes related to incorporating polyunsaturated fatty acids into phospholipids (ACSL4, LPCAT3), and parallel lipidomic analysis demonstrated that hypoxia significantly decreased the levels of the ferroptosis-prone lipid class, phosphatidylethanolamine (PE) and increased production of neutral lipid species, cholesteryl ester (ChE (22:5)) and triglycerides (TG(48:1), TG:(50:4), and TG(58:4)).”

This research highlights the importance of the tumor microenvironment, particularly oxygen levels, in shaping how cancer cells respond to therapy. By altering their metabolism and storing lipids, prostate tumors may evade treatments designed to trigger ferroptosis. These findings underscore the need to develop new strategies targeting LD dynamics or lipid metabolism to overcome this resistance.

Understanding how prostate cancer (Pca) adapts to survive in hypoxic conditions offers a potential avenue for improving therapies. For example, preventing lipid accumulation in cancer cells or releasing stored fats may restore their sensitivity to ferroptosis and improve the effectiveness of current therapies. This approach could have broader implications for treating other solid tumors that share similar metabolic features.

DOI - https://doi.org/10.18632/oncotarget.28750

Correspondence to - Noel A. Warfel - warfelna@arizona.edu, and Shailender S. Chauhan - shailenderc@arizona.edu

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Keywords - cancer, hypoxia, lipid droplets, ferroptosis, resistance, prostate

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Prostate Cancer Cells Survive Treatment by Storing Fat in Low Oxygen Conditions

BUFFALO, NY — July 15, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 5, 2025, titled “Senescence caused by telomerase inactivation in myeloid, mesenchymal, and endothelial cells has distinct effects on cancer progression.”

In this study, first author Joseph Rupert, along with corresponding author Mikhail G. Kolonin and colleagues from The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, McGovern Medical School, at The University of Texas Health Sciences Center at Houston, investigated how aging-related changes in different cell types affect cancer progression. By turning off telomerase in specific cell populations in mice, the researchers discovered that cell aging, or senescence, can slow primary tumor growth but also trigger unexpected effects. This work sheds light on the complex relationship between aging cells and cancer and may help guide future anti-cancer strategies.

The team used genetically modified mice to deactivate telomerase, the enzyme that maintains chromosome ends, specifically in immune, connective tissue, and blood vessel cells. This caused these cells to enter a state of senescence, where they stop dividing and release inflammatory signals. The researchers then implanted breast, prostate, and pancreatic cancer cells into the mice and tracked how tumors developed. They found that when telomerase was inactivated in immune cells or connective tissue cells, tumors grew more slowly. However, these tumors showed signs of increased tissue damage and potential aggressiveness.

Interestingly, when telomerase was turned off in endothelial cells, which cover blood vessels, tumors shrank and became poorly supplied with blood, leading to oxygen deprivation. In the case of pancreatic cancer cells, this low-oxygen environment made them more likely to spread to the liver, highlighting a potential risk of targeting these cells.

“[…] this study shows that senescence and metabolic dysfunction resulting from telomerase inactivation in distinct cells in the tumor microenvironment have different effects on tumor growth and metastasizing of carcinomas.”

This research provides important insights into how aging cells within the tumor microenvironment (TME) influence cancer behavior. While senescence in certain cell types can help suppress tumor growth, it may also create conditions that favor cancer metastasis. These findings highlight the need to consider cell type-specific effects when developing therapies that target senescent cells. By mapping how different cell populations contribute to cancer progression in aging tissues, this study opens the door for more precise approaches to prevent both tumor growth and spread.

DOI - https://doi.org/10.18632/aging.206268

Corresponding author - Mikhail G. Kolonin - mikhail.g.kolonin@uth.tmc.edu

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Keywords - aging, senescence, telomerase, myeloid, mesenchymal, endothelial

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How Telomerase Inactivation in Aging Cells Influences Cancer Growth and Metastasis

BUFFALO, NY – July 24, 2025 – A new #casereport was #published in Volume 16 of Oncotarget on July 23, 2025, titled “Extracorporeal blood filtration leading to tumor growth arrest and reduced analgesic requirements in Stage IV poorly differentiated pancreatic adenocarcinoma: A case report.”

In this report, Susanna Ulahannan from the University of Oklahoma Health Sciences Center and colleagues describe the use of extracorporeal blood filtration in a patient with metastatic pancreatic cancer. The patient experienced clinical improvement, reduced pain, and no signs of new tumor growth over 12 months of follow-up.

Metastatic pancreatic cancer is difficult to treat and is often diagnosed at an advanced stage. In this case, a 51-year-old woman with stage IV poorly differentiated adenocarcinoma chose not to undergo standard chemotherapy. Instead, she received extracorporeal blood filtration with the Seraph® 100 device, which is designed to remove circulating tumor cells (CTCs) from the bloodstream. CTCs are thought to contribute to the spread of cancer to other organs.

“Circulating tumor cells (CTC’s) are tumor cells that are shed from the primary tumor and travel via blood or lymphatic system to form micro metastases in distant organs under a suitable environment.“

The patient received between nine and twelve treatments over the course of a year. These treatments were performed both abroad, where the device is approved for this use, and under a clinical protocol in the United States. Medical imaging showed that her disease remained stable, with no new metastases detected. She also reported improvements in appetite, energy levels, and pain control. Her opioid use was reduced by 90%.

Blood samples confirmed a drop in CTC levels after treatment. This observation supports the idea that removing CTCs might help limit cancer progression in some patients. However, given that this is a single case report, larger clinical studies are needed to evaluate the effectiveness of this approach.

The mechanism behind the patient’s pain relief is not fully understood. Authors suggest that it may be related to the reduction of tumor cells or inflammatory molecules in the blood. Researchers noted that pro-inflammatory cytokines, known to influence pain, could also have been affected by the filtration process.

This is the first documented case of stable disease and reduced symptoms following CTC filtration in advanced pancreatic cancer. While these findings should not be generalized, they highlight an approach outside standard protocols that should be further explored in clinical research. Future studies will be needed to determine whether this method can contribute to symptom management or disease control in other patients with metastatic pancreatic cancer.

DOI - https://doi.org/10.18632/oncotarget.28756

Correspondence to - Susanna Ulahannan - susanna-ulahannan@ouhsc.edu

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Keywords - cancer, extracorporeal blood filtration, circulating tumor cells, metastatic pancreatic cancer, seraph 100, OncoBind

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Blood Filtration Stabilizes Advanced Pancreatic Cancer: A Case Report

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

Cancer and aging are two sides of age-related tumorigenesis.

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

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