BUFFALO, NY- March 19, 2024 – A new #research perspective was #published by Mikhail V. Blagosklonny M.D., Ph.D., from Roswell Park Comprehensive Cancer Center in Oncotarget's Volume 15 on March 15, 2024, entitled, “From osimertinib to preemptive combinations.”

“Here, I suggest that while first-line osimertinib extends median progression-free survival (PFS) in EGFR-mutant lung cancer compared to first-generation TKIs, it reduces individual PFS in 15–20% of patients compared to first-generation TKIs. Since detecting a single resistant cell before treatment is usually impossible, osimertinib must be used in all patients as a first-line treatment, raising median PFS overall but harming some. 

The simplest remedy is a preemptive combination (PC) of osimertinib and gefitinib. A comprehensive PC (osimertinib, afatinib/gefitinib, and capmatinib) could dramatically increase PFS for 80% of patients compared to osimertinib alone, without harming anyone. This article also explores PCs for MET-driven lung cancer.”

DOI - https://doi.org/10.18632/oncotarget.28569

Correspondence to - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com

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Keywords - cancer, lung cancer, NSCLC, EGFR, resistance, afatinib, gefitinib, capmatinib

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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Oncotarget

“From Osimertinib to Preemptive Combinations” by Dr. Blagosklonny

BUFFALO, NY- June 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 10, entitled, “Serine racemase expression profile in the prefrontal cortex and hippocampal subregions during aging in male and female rats.”

Aging is associated with a decrease in N-methyl-D-aspartate (NMDA) receptor function, which is critical for maintaining synaptic plasticity, learning, and memory. Activation of the NMDA receptor requires binding of the neurotransmitter glutamate and also the presence of co-agonist D-serine at the glycine site. The enzymatic conversion of L-serine to D-serine is facilitated by the enzyme serine racemase (SR). 

Subsequently, SR plays a pivotal role in regulating NMDA receptor activity, thereby impacting synaptic plasticity and memory processes in the central nervous system. As such, age-related changes in the expression of SR could contribute to decreased NMDA receptor function. However, age-associated changes in SR expression levels in the medial and lateral prefrontal cortex (mPFC, lPFC), and in the dorsal hippocampal subfields, CA1, CA3, and dentate gyrus (DG), have not been thoroughly elucidated. 

In this new study, researchers Linda Bean, Prodip K. Bose, Asha Rani, and Ashok Kumar from Indiana University School of Medicine, North Florida/South Georgia Veterans Health System, and the University of Florida aimed to determine the SR expression profile, including protein levels and mRNA, for these regions in aged and young male and female Fischer-344 rats. Their results demonstrate a significant reduction in SR expression levels in the mPFC and all hippocampal subfields of aged rats compared to young rats. No sex differences were observed in the expression of SR. 

“These findings suggest that the decrease in SR levels may play a role in the age-associated reduction of NMDA receptor function in brain regions crucial for cognitive function and synaptic plasticity.”

DOI - https://doi.org/10.18632/aging.205841

Corresponding author - Ashok Kumar - kash@ufl.edu

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Keywords - aging, serine racemase, hippocampus, medial prefrontal cortex (mPFC), NMDA receptor

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.

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.)

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Aging (Aging-US)

Serine Racemase Expression in the Brain During Aging in Male and Female Rats

BUFFALO, NY- June 5, 2024 – A new research paper was published in Oncotarget's Volume 15 on June 3, 2024, entitled, “Synergistic cytotoxicity of histone deacetylase and poly-ADP ribose polymerase inhibitors and decitabine in pancreatic cancer cells: Implications for novel therapy.”

Histone deacetylase inhibitors (HDACi) can modulate the acetylation status of proteins, influencing the genomic instability exhibited by cancer cells. Poly (ADP ribose) polymerase (PARP) inhibitors (PARPi) have a direct effect on protein poly (ADP-ribosyl)ation, which is important for DNA repair. Decitabine is a nucleoside cytidine analogue, which when phosphorylated gets incorporated into the growing DNA strand, inhibiting methylation and inducing DNA damage by inactivating and trapping DNA methyltransferase on the DNA, thereby activating transcriptionally silenced DNA loci.

In this new study, researchers Benigno C. Valdez, Apostolia M. Tsimberidou, Bin Yuan, Yago Nieto, Mehmet A. Baysal, Abhijit Chakraborty, Clark R. Andersen, and Borje S. Andersson from The University of Texas MD Anderson Cancer Center explored various combinations of HDACi and PARPi +/− decitabine (hypomethylating agent) in pancreatic cancer cell lines BxPC-3 and PL45 (wild-type BRCA1 and BRCA2) and Capan-1 (mutated BRCA2). 

“[...] we explored various combinations of HDACis and PARPis, with or without decitabine, in pancreatic cancer cell lines.”

The combination of HDACi (panobinostat or vorinostat) with PARPi (talazoparib or olaparib) resulted in synergistic cytotoxicity in all cell lines tested. The addition of decitabine further increased the synergistic cytotoxicity noted with HDACi and PARPi, triggering apoptosis (evidenced by increased cleavage of caspase 3 and PARP1). 

The 3-drug combination treatments (vorinostat, talazoparib, and decitabine; vorinostat, olaparib, and decitabine; panobinostat, talazoparib, and decitabine; panobinostat, olaparib, and decitabine) induced more DNA damage (increased phosphorylation of histone 2AX) than the individual drugs and impaired the DNA repair pathways (decreased levels of ATM, BRCA1, and ATRX proteins). The 3-drug combinations also altered the epigenetic regulation of gene expression (NuRD complex subunits, reduced levels). 

“This is the first study to demonstrate synergistic interactions between the aforementioned agents in pancreatic cancer cell lines and provides preclinical data to design individualized therapeutic approaches with the potential to improve pancreatic cancer treatment outcomes.”

DOI - https://doi.org/10.18632/oncotarget.28588

Correspondence to - Apostolia M. Tsimberidou - atsimber@mdanderson.org

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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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Synergistic Cytotoxicity of HDAC and PARP Inhibitors and Decitabine in Pancreatic Cancer Cells

Feeling lonely in a world more connected than ever? You're not alone.

On this episode of YJBM, join our host, Shankeri Vijayakumar, as she chats with our guest Blake Waranch about how loneliness is affecting our lives today. Whether you're feeling a bit isolated or just want to understand more about why loneliness is such a big deal right now, this episode has something for everyone. Tune in to learn more about what’s causing this silent epidemic and how we can all work towards a more connected and supportive world.

We want to credit Shivani Dayal for creating this interview series and for the format of interviews in this series.

Links and resources:
The Dinner Party: https://www.thedinnerparty.org/ 
Surgeon General’s Advisory on Loneliness: https://www.hhs.gov/sites/default/files/surgeon-general-social-connection-advisory.pdf 
“Together: The Healing Power of Human Connection in a Sometimes Lonely World” by Vivek Murthy, MD

More about YJBM at:
https://medicine.yale.edu/yjbm/ 

Our Instagram:
https://www.instagram.com/theyjbm/

Reflecting on the Loneliness Epidemic: Interview with Blake Waranch

In the relentless battle against non-small cell lung cancer (NSCLC) driven by epidermal growth factor receptor (EGFR) mutations, the development of resistance has long been a formidable obstacle. Historically, first- and second-generation EGFR tyrosine kinase inhibitors (TKIs) like gefitinib, erlotinib, afatinib, and dacomitinib have faced a significant hurdle: the emergence of the T790M point mutation in approximately 50% of patients, rendering the tumor resistant to these therapies.

This resistance stems from a sobering reality – before treatment, a small subset of cancer cells already harbor the T790M mutation, conferring no selective advantage initially. However, once treatment commences, these rare mutated cells proliferate selectively, eventually dominating the tumor population and diminishing the effectiveness of first- and second-generation TKIs.

Full blog - https://www.oncotarget.org/2024/06/06/dr-blagosklonnys-strategy-from-osimertinib-to-preemptive-combinations/

Paper DOI - https://doi.org/10.18632/oncotarget.28569

Correspondence to - Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com

Video short - https://www.youtube.com/watch?v=UO5BGLIggTE

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Keywords - cancer, lung cancer, NSCLC, EGFR, resistance, afatinib, gefitinib, capmatinib

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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Dr. Blagosklonny’s Strategy: From Osimertinib to Preemptive Combinations

Yale Center for Emotional Intelligence co-founder Dr. Robin Stern discusses the role of spirituality and religion in understanding and managing emotions, the danger of suppressing emotions like anger, and her groundbreaking work on gaslighting.

For more information and a transcript, please visit: https://divinity.yale.edu/news/emotional-intelligence-and-spirituality-dr-robin-stern

Emotional Intelligence and Spirituality with Dr. Robin Stern

BUFFALO, NY- June 10, 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 10, entitled, “Relationships of depression and antidepressant use with epigenetic age acceleration and all-cause mortality among postmenopausal women.”

In this new study, researchers May A. Beydoun, Hind A. Beydoun, Jason Ashe, Michael F. Georgescu, Steve Horvath, Ake Lu, Anthony S. Zannas, Aladdin H. Shadyab, Su Yon Jung, Sylvia Wassertheil-Smoller, Ramon Casanova, Alan B. Zonderman, and Robert L. Brunner from the National Institute on Aging, U.S. Department of Veterans Affairs (Washington, DC), University of Texas Health Science Center at Houston, University of California Los Angeles, University of North Carolina at Chapel Hill, University of California San Diego, Albert Einstein College of Medicine, Wake Forest University School of Medicine, and University of Nevada Reno investigated relations of depressive symptoms, antidepressant use, and epigenetic age acceleration with all-cause mortality risk among postmenopausal women. 

“Frequently under-recognized depression is a major contributor to the Global Burden of Diseases [1, 2] while being the most prevalent mental illness among geriatric populations [2].”

Data were analyzed from ≤1,900 participants in the Women's Health Initiative study testing four-way decomposition models. After a median 20.4y follow-up, 1,161 deaths occurred. Approximately 11% had elevated depressive symptoms (EDS+), 7% were taking antidepressant medication at baseline (ANTIDEP+), while 16.5% fell into either category (EDS_ANTIDEP+). 

Baseline ANTIDEP+, longitudinal transition into ANTIDEP+ and accelerated epigenetic aging directly predicted increased mortality risk. GrimAge DNA methylation age acceleration (AgeAccelGrim) partially mediated total effects of baseline ANTIDEP+ and EDS_ANTIDEP+ on all-cause mortality risk in socio-demographic factors-adjusted models (Pure Indirect Effect >0, P < 0.05; Total Effect >0, P < 0.05). Thus, higher AgeAccelGrim partially explained the relationship between antidepressant use and increased all-cause mortality risk, though only prior to controlling for lifestyle and health-related factors. 

“Antidepressant use and epigenetic age acceleration independently predicted increased all-cause mortality risk. Further studies are needed in varying populations.”

DOI - https://doi.org/10.18632/aging.205868

Corresponding author - May A. Beydoun - baydounm@mail.nih.gov

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Keywords - aging, depressive symptoms, epigenetic age acceleration, mortality

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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Depression, Antidepressants, Epigenetic Age Acceleration, and Mortality in Postmenopausal Women

BUFFALO, NY- June 11, 2024 – The Ride for Roswell is one of the nation’s largest cycling events—hosted by Roswell Park Comprehensive Cancer Center—to raise awareness and funds for cancer research and patient care. This charity bike ride, based out of Buffalo, New York, has brought people together for 28 years to celebrate cancer survivors, pay tribute to lives that have been lost, and to work together to support research and find a cure.

THE ORIGIN OF THE RIDE

The Ride for Roswell started in 1989 when Mitch Flynn, owner of the advertising agency Flynn & Friends, met Katherine Gioia. Katherine was a four-year-old patient battling a rare form of cancer. After Katherine’s death (less than a year after her diagnosis), Katherine’s mother, Anne Gioia, and aunt, Donna Gioia, founded the Roswell Park Alliance Foundation in her memory to raise money for cancer research and treatment. On June 29, 1996, Mitch and Alliance Foundation staff launched the first Ride for Roswell.

In the 28 years since then, thanks to over 135,000 riders and thousands of volunteers, the Ride for Roswell has raised over $72 million to fund cancer research. The event has become one of the largest charity rides in the United States. 

THIS YEAR

This year, Ride Day is on Saturday, June 22, 2024, and will once again begin at the University at Buffalo North Campus. There are nine routes to choose from, ranging from five to 100 mile distances. All riders are encouraged to check in on the Thursday or Friday before Ride Day. 

Learn more about The Ride, check in, and routes: https://www.rideforroswell.org/routes/

JOIN A TEAM: TEAM OPEN ACCESS

Impact Journals has been a part of this event since 2018 and continues to sponsor captain Sergei Kurenov’s peloton, Team Open Access. Team Open Access was named in honor of all open-source online medical journals, such as Aging, Oncotarget, Genes & Cancer, and Oncoscience. Sergei works at Roswell Park Comprehensive Cancer Center to create, develop, and implement innovative diagnostic and surgical pre-planning software used in cancer treatment. He has been riding in the event since 2016.

“I am proud to [say] that our team is supported again by open source cancer-related scientific journals: Oncotarget and Aging! Both of these journals publish high-impact research papers of general interest and biological significance in all fields of cancer research,” Sergei said.

There is still time to join Team Open Access in the Ride for Roswell. You can also support the team by giving a donation of any size. Any avenue of support you may choose to donate to the Ride for Roswell will make a difference and change lives.

“Finding a cure for cancer is something we are all incredibly passionate about, and we are so thankful and grateful for your support. Together, we can make a difference!” Sergei said. “Thank you so much for your donations, your support, and well wishes!”

Visit the Open Access team page to join or donate today: 
https://give.roswellpark.org/site/TR/SpecialEvents/General?team_id=19666&pg=team&fr_id=1940

For media requests, please contact media@impactjournals.com.

Impact Journals Sponsors 2024 Ride for Roswell

BUFFALO, NY- June 11, 2024 – The Ride for Roswell is one of the nation’s largest cycling events—hosted by Roswell Park Comprehensive Cancer Center—to raise awareness and funds for cancer research and patient care. This charity bike ride, based out of Buffalo, New York, has brought people together for 28 years to celebrate cancer survivors, pay tribute to lives that have been lost, and to work together to support research and find a cure.

THE ORIGIN OF THE RIDE

The Ride for Roswell started in 1989 when Mitch Flynn, owner of the advertising agency Flynn & Friends, met Katherine Gioia. Katherine was a four-year-old patient battling a rare form of cancer. After Katherine’s death (less than a year after her diagnosis), Katherine’s mother, Anne Gioia, and aunt, Donna Gioia, founded the Roswell Park Alliance Foundation in her memory to raise money for cancer research and treatment. On June 29, 1996, Mitch and Alliance Foundation staff launched the first Ride for Roswell.

In the 28 years since then, thanks to over 135,000 riders and thousands of volunteers, the Ride for Roswell has raised over $72 million to fund cancer research. The event has become one of the largest charity rides in the United States.

THIS YEAR

This year, Ride Day is on Saturday, June 22, 2024, and will once again begin at the University at Buffalo North Campus. There are nine routes to choose from, ranging from five to 100 mile distances. All riders are encouraged to check in on the Thursday or Friday before Ride Day.

Learn more about The Ride, check in, and routes: www.rideforroswell.org/routes/

JOIN A TEAM: TEAM OPEN ACCESS

Impact Journals has been a part of this event since 2018 and continues to sponsor captain Sergei Kurenov’s peloton, Team Open Access. Team Open Access was named in honor of all open-source online medical journals, such as Oncotarget, Aging, Genes & Cancer, and Oncoscience. Sergei works at Roswell Park Comprehensive Cancer Center to create, develop, and implement innovative diagnostic and surgical pre-planning software used in cancer treatment. He has been riding in the event since 2016.

“I am proud to [say] that our team is supported again by open source cancer-related scientific journals: Oncotarget and Aging! Both of these journals publish high-impact research papers of general interest and biological significance in all fields of cancer research,” Sergei said.

There is still time to join Team Open Access in the Ride for Roswell. You can also support the team by giving a donation of any size. Any avenue of support you may choose to donate to the Ride for Roswell will make a difference and change lives.

“Finding a cure for cancer is something we are all incredibly passionate about, and we are so thankful and grateful for your support. Together, we can make a difference!” Sergei said. “Thank you so much for your donations, your support, and well wishes!”

Visit the Open Access team page to join or donate today:
give.roswellpark.org/site/TR/Specia…eam&fr_id=1940

For media requests, please contact media@impactjournals.com.

BUFFALO, NY- June 11, 2024 – A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “CCR4-NOT complex in stress resistance and longevity in C. elegans.”

The ability to mount an adaptive response to environmental stress is crucial in organismal survival and overall fitness. In the context of aging, many genes that mediate resistance to stressors are also important in longevity, and aging has been shown to cause a decline in stress resistance. In their new editorial, researchers Cheng-Wei Wu and Hadi Tabarraei from the University of Saskatchewan wrote that recently, during a screening for genes that are required for the transcriptional response to heavy metal and oxidative stress in C. elegans, they found that depletion of subunits within the evolutionarily conserved CCR4-NOT protein complex compromises stress resistance and decreases lifespan.

“The CCR4-NOT (Carbon Catabolite Repression 4 – Negative On TATA-less) is a multi-protein complex tasked with regulating RNA metabolism across multiple steps including mRNA decay, transcription initiation and elongation, mRNA quality control and export, and mRNA translatability (reviewed in [3]).”

Studies in yeast have shown that CCR4-NOT is required for transcriptional elongation of stress responsive genes and that loss of function mutants of this protein complex have increased sensitivity to replication stress caused by DNA damaging agents [4, 5]. An expansive role for the CCR4-NOT complex in stress-induced transcriptional programming was demonstrated in C. elegans via whole-transcriptome sequencing analysis [2]. 

“Together, while the CCR4-NOT complex has been extensively studied for the past 3 decades, new studies in the model organism C. elegans have revealed an important new role for this protein complex in regulating normal aging as well as a requirement for many well-characterized and evolutionarily conserved pro-longevity pathways including reduced insulin signaling, mitochondrial suppression, enhanced stress response, and dietary restriction.”

DOI - https://doi.org/10.18632/aging.205918

Corresponding author - Cheng-Wei Wu - michael.wu@usask.ca

Video short - https://www.youtube.com/watch?v=UFi7Dq5JXJ4

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Keywords - aging, oxidative stress, C. elegans, CCR4-NOT

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.

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​​ and connect with us:

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CCR4-NOT Complex in Stress Resistance and Longevity in C. elegans

BUFFALO, NY- June 12, 2024 – A new review paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Peripheral vascular dysfunction and the aging brain.”

Aging is the greatest non-modifiable risk factor for most diseases, including cardiovascular diseases (CVD), which remain the leading cause of mortality worldwide. In their new review, researchers Devin Wahl and Zachary S. Clayton from Colorado State University and the University of Colorado note that robust evidence indicates that CVD are a strong determinant for reduced brain health and all-cause dementia with advancing age. 

“CVD are also closely linked with peripheral and cerebral vascular dysfunction, common contributors to the development and progression of all types of dementia, that are largely driven by excessive levels of oxidative stress (e.g., reactive oxygen species [ROS]).”

Emerging evidence suggests that several fundamental aging mechanisms (e.g., “hallmarks” of aging), including chronic low-grade inflammation, mitochondrial dysfunction, cellular senescence and deregulated nutrient sensing contribute to excessive ROS production and are common to both peripheral and cerebral vascular dysfunction. Therefore, targeting these mechanisms to reduce ROS-related oxidative stress and improve peripheral and/or cerebral vascular function may be a promising strategy to reduce dementia risk with aging. Investigating how certain lifestyle strategies (e.g., aerobic exercise and diet modulation) and/or select pharmacological agents (natural and synthetic) intersect with aging “hallmarks” to promote peripheral and/or cerebral vascular health represent a viable option for reducing dementia risk with aging. 

“Therefore, the primary purpose of this review is to explore mechanistic links among peripheral vascular dysfunction, cerebral vascular dysfunction, and reduced brain health with aging. Such insight and assessments of non-invasive measures of peripheral and cerebral vascular health with aging might provide a new approach for assessing dementia risk in older adults.”

DOI - https://doi.org/10.18632/aging.205877

Corresponding authors - Devin Wahl - devin.wahl@colostate.edu, and Zachary S. Clayton - zachary.clayton@colorado.edu

Video short - https://www.youtube.com/watch?v=0gx9DklNZVM

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Keywords - aging, peripheral vascular health, cerebrovascular health, cognitive function, dementia

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.

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​​ and connect with us:

Facebook - https://www.facebook.com/AgingUS/
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LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc

MEDIA@IMPACTJOURNALS.COM

The Aging Brain and Peripheral Vascular Dysfunction

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/

“From Osimertinib to Preemptive Combinations” by Dr. Blagosklonny

Oncotarget Podcast

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