BUFFALO, NY – October 20, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on October 16, 2025, titled “Widespread folate receptor expression in pediatric and adolescent solid tumors – opportunity for intraoperative visualization with the novel fluorescent agent pafolacianine.”

In this study, led by first author Ashley C. Dodd from Ann & Robert H. Lurie Children’s Hospital and corresponding author Timothy B. Lautz from the same institution and Northwestern University Feinberg School of Medicine, researchers discovered that folate receptor beta (FRβ) is widely expressed in various pediatric and adolescent solid tumors. This finding highlights FRβ as a promising target for improving the accuracy of tumor surgery using a fluorescent imaging agent known as pafolacianine.

Pediatric cancers are often challenging to remove completely during surgery, particularly when tumors spread or form small metastases. Fluorescence-guided surgery is a method that helps surgeons better identify tumors during operations using special imaging dyes. However, commonly used dyes such as indocyanine green are not tumor-specific and rely on general features of blood vessel permeability, limiting their precision.

In this study, researchers investigated the potential of pafolacianine, a next-generation dye that targets folate receptors, for pediatric use. Folate receptors are proteins commonly found on the surface of cancer cells. Pafolacianine is already FDA-approved for adults with ovarian and lung cancers due to its ability to bind these receptors and highlight tumors during surgery. 

The research team analyzed tissue samples from 13 young patients diagnosed with various cancers, including Wilms tumor, osteosarcoma, synovial sarcoma, rhabdomyosarcoma, Ewing sarcoma, and neuroblastoma. The results showed that FRα was predominantly absent, whereas FRβ was present in 100% of the tumor samples. Notably, FRβ appeared both on the tumor cells and in the surrounding tumor microenvironment but showed little to no expression in normal tissue, making it an excellent candidate for targeted imaging.

“In this study, we performed immunohistochemistry staining on slides obtained from a range of pediatric patients with solid tumors.”

This consistent expression of FRβ in pediatric tumors is a significant and novel finding. Earlier studies primarily linked FRβ to immune cells called tumor-associated macrophages. This study reveals that FRβ is also expressed directly on tumor tissue, which could help surgeons better distinguish cancer from healthy tissue during procedures.

Based on these results, the team has launched a clinical trial to evaluate pafolacianine in children undergoing surgery for metastatic lung tumors. If successful, this method could make pediatric cancer surgery safer and more effective.

Overall, this study suggests that targeting FRβ with pafolacianine could serve as a tumor-agnostic imaging strategy, applicable across a wide range of pediatric solid tumors. This represents a potential advancement in real-time surgical imaging and a step forward in pediatric cancer care.

DOI - https://doi.org/10.18632/oncotarget.28772

Correspondence to - Timothy B. Lautz - TLautz@luriechildrens.org

Abstract video - https://www.youtube.com/watch?v=0its0QkOcwM

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Oncotarget

Folate Receptor Beta Found in Pediatric Tumors May Improve Fluorescence-Guided Cancer Surgery

Beat by @comfortfabricritual, additional melodies, samples, sound design, drums and rapping by DJ Chud

Strains and Dextro move me slow like a wounded stormtrooper, those pussy boys square like tabs, claim they dogs, you must be neutered
You off X instead of CBD in a laced stupor, DJ Chud can and will take the beef outside of the computers
Come to the show on that same time if you want yo ass booted up, I live life on one chance with a debilitating lack of fucks
Live it like my last, and make shit tight like tourniquet, I’m passionate, if money gets in the way of my dreams then I’ll gladly burn through it

But you know I stack it from doing this shit, so that’ll never be a problem, I got the beauty:beast on cause I’m both, hot mess with problems
I hate the game more than The Manic Street Preachers, I hate these niggas more than Piper Thiel Peter
I cloud my brain up with the packs spring green reefer, I know I’m bound to blow up like a same colored Creeper
Niggas who say shit ain’t that deep haven’t been deeper than the surface level ‘cause they know if they do they’ll become seethers

They’re cattle, I count and smoke Sour Apple and lick Granny Smith tadpoles sprinkled with the bud that’s colored a shade of cantaloupe
Higher than Building 7, yeah, that’s fo’ sho, AW98 garments got me in a chokehold like Austin, stone cold
Coldsteel The Hedgeheg, psssh, nothin personnel, Prada bags on my personal, don’t get blood on my Monolith Leather Loafs
Once she make them ankles cuff, then I bust rose gold, Cash Domain Motorsports, we blow up the game’s Walls Of Jericho

All about my chips, no Fritos, MLG timing, Obey snapback, Mtn Dew and Doritos
Build yo whole gang up just to put y’all down, Home Depot, demolish the scene is the M.O
‘Cause I know I’ll be alienated from the game no matter how hard the music go, that’s cool, I’ll just drift my own tides mad slow
In the corner, staring at the walls, Blair Witch Project or Dizzee Rascal, after BT dropped, I went Pluto, took my mask off

Dress New Weird America, hysteria is glamorous, met some Freaky Folk on Babcock trying to catch a Lyft
Off the blocks of kush, I see aliens like Nowhere by Gregg Araki, don’t even try to stop me, I’m Dark Smith and Darko Donnie
If everyone in the game my son, I failed as a father, I taught you niggas better than to copy


Computers (Prod Comfort Fabric Ritual 🤝 DJ Chud)

BUFFALO, NY — October 21, 2025 — A new #editorial was #published in Aging-US on October 13, 2025, titled “Longevity clinics: between promise and peril.”

In this editorial, Marco Demaria, Editor-in-Chief of Aging-US, from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), reviews the rapid rise of longevity clinics worldwide. 

Longevity clinics have emerged globally in response to increasing demand for personalized, preventive healthcare. Located in countries such as the United States, Switzerland, and the United Arab Emirates, these centers offer advanced diagnostic services, including genomic testing, advanced imaging, and multi-omics profiling. Their goal is to extend healthspan—the number of years a person lives in good health—through customized lifestyle interventions, nutritional guidance, and, in some cases, experimental therapies.

“Longevity clinics embody an important vision: healthcare is personalized, preventive, and engaged.”

Although the concept of proactive aging care is attractive, the editorial raises serious concerns about the scientific and ethical foundations of these clinics. Many operate outside conventional medical systems and lack connections to academic geroscience. This disconnection allows them to market expensive interventions without sufficient clinical validation. Program costs can range from €10,000 to over €100,000 per year, limiting access to wealthy individuals while leaving out populations most at risk for premature aging.

Despite these challenges, Dr. Demaria notes that longevity clinics may contribute meaningfully to innovation. By collecting extensive, long-term health data from clients, these clinics have the potential to identify early biomarkers of aging and detect signs of age-related diseases. Unlike traditional clinical trials, which are limited in scope and duration, longevity clinics track a wide range of health data over time. When paired with artificial intelligence tools, this information could help advance the science of healthy aging.

However, several risks remain. Many clinics lack standardized protocols, and the tools they use, such as biological age calculators or hormone therapies, often lack accuracy or clear clinical value. Without proper guidelines, clients may receive advice that is confusing or not scientifically supported. This can reduce public trust in the broader field of longevity research.

To ensure these clinics contribute positively to health innovation, the editorial outlines different key steps: greater collaboration with academic researchers, the adoption of standardized protocols, increased transparency, and work toward regulatory clarity. Broader access must also be considered by developing scalable and more affordable models, possibly through partnerships with public health systems.

Ultimately, longevity clinics represent both a major opportunity and a serious concern. If integrated responsibly with science, policy, and public health, they could support a shift toward personalized, preventive healthcare. Without this alignment, however, they risk reinforcing inequality and weakening the credibility of the science behind aging.

DOI - https://doi.org/10.18632/aging.206330

Corresponding author - Marco Demaria — m.demaria@umcg.nl

Abstract video - https://www.youtube.com/watch?v=Bt84xBdii0s

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Aging-US

The Rise of Longevity Clinics: Promise, Risk, and the Future of Aging

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare blood cancer that primarily affects older adults. One of the key challenges in diagnosing and treating BPDCN is that it closely resembles other forms of leukemia in both appearance and behavior. This overlap often leads to delays or uncertainty in diagnosis, especially since currently there is no single, reliable marker that clearly distinguishes BPDCN from related diseases.

To address this issue, researchers from the City of Hope Comprehensive Cancer Center investigated the genetic profile of BPDCN.  Their study, titled “Genetic characteristics of blastic plasmacytoid dendritic cell neoplasm: A single institution experience,” was published in Oncotarget (Volume 16).

Full blog - https://www.oncotarget.org/2025/10/22/genetic-study-identifies-potential-diagnostic-marker-for-rare-blood-cancer-bpdcn/

Paper DOI - https://doi.org/10.18632/oncotarget.28742

Correspondence to - Michelle Afkhami - mafkhami@coh.org

Abstract video - https://www.youtube.com/watch?v=wUjr3uU3onI

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Keywords - cancer, Blastic plasmacytoid dendritic cell neoplasm (BPDCN), Next-generation sequencing (NGS), CCDC50

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Genetic Study Identifies Potential Diagnostic Marker for Rare Blood Cancer BPDCN

Produced by 54V4G3 B4ND1T

LYRICS:

Hey you
I see you in your room
Wondering what to do
They made you look a fool
But you are no fool

Ok, I’m no fool but why’d I have to go through it
I’m stuck maneuvering whether to tell or hush
A broken innocence don’t wanna make a fuss
But it weighs on my consciousness, so what’s up

Let’s weigh the pros and cons since you won’t let me leave
I’m tryna stand up but an angel’s blocking me
God since you know best how come I was so deceived
How come the world spins in your hands but I’m here with broken wings

This is my grave song
Maybe I take it to the grave
Don’t let them hear something
Not from me, no

But I want to be free
It’s not my fault, no it’s not
The devil thought
He had me down
But I stood up
I stood up

No whispering
Stop it, make some noise
No pros and cons to the sin
Come on and make some noise
It’s getting loud in here
I’m filling up with fear
But in my mind it’s clear
Take back your power dear
Oh dear oh dear
Oh dear
I see your little tears
Know that they aren’t in vain
There’s comfort in the pain

Grave Song (Prod. 54V4G3 B4ND1T)

BUFFALO, NY — October 23, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 11, 2025, titled “Roles of plasminogen activator inhibitor-1 in aging-related muscle and bone loss in mice.”

In this study led by first author Takashi Ohira and corresponding author Hiroshi Kaji from Kindai University Faculty of Medicine, researchers found that female mice lacking the gene for plasminogen activator inhibitor-1 (PAI-1) were protected from age-related muscle weakness and bone thinning. This suggests that PAI-1 could be a potential target for future treatments to reduce frailty in aging populations.

As the global population continues to age, more people are affected by conditions such as sarcopenia and osteoporosis. These disorders involve the progressive loss of skeletal muscle mass and bone density, leading to reduced mobility, a greater risk of falls, and a lower quality of life.

To investigate the role of PAI-1 in aging, researchers compared young (6-month-old) and aged (24-month-old) male and female mice, with and without the PAI-1 gene. They found that PAI-1 levels increased with age in both sexes. However, only female mice lacking the PAI-1 gene experienced a significant reduction in age-related muscle and bone loss.

Female mice without PAI-1 maintained stronger grip strength and greater muscle mass in their lower limbs. They also showed less cortical bone loss in their femurs and tibias. In contrast, male mice did not experience the same benefits, despite also showing increased levels of PAI-1 with age. These results suggest that PAI-1 contributes to aging-related decline in a sex-specific manner.

“The present study found that lower limb muscle mass, gastrocnemius and soleus muscle tissue weights, and grip strength were significantly lower in 24-month-old male and female wild-type mice than in their 6-month-old counterparts.”

PAI-1 plays key roles in blood clotting, inflammation, and cellular senescence—a process in which aging cells release harmful molecules that affect nearby tissues. One of these molecules, interleukin-6 (IL-6), is a major driver of inflammation. The researchers found that aged female mice lacking PAI-1 had lower IL-6 levels in both muscle and blood, suggesting that PAI-1 may contribute to muscle and bone loss by promoting inflammation. These protective effects were also not associated with changes in muscle protein turnover or reductions in fibrous tissue, reinforcing the idea that PAI-1’s impact is likely driven by inflammatory signaling.

This study highlights PAI-1 as a promising therapeutic target for slowing or preventing age-related declines in muscle and bone health, particularly in women. Since postmenopausal women are especially vulnerable to osteoporosis and frailty, a better understanding of how PAI-1 contributes to aging could lead to new strategies for maintaining strength and mobility in later life. Further research is needed to explore how PAI-1 interacts with other age-related biological changes and why its effects differ between sexes.

DOI - https://doi.org/10.18632/aging.206318

Corresponding author - Hiroshi Kaji - hkaji@med.kindai.ac.jp

Abstract video - https://www.youtube.com/watch?v=hg4qKf-oO2I

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PAI-1 Deficiency Protects Aging Female Mice from Muscle and Bone Loss

(prod.kash)

 [Lyrics]
my heart it dosent move, it dosent know where to go 
if u leave, don't go far away 
i kinda of hate when people change

my heart it dosent move, it dosent know where to go 

the pills won't help, the friends won't help
family askin why I 
askin why I 
never mind 

why wont you try to belive in me
said i was jus wastin you time (wastin your time)
why am i still stuck on the first season 
does pain ever go away

my heart it dosent move, it dosent know where to go 
if u leave, don't go far away 
I kinda of hate when people change
my heart it dosent move, it doesn't know where to go

my heart is lost/ no one cares to help

(prod.kash)

[Lyrics]

you knew why i didnt say anything when u left
did it make me mad i guess
was that last text a threat
you knew why i didnt say anything when u left

why dont you just tell the truth 
cus my mind is tryna loose
itself 

i dont know why its tryna do that
my heart was beating so fast when i was talked to you 
guess that shows how much i cared

you knew why i didnt say anything when u left
did it make me mad i guess
was that last text a threat

i didn’t say anything/ you knew why

Découvrez des confidences inédites, surprenantes et véridiques racontées par 
Cindy Cinnamon, personnalité publique Québécoise
www.CindyCinnamon.com 

Site Officiel du Podcast:  www.CindylaDit.com 

Pour une meilleure compréhension et mieux suivre l’évolution de ce témoignage, il est recommandé de commencer par le premier épisode.

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Bonne Écoute et Gardez l’Esprit Ouvert 

73 - Quand on débute, on prend ce qui passe - Episode 73

BUFFALO, NY — October 27, 2025 — A new #research paper was #published in Volume 17, Issue 9 of Aging-US on September 17, 2025, titled “Depletion of the TRF1 telomere-binding protein leads to leaner mice with altered metabolic profiles.”

In this study led by first author Jessica Louzame Ruano and corresponding author Maria A. Blasco from the Spanish National Cancer Centre (CNIO), researchers investigated the role of TRF1, a protein known for protecting telomeres, in regulating whole-body metabolism. The results suggest that TRF1 influences metabolic health through mechanisms unrelated to its known function in telomere maintenance.

Obesity and metabolic disorders are major health concerns, especially as people age. To explore TRF1’s role beyond telomere protection, the research team studied both normal mice and genetically modified mice that lacked TRF1. Mice without TRF1 remained leaner over time, resisted fat accumulation, and showed healthier blood sugar and insulin levels compared to normal mice. Importantly, these benefits occurred without any detectable shortening of telomeres.

The leaner body composition in TRF1-deficient mice was not due to reduced food intake or increased physical activity. Instead, the fat loss appeared to result from biological changes in how energy was processed and stored. Male mice without TRF1 gained less weight and had lower LDL cholesterol levels, even on a high-fat diet. Female mice showed milder effects, reflecting known sex-based differences in susceptibility to diet-induced obesity. This highlights the importance of including both sexes in metabolic research.

“Major metabolic pathways related with energy production and regulation of metabolism homeostasis were also found downregulated in Trf1-deficient mice.”

Gene expression analysis in the liver revealed shifts in several key pathways. Genes related to fat production, energy generation, and muscle growth were downregulated, while genes linked to inflammation and cholesterol synthesis were upregulated. The mice also showed signs of higher energy expenditure and a shift from using fat to protein as an energy source, possibly due to their reduced fat reserves. However, some older mice developed mild liver stress, including fibrosis and DNA damage, suggesting a possible long-term trade-off.

Overall, this study expands the understanding of how telomere-related proteins influence more than just cellular aging. By identifying a connection between TRF1 and metabolism, the research opens new possibilities for targeting TRF1 or its pathways to address obesity and related conditions. Still, further studies are needed to clarify how TRF1 affects fat development and whether similar effects occur in humans.

DOI - https://doi.org/10.18632/aging.206320

Corresponding author - Maria A. Blasco — mblasco@cnio.es

Abstract video - https://www.youtube.com/watch?v=7AG3TBgDZIw

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Keywords - aging, Trf1, metabolism, leaner, fat, telomeres

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TRF1 Protein Loss Reduces Body Fat and Improves Metabolic Health in Mice Without Shortening Telomeres

TRF1 Protein Loss Reduces Fat and Improves Metabolic Health in Mice Without Shortening Telomeres

Découvrez des confidences inédites, surprenantes et véridiques racontées par Cindy Cinnamon, personnalité publique québécoise
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BLUE TIGER Out Now all plats
CD-Rs For Sale @ https://go-harder.neocities.org/
⠀⠀
⠀DJ (C)annibalistic (H)umanoid (U)nderground (D)weller 

https://go-hard.neocities.org 
 1/2 of @cashismydomain⠀Every song prod me unless specified

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/

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease.

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

👆God first, God leads the way
💿 ‘Phases’ EP… OUT NOW
🎧 Producer-wise, I go by Raccoon Peanut

New tracks tagged #journal