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BUFFALO, NY- October 30, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on March 24, 2023, entitled, “Neutrophil PAD4: how does it function in cancer beyond promoting NETosis?”

Expansion of pathologically activated immune suppressive myeloid cells called myeloid-derived suppressor cells (MDSC) is one of the hallmarks of cancer. In most tumor types, MDSC are represented primarily by pathologically activated neutrophils (PMN-MDSC). In this new editorial, researchers Laura Garcia-Gerique and Yulia Nefedova from the Wistar Institute discussed their team’s recent study identifying a novel mechanism by which neutrophil PAD4 promotes cancer progression. 

“Using several transplantable and genetically engineered mouse models, we demonstrated that tumor growth was accompanied by significantly elevated enzymatic activity of neutrophil PAD4 [10]. To further clarify the role of PAD4 in tumor progression, we utilized PAD4fl/fl MRP8Cre mice with targeted deletion of PAD4 in myeloid cells, primarily neutrophils.”

PMN-MDSC originate in the bone marrow and migrate to various sites including tumor tissues and premetastatic niches. These cells have a relatively short lifespan (less than 48 hours) and, therefore, are continually replaced from the bone marrow. Tumor-infiltrating PMN-MDSC possess a potent suppressive activity as they are able to inhibit both antigen-specific immune responses of T cells and non-specific anti-CD3/CD28-stimulated responses. As a result, a highly immunosuppressive environment is created in tumors, which prevents their rejection via immunological mechanisms. 

In addition, PMN-MDSC employ non-immunological mechanisms to facilitate tumor progression, including angiogenesis, remodeling of extracellular matrix, and production of cytokines. In patients with solid tumors, levels of MDSC in circulation and tumor tissues have been positively associated with a poor response to the therapy in many types of cancer and represent an independent indicator of poor outcomes. However, many of the details about how PMN-MDSC support cancer progression, and thus approaches for therapeutically targeting these cells, remain enigmatic.

“Taken together, our study identified a new mechanism responsible for transcriptional regulation of neutrophil migration and a new mechanism by which neutrophil PAD4 is contributing to tumor progression. PAD4 inhibitors are in development and may enter early phase clinical trials in the future.”

DOI - https://doi.org/10.18632/oncotarget.28369

Correspondence to - Yulia Nefedova - ynefedova@wistar.org

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Keywords - cancer, PAD4, PMN-MDSC, neutrophils, neutrophil migration

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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Oncotarget

Neutrophil PAD4 in Cancer, Beyond Promoting NETosis

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BUFFALO, NY- January 22, 2024 – A new #research perspective was #published in Oncotarget's Volume 15 on January 16, 2024, entitled, “Bone marrow adipocytes provide early sign for progression from MGUS to multiple myeloma.”

Multiple Myeloma (MM) is the second most common hematological malignancy and is characterized by clonal expansion of malignant plasma cells in the bone marrow. In spite of recent advances in the field of MM, the disease has remained incurable. MM is preceded by a premalignant state known as monoclonal gammopathy of undetermined significance (MGUS), with a risk of progression to MM of 1% per year. Establishing a scalable approach that refines the identification of MGUS patients at high risk of progression to MM can transform the clinical management of the disease, improve the patient’s quality of life, and will have significant socioeconomic implications. 

In this new perspective, researchers Bilal M. El-Masri, Benedeta Leka, Fatima Mustapha, Michael Tveden Gundesen, Maja Hinge, Thomas Lund, Thomas L. Andersen, Marta Diaz-delCastillo, and Abbas Jafari from the Danish Spatial Imaging Consortium, University of Southern Denmark, University of Copenhagen, University of Aarhus, Odense University Hospital, and Lillebaelt Hospital provide evidence that changes in the bone marrow adipose tissue (BMAT) provide an early sign for progression from MGUS to MM. 

“We employed AI-assisted histological analysis of unstained bone marrow biopsies from MGUS subjects with or without progression to MM within 10 years (n = 24, n = 17 respectively).” 

Although the BMAT fraction was not different between the two groups, bone marrow adipocyte (BMAd) density was decreased in MGUS patients who developed MM, compared to non-progressing MGUS patients. Importantly, the distribution profile for BMAd size and roundness was significantly different between the two groups, indicating a shift toward increased BMAd size and roundness in MGUS patients who developed MM. These early changes in the BMAT could serve as valuable early indicators for the transition from MGUS to MM, potentially enabling timely interventions and personalized treatment strategies. 

“[...] the AI-based approach for histological characterization of unstained bone marrow biopsies is cost-effective and fast, rendering its clinical implementation feasible.”

DOI - https://doi.org/10.18632/oncotarget.28548

Correspondence to - Abbas Jafari - ajafari@sund.ku.dk, Marta Diaz-delCastillo - marta@forens.au.dk, and Thomas L. Andersen - thomas.levin.andersen@rsyd.dk

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Keywords - cancer, multiple myeloma, MGUS, bone marrow adipocyte

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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Bone Marrow Adipocytes Provide Early Sign of Progression from MGUS to Multiple Myeloma

Damian describes his story of diagnosis, treatment, and bone marrow transplant in this compelling episode.

Athletic Service Member Conquers Aplastic Anemia and MDS with Transplant

[HOOK: VAGUE]

I’ve been reminiscing ever since the other day
Just another fucken soul that’s been lost away
I’ve been trapped in the motion and It cannot fade
Tried to get a hold of it but lost the grip, it got away
I’ve been reminiscing ever since the other day
Just another fucken soul that’s been lost away
I’ve been trapped in the motion and It cannot fade
Tried to get a hold of it but lost the grip, it got away

[VAGUE]

I'm combinin and ignoring the visions
I never talk about the future
Cause I’m still in the picture
And that’s just how it goes
In a world of bad habits
And it’s weighin on my peace
Being raised by drug addicts
And It always seemin like it’s never endin
Gotta be more careful
Gotta to take control of your all spendin
The world is so fucked
It needed to much
To keep you independent
While the ones you love
Are defendants
It’s the cycle of life to feel the pressure
But what you doin
With your time to put in all the effort?
I’m really trying hard just to find the right measure
Find the balance in between, its for business or for pleasure
A lot of people always losin themselves
Instead of runnin the world
They stay sheepin themselves
And it’s quite sad, that you can’t get out of this hell
Don’t wanna be just another person trapped in a cell

[HOOK: VAGUE]

I’ve been reminiscing ever since the other day
Just another fucken soul that’s been lost away
I’ve been trapped in the motion and It cannot fade
Tried to get a hold of it but lost the grip, it got away
I’ve been reminiscing ever since the other day
Just another fucken soul that’s been lost away
I’ve been trapped in the motion and It cannot fade
Tried to get a hold of it but lost the grip, it got away

[T.R.I.P.]

I think i’m cursed riding round Vegas
In that hearse shooting up your body
Like a mothafuckin nurse 
Had to go berserk up on this track
Now watch 'em burn 
Training day with the devil
Putting these rappers in the dirt yuh
Slide with that heater on me
Talking to the dead 
Resurrected from the depths
I’m coming for your head
Shame on you pussy boys for talking out your neck
If you really want the smoke
I put it down for my set 
I got two whips, ones my bitch and ones my daily 
UAV Records is the label that be paying me 
Fuck a flex, my boys ain’t rockin any reps 
Mob with the squad, UAV until the death 
Every scene that i’m in
They be treating me like a grinch
Scared as fuck
When I pull up with them hallow tips
These rappers can’t compete with us
Please do not attempt
Snatch your fuckin soul
And take you down to the abyss, lil bitch

Bone Marrow

Bone Marrow [Prod. Roosevelt]

Book an Appointment for Bone Marrow Transpalnt 
https://healthcheckbox.com/organ-transplant/bone-marrow-transplant/

Bone Marrow Transplant in India (ভারতে বোন ম্যারো ট্রান্সপ্লান্ট)

একটি অস্থি মজ্জা প্রতিস্থাপন কি?
অস্থি মজ্জা প্রতিস্থাপন (BMT) নির্দিষ্ট ক্যান্সার বা অন্যান্য রোগের রোগীদের জন্য একটি বিশেষ থেরাপি। একটি অস্থিমজ্জা প্রতিস্থাপনের মধ্যে সাধারণত অস্থি মজ্জা (স্টেম কোষ) তে পাওয়া কোষগুলি গ্রহণ করা, সেই কোষগুলিকে ফিল্টার করা এবং সেগুলি দাতা (রোগী) বা অন্য ব্যক্তির কাছে ফেরত দেওয়া জড়িত। বিএমটি-এর লক্ষ্য হল স্বাস্থ্যকর অস্থি মজ্জা কোষগুলিকে একজন ব্যক্তির মধ্যে স্থানান্তর করা তার নিজের অস্বাস্থ্যকর অস্থিমজ্জার অস্বাভাবিক কোষগুলিকে মেরে ফেলার পরে।
1968 সাল থেকে লিউকেমিয়া, লিম্ফোমাস, অ্যাপ্লাস্টিক অ্যানিমিয়া, ইমিউন ডেফিসিয়েন্সি ডিসঅর্ডার এবং কিছু কঠিন টিউমার ক্যান্সারের মতো রোগের চিকিৎসার জন্য অস্থি মজ্জা প্রতিস্থাপন সফলভাবে ব্যবহার করা হয়েছে।
অস্থি মজ্জা কি?
অস্থি মজ্জা হাড়ের ভিতরে পাওয়া নরম, স্পঞ্জি টিস্যু। এটি যেখানে শরীরের বেশিরভাগ রক্তকণিকা বিকাশ করে এবং সংরক্ষণ করা হয়।

Bone Marrow Transplant in India (

BUFFALO, NY- December 4, 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 21 on November 22, 2024, entitled, “The effects of young and aged, male and female megakaryocyte conditioned media on angiogenic properties of endothelial cells.”

Researchers Murad K. Nazzal, Hanisha L. Battina, Nikhil P. Tewari, Sarah L. Mostardo, Rohit U. Nagaraj, Donghui Zhou, Olatundun D. Awosanya, Saveda K. Majety, Sue Samson, Rachel J. Blosser, Ushashi C. Dadwal, Patrick L. Mulcrone, and Melissa A. Kacenaat from Indiana University School of Medicine and Richard L. Roudebush Veterans' Administration Medical Center, have uncovered how certain bone marrow cells, called megakaryocytes (MKs), promote the growth of new blood vessels (angiogenesis) to aid in bone healing. Their findings help explain why healing slows with age and offer insights into potential treatments to accelerate fracture recovery in older adults.

Broken bones are common in older adults, and slower healing can lead to complications and longer hospital stays. Accelerating the healing process could significantly improve the quality of life for millions.

In this study, researchers investigated the effects of substances secreted by MKs, collected from young and older male and female mice. These substances, known as conditioned media (CM), were tested for their ability to stimulate the growth and function of endothelial cells (EC), which form the building blocks of blood vessels. Blood vessels play a critical role in healing by delivering oxygen and nutrients to damaged areas, making angiogenesis a vital part of the recovery process.

The results showed that CM from younger MKs mice was more effective at helping blood vessels grow. Interestingly, MKs from female mice performed better than those from males, regardless of age. For example, substances from female MKs mice boosted blood vessel growth by over 115% and significantly improved the movement of cells needed for healing. 

The researchers also studied changes in genes related to blood vessel growth, and found that aging affects how these genes work. These changes may explain why older people heal more slowly after breaking a bone. 

“An understanding of which factors regulate which mechanisms of EC functionality may allow for isolation of one or a few factors that influence EC migration changes with aging, resulting in the development of targeted therapy to improve EC migration, subsequent angiogenesis, and fracture healing.” 

In conclusion, this research paves the way for developing new therapies to help older individuals recover from fractures more quickly, reducing pain and improving mobility. One potential approach could involve creating treatments that replicate the effects of MKs from younger individuals or isolating the specific substances that promote blood vessel growth. This represents an important step toward addressing the growing challenge of delayed healing in an aging population.

DOI - https://doi.org/10.18632/aging.206077

Corresponding authors - Patrick L. Mulcrone - pamulcro@iu.edu, and Melissa A. Kacena - mkacena@iupui.edu

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.

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.)

Please visit our website at https://www.Aging-US.com​​.

MEDIA@IMPACTJOURNALS.COM

Aging (Aging-US)

Effects of Megakaryocyte Conditioned Media on Endothelial Cell Angiogenesis

BUFFALO, NY - April 2, 2025 – A new #research paper was #published in Oncotarget, Volume 16, on March 21, 2025, titled “NSD2-epigenomic reprogramming and maintenance of plasma cell phenotype in t(4;14) myeloma."

Researchers Andrea Gunnell, Scott T. Kimber, Richard Houlston, and Martin Kaiser from The Institute of Cancer Research, London, studied how a gene called NSD2 affects the behavior of multiple myeloma (MM) cells. Their findings reveal that NSD2 plays a key role in helping cancer cells retain their identity as plasma cells—white blood cells that normally help the immune system fight infections. This discovery could shape future treatment strategies for patients with a high-risk form of MM known as t(4;14) myeloma.

Multiple myeloma is a type of blood cancer that begins in plasma cells found in the bone marrow. About 20% of patients have a genetic change called t(4;14), which makes the NSD2 gene highly active. The research team compared two types of myeloma cells: one with high NSD2 activity and one where NSD2 was turned off. They found that when NSD2 is active, it changes how DNA is folded and how genes are switched on or off, especially genes that help the cells act like plasma cells. When NSD2 was turned off, important markers like CD38 were reduced, and other genes normally silent in plasma cells were activated.

The study indicated that NSD2 does not directly affect the main genes responsible for plasma cell creation. Instead, it influences many other genes that help maintain the cancer cell’s identity, which contributes to cancer growth and survival. 

The researchers also observed physical changes in the cancer cells. Cells with active NSD2 looked and behaved more like typical plasma cells, while cells without NSD2 appeared more immature and lost important surface markers. These changes were linked to differences in how the DNA was organized inside the cells.

These findings are especially important as new drugs are being developed to block NSD2. The study suggests that turning off NSD2 could change how MM cells respond to existing treatments. For example, if NSD2 is blocked and CD38 levels drop, the change might affect therapies that target CD38. However, the rise of other immune-related genes might make certain immunotherapies more effective.

“Identifying the biological consequences of NSD2 over-expression in MM is not only relevant to informing new therapeutic interventions through indirect targeting of downstream effectors, but also to anticipate possible consequences of targeting NSD2 directly.”

In summary, this study shows how NSD2 helps myeloma cells keep their cancerous identity by reorganizing the DNA and influencing gene activity. Understanding this role could help researchers design better treatment approaches and possibly overcome resistance to current therapies in t(4;14) myeloma.

DOI - https://doi.org/10.18632/oncotarget.28706

Correspondence to - Andrea Gunnell - andrea.gunnell@icr.ac.uk

Video short - https://www.youtube.com/watch?v=hibkjUpRq7I

Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/

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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NSD2 Gene Drives Cancer Cell Identity in Multiple Myeloma

BUFFALO, NY - July 7, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 17, 2025, titled “Genetic characteristics of blastic plasmacytoid dendritic cell neoplasm: A single institution experience.”

In this study, a research team led by first author Fei Fei and corresponding author Michelle Afkhami from the City of Hope Comprehensive Cancer Center investigated a rare and aggressive type of blood cancer called blastic plasmacytoid dendritic cell neoplasm (BPDCN). Their research uncovered frequent mutations in key genes and identified CCDC50 as a potential biomarker for diagnosis and disease monitoring. These findings could help improve how this cancer is detected and treated in the future.

BPDCN most often affects older adults and is known for its rapid progression and poor survival rates. The researchers performed genetic sequencing on 21 patients to better understand the disease. They found that two genes, TET2 and ASXL1, were frequently mutated in these patients and were linked to worse survival, especially in those over 65 years old.

“Our study revealed that TET2 (57%) and ASXL1 (33%) were the most frequently mutated genes, followed by NRAS (29%), SRSF2 (14%), ZRSR2 (14%), and KMT2D (14%).”

The study also discovered that a gene called CCDC50 was expressed at much higher levels in BPDCN samples compared to other blood cancers, such as acute myeloid leukemia and chronic monomyelocytic leukemia. This suggests that CCDC50 may help clinicians distinguish BPDCN from other similar diseases. Importantly, CCDC50 levels dropped significantly in patients whose disease went into remission, highlighting its potential as a tool for tracking disease activity over time.

Researchers further observed that patients who received stem cell transplants lived longer than those who did not, reinforcing the importance of this treatment approach. However, BPDCN remains a challenging disease with an overall poor outlook, making these findings an important step toward better care.

This research provides new insights into the genetic changes behind BPDCN and points to CCDC50 as a promising marker to improve diagnosis and monitor treatment success. Larger studies will be needed to confirm these results and bring these discoveries closer to use in routine medical practice.

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

Correspondence to - Michelle Afkhami - mafkhami@coh.org

Video short - 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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Key Genetic Alterations and Biomarker for Blastic Plasmacytoid Dendritic Cell Neoplasm

BUFFALO, NY — August 1, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 7 of Aging (Aging-US) was #published on July 25, 2025, titled “Systemic factors in young human serum influence in vitro responses of human skin and bone marrow-derived blood cells in a microphysiological co-culture system.”

The study, led by first author Johanna Ritter and corresponding author Elke Grönniger from Beiersdorf AG, Research and Development Hamburg, shows that components in young human blood serum can help restore youthful properties to skin, but only when bone marrow cells are also present. This discovery highlights the role of bone marrow in supporting skin health and may allow for novel approaches aimed at slowing or reversing visible signs of aging.

The research explored how factors present in blood serum, already known to influence aging in animal studies, act on human cells. Using an advanced system that mimics human circulation, the researchers connected a 3D skin model with a 3D bone marrow model. They found that young human serum alone was not enough to rejuvenate skin. However, when bone marrow cells were present, these serum factors changed the activity of those cells, which then secreted proteins that rejuvenated skin tissue.

“Interestingly, we detected a significant increase in Ki67 positive cells in the dynamic skin model co-cultured with BM model and young serum compared to the model co-cultured with BM and old serum, indicating an improved regenerative capacity of the tissue.”

Detailed analysis indicated that young serum stimulated the bone marrow to produce a group of 55 proteins, with 7 of them demonstrating the ability to boost cell renewal, collagen production, and other features associated with youthful skin. These proteins included factors that improved energy production in cells and reduced signs of cellular aging. Without the interaction between skin and bone marrow cells, these rejuvenating effects did not occur.

This finding explains why earlier experiments in mice, where young and old animals shared a blood supply, showed rejuvenation across organs. It suggests that bone marrow-derived cells are critical messengers that transform signals from blood into effects on other tissues, including the skin.

While these results are preclinical and not from human trials, they offer a starting point for new strategies in regenerative medicine and skin care. By identifying specific proteins that may carry rejuvenating signals, the study points to a new way to address age-related changes. Researchers emphasize that further studies will be needed to confirm these effects in humans and to test how these proteins can be safely and effectively applied in future therapies.

Overall, this research is an important step in understanding how young blood serum factors influence human tissue and could guide the development of novel methods to maintain healthier skin as people age.

DOI - https://doi.org/10.18632/aging.206288

Corresponding author - Elke Grönniger - elke.groenniger@beiersdorf.com

Video short - https://www.youtube.com/watch?v=_4spcgzPcEk

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Young Human Blood Serum Factors Show Potential to Rejuvenate Skin Through Bone Marrow

A new #study published as the #cover of Aging (Aging-US) Volume 17, Issue 7, explores how factors in young human blood may affect the biological age of human skin. Researchers from Beiersdorf AG, Research and Development Hamburg in Germany, used a microphysiological co-culture system—a lab-based model simulating human circulation—to test the effects of young versus old blood serum on skin cells. The findings suggest that bone marrow-derived cells play a key role in converting blood-borne signals into effects that support skin rejuvenation.

Understanding Skin Aging and Systemic Influence

As we age, the skin’s ability to regenerate declines, while its biological age increases. This contributes to visible signs of aging and a weakened barrier function. While cosmetic treatments can improve appearance, they rarely target the cellular processes underlying skin aging.

Animal studies have shown that exposure to young blood can promote tissue repair and rejuvenation, likely due to molecules circulating in the bloodstream. However, reproducing these effects in human skin has proven difficult. Applying young serum directly to skin tissue has not produced significant results, indicating that additional cellular interactions may be required.

Full blog - https://aging-us.org/2025/08/skin-rejuvenation-how-young-blood-and-bone-marrow-influence-it/

Paper DOI - https://doi.org/10.18632/aging.206288

Corresponding author - Elke Grönniger - elke.groenniger@beiersdorf.com

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Keywords - aging, skin rejuvenation, microphysiological systems, systemic factors, bone marrow model, human serum

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Skin Rejuvenation: How Young Blood and Bone Marrow Influence It

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

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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

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