Oncotarget

In February, 2021, researchers from Spain conducted a study published in Oncotarget, titled: “Head to head evaluation of second generation ALK inhibitors brigatinib and alectinib as first-line treatment for ALK+ NSCLC using an in silico systems biology-based approach.”

This trending paper was authored by researchers practicing at the Hospital Germans Trias i Pujol, Takeda Farmacéutica España, Anaxomics Biotech, and Universitat Pompeu Fabra.

The researchers used a computer simulated modeling system to highlight the strengths and weaknesses of two ALK inhibitors. They first began their study by characterizing the pathophysiology of ALK+ NSCLC after completing a detailed review of review papers published in PubMed between 2013 and 2018.

Read the full study here: https://www.oncotarget.com/article/27875/text/

The Trending with Impact series highlights Oncotarget publications attracting higher visibility among readers around the world online, in the news, and on social media—beyond normal readership levels.

More from Trending with Impact: www.oncotarget.org/tag/trending-with-impact/

About Oncotarget:

Oncotarget is a bi-weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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In the cover paper of this week's issue of Oncotarget, titled: "The cancer testis antigens CABYR-a/b and CABYR-c are expressed in a subset of colorectal cancers and hold promise as targets for specific immunotherapy," researchers evaluate CABYR isoforms a/b and c mRNA expression in colorectal cancer in hopes of determining whether or not these proteins may be promising vaccine targets.

Read the full study here: https://doi.org/10.18632/oncotarget.27897

Oncotarget Volume 12, Issue 5: https://www.oncotarget.com/archive/v12/i5/

About Oncotarget:

Oncotarget is a bi-weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Listen to short summaries of the latest oncology-focused research literature published in this week's issue of Oncotarget Volume 12, Issue 5.

Click here for the complete issue: https://www.oncotarget.com/archive/v12/i5/

Oncotarget Volume 12, Issue 5 features:

Cover Paper: "The cancer testis antigens CABYR-a/b and CABYR-c are expressed in a subset of colorectal cancers and hold promise as targets for specific immunotherapy." https://doi.org/10.18632/oncotarget.27897

Research Perspective: "Tumor mutational burden as a predictor of immunotherapy response in breast cancer." https://doi.org/10.18632/oncotarget.27877

Research Paper: "STAT3 induces the expression of GLI1 in chronic lymphocytic leukemia cells." https://doi.org/10.18632/oncotarget.27884

Research Paper: "Multi-modal effects of 1B3, a novel synthetic miR-193a-3p mimic, support strong potential for therapeutic intervention in oncology." https://doi.org/10.18632/oncotarget.27894

Research Paper: "Mutational profile of skin lesions in hepatocellular carcinoma patients under tyrosine kinase inhibition: a repercussion of a wide-spectrum activity." https://doi.org/10.18632/oncotarget.27891

Research Paper: "Development of a ghrelin receptor inverse agonist for positron emission tomography." https://doi.org/10.18632/oncotarget.27895

Research Paper: "Global DNA hypermethylation pattern and unique gene expression signature in liver cancer from patients with Indigenous American ancestry." https://doi.org/10.18632/oncotarget.27890

Research Paper: "Fine–mapping of two differentiated thyroid carcinoma susceptibility loci at 2q35 and 8p12 in Europeans, Melanesians and Polynesians." https://doi.org/10.18632/oncotarget.27888

Research Paper: "Quantitative proteome profiling stratifies fibroepithelial lesions of the breast." https://doi.org/10.18632/oncotarget.27889

About Oncotarget:

Oncotarget is a bi-weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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A review paper published this month in Oncotarget by researchers from the University of Modena and Reggio Emilia in Italy and the Sulaiman AlRajhi Medical School in Saudi Arabia is trending, and titled, “Cancer stem cells and macrophages: molecular connections and future perspectives against cancer.”

(Read the paper here: https://www.oncotarget.com/article/27870/text/)

Two authors of this review paper, Dr. Beatrice Aramini and Dr. Valentina Masciale, provide an overview of their research on the complex crosstalk between cancer stem cells and macrophages, and potential anti-cancer strategies for future studies.

The Trending with Impact series highlights Oncotarget publications attracting higher visibility among readers around the world online, in the news, and on social media—beyond normal readership levels.

(More from Trending with Impact: https://www.oncotarget.org/tag/trending-with-impact/)

About Oncotarget:

Oncotarget is a bi-weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Hundreds of scientific studies, reviews, and analyses are being published from around the world at any given time. This can make reading the latest research literature a time consuming task—depending, of course, on the quantity of papers one hopes to consume. As a tool to help alleviate this important undertaking, many researchers have taken to listening to one of the top open-access podcasts of 2020 and 2021: The Oncotarget Podcast.

After a paper is published, it is added to an enhanced post-publication service provided by Oncotarget, in an effort to help authors reach a wider audience. This podcast series is another way to widely distribute the research that is published with free access by Oncotarget. Oncotarget Podcast episodes regularly include audio readings, press releases, and interviews with authors about their latest and trending papers published by Oncotarget. Player.fm (https://player.fm/podcasts/open-access) rated the Oncotarget Podcast on their lists of Best Open Access Podcasts of 2020 and 2021.

Oncotarget, and Impact Journals as a whole, is constantly expanding the definition of open-access to include a wide variety of accessibility-based audio and visual media to support researchers and readers with disabilities. Creators of the Oncotarget Podcast hope that offering audible renderings of literature from Oncotarget.com, and of blog posts from Oncotarget.org and Oncotarget.net, will be helpful for the vision impaired community.

Stay up-to-date with all of the latest oncology-focused research literature published by Oncotarget by subscribing to the Oncotarget Podcast, which can be found on Soundcloud, Apple, Stitcher, and Blubrry podcast streaming services.

About Oncotarget:

Oncotarget is a bi-weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Dr. Mikhail V. Blagosklonny, M.D., Ph.D., Editor-in-Chief of Oncotarget, and Professor, at Roswell Park Cancer Institute, published "The goal of geroscience is life extension" which was selected as the Featured Cover Paper for Volume 12 Issue 3 and reported that although numerous drugs seemingly extend healthspan in mice, only a few extend lifespan in mice and only one does it consistently. Some of them, alone or in combination, can be used in humans, without further clinical trials.

Dr. Mikhail V. Blagosklonny from The Roswell Park Cancer Institute said, "Although we do not know everything about aging, we now know enough to start its pharmacologic suppression using clinically approved drugs."

Published in 2010, these opening words of the paper entitled "Increasing healthy lifespan by suppressing aging in our lifetime: preliminary proposal" are still relevant today.

Hyperfunction of these signaling pathways directly drive all age-related diseases, which are manifestations of aging. We just need clinically available inhibitors of these signaling pathways to extend both healthspan and lifespan, by slowing aging.

A mere extension of healthspan is not enough: drugs that fail to extend lifespan in mice will fail to extend lifespan in humans, if used as a monotherapy.

Yet, in rational combinations with life-extending drugs, "healthspan-only" drugs may extend lifespan further.

In this Oncotarget publication, Dr. Blagosklonny reviews drugs that extend lifespan and healthspan in mammals, in contrast to those that may affect only healthspan without lifespan, and discusses how to proceed with clinical application of lifespan-extending drugs.

Blagosklonny concluded in their Oncotarget Research Perspective, "If we want to live longer, we have no choice, but to use drugs such as rapamycin, which extends life in short-lived mammals and is approved for humans use. After all, humans are mammals, and there is no reason to think that they will not work in humans."

Please note: This review is intended for a professional audience. This article does not represent medical advice or recommendations to patients. The media should exercise caution and seek expert medical advice for interpretation, when referring to this article. Medical doctors interested in this topic may e-mail the author at [email protected] or follow on Twitter @Blagosklonny

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DOI - https://doi.org/10.18632/oncotarget.27882

Full text - https://www.oncotarget.com/article/27882/text/

Correspondence to - Mikhail V. Blagosklonny - [email protected], [email protected]

Keywords - aging, longevity, rapamycin, mTOR, metformin

About Oncotarget

Oncotarget is a weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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The cover for issue 2 of Oncotarget features Figure 4, "Combination therapy TA99/ICB reduced the lung tumor burden in the B16 model of metastases," published in "Improved therapeutic efficacy of unmodified anti-tumor antibodies by immune checkpoint blockade and kinase targeted therapy in mouse models of melanoma" by Pérez-Lorenzo, et al. which reported that here, the authors showed that removing immune suppression and enhancing stimulatory signals increased the anti-tumor activity of unmodified TA99 antibodies with a significant reduction of growth of solid tumors and lung metastases in mouse models of melanoma.

Immune checkpoint blockade enhanced the efficacy of TA99, which was associated with greater CD8 /Foxp3 , NK1.1 and dendritic cell infiltrates, suggestive of an increased anti-tumor innate and adaptive immune responses.

Moreover, they found an improved therapeutic effect when YUMM tumor-bearing mice were treated with TA99 combined with MEKi and immune checkpoint blockade.

The Oncotarget findings suggest that MEKi induced an increased expression of tumor-associated antigens, which in combination with anti-tumor antibodies, generated a robust adaptive anti-tumor response that was sustained by immune checkpoint inhibition therapy.

The authors postulate that combining anti-tumor antibodies with standard-of-care strategies such as immune checkpoint blockade or targeted therapy, will improve therapeutic outcomes in cancer.

Dr. Angela M. Christiano from The Columbia University said, "It is well accepted that tumor development and progression is usually controlled by immunosurveillance mechanisms in which specific and non-specific immunological responses are constantly mounted against tumor cells."

Passive administration of anti-tumor antibodies generally functions by targeting malignant cells through IgG-mediated antibody-dependent cellular cytotoxicity, which is a rapid but relatively short-acting anti-tumor response.

Alternatively, they and others also demonstrated that the administration of anti-tumor antibodies induces long-lasting FcR-dependent tumor specific immunity in the host, with kinetics consistent with an induced adaptive immune response against the tumor.

In this model, anti-tumor antibodies, alone or in combination with chemotherapy, will promote innate cell-mediated ADCC, and the capture and processing of antigens by antigen presenting cells, with the subsequent stimulation and homing of antigen-specific effector T lymphocytes to the tumor site, leading to tumor elimination, a phenomenon the researchers and others referred to as the “vaccinal effect”.

With the use of the B16 and YUMM mouse models of melanoma and the anti-TYRP1 mouse monoclonal antibody TA99, we demonstrated that the therapeutic effects of these unmodified anti-tumor antibodies can be enhanced by ICB through the stimulation of both innate and adaptive anti-tumor immune responses.

In addition, they found that the MEK inhibitor -induced increased expression of melanosomal antigens further enhanced the anti-melanoma response to combination therapy with anti-tumor antibodies and immune checkpoint blockade in mouse models of melanoma.

The Christiano Research Team concluded in their Oncotarget Research Paper, "Together with our preclinical data, these results invite further clinical investigation of unmodified anti-tumor antibodies in combination with ICB and targeted therapies, and may represent promising and innovative therapeutic interventions for the successful management of patients with advanced melanoma and other cancers."

Full text - https://www.oncotarget.com/article/27868/text/

Correspondence to - Angela M. Christiano - [email protected]

Keywords - anti-tumor antibodies, targeted therapy, immunotherapy, combination therapies, melanoma

The cover for issue 28 of Oncotarget features Figure 5, "TMEM165 expression levels alters N-linked glycosylation," by Murali, et al., and reported that the TMEM165 protein was not detected in non-malignant matched breast tissues and was detected in invasive ductal breast carcinoma tissues by mass spectrometry.

The hypothesis is that the TMEM165 protein confers a growth advantage to breast cancer.

The authors created a CRISPR/Cas9 knockout of TMEM165 in the human invasive breast cancer cell line MDAMB231.

Furthermore, they find that TMEM165 expression alters the glycosylation of breast cancer cells and these changes promote the invasion and growth of breast cancer by altering the expression levels of key glycoproteins involved in the regulation of the epithelial to mesenchymal transition such as E-cadherin.

These studies illustrate new potential functions for this Golgi membrane protein in the control of breast cancer growth and invasion.

Dr. Karen L. Abbott from The University of Oklahoma Health Sciences Center, Department of Biochemistry and Molecular Biology said "Breast cancer is the most commonly diagnosed cancer in women."

The TMEM165 protein was identified by mass spectrometry in invasive breast carcinoma tissue with no detection in patient-matched adjacent normal breast tissues.

The authors analyzed TCGA breast cancer cases to examine TMEM165 expression levels in all molecular types of human breast cancer using UALCAN.

They found that TMEM165 is amplified across all types of breast cancer compared to normal breast tissue with IDC cases having the highest levels of TMEM165 expression.

In the present study, the authors report that TMEM165 is upregulated in human breast cancer cell lines and patient tumor tissues and increased expression of TMEM165 correlates with poor prognosis in breast cancer patients.

Collectively, the data demonstrate that overexpression of TMEM165 promotes EMT in breast cancer suggesting a novel role for TMEM165 as a driver of tumor invasion making it a prognostic marker and potential therapeutic target for breast cancer.

The Abbott Research Team concluded in their Oncotarget Research Paper, "we have expanded on our initial 2012 glycoproteomic study that was the first to identify TMEM165 protein as a potential biomarker for breast carcinoma. In this study, we have provided initial mechanistic studies that indicate that TMEM165 expression drives the growth and invasion of breast cancer. TMEM165 expression levels could be a potential prognostic marker for predicting DCIS cases that may progress to invasive disease. Larger prospective cohorts will need to be analyzed to determine the link between TMEM165 levels and the progression to IDC. We find that IDC patients with higher TMEM165 expression levels have reduced overall survival making this protein a target for the development of new therapeutic strategies to limit the progression of breast cancer."

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DOI - https://doi.org/10.18632/oncotarget.27668

Full text - https://www.oncotarget.com/article/27668/text/

Correspondence to - Karen L. Abbott - [email protected]

Keywords - TMEM165, migration, invasion, breast cancer, glycosylation

About Oncotarget

Oncotarget is a weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Volume 11, Issue 28 of Oncotarget features "Rapid onset type 1 diabetes with anti-PD-1 directed therapy", by Yun et al. and reported that Type 1 diabetes is a rare immune-related adverse event caused by checkpoint inhibitors with serious risk for diabetic ketoacidosis.

Of the patients who received immunotherapy, 5 patients were found to have type 1 diabetes, all of whom presented with DKA requiring insulin at 20 to 972 days from their first anti-PD- 1 dose.

Four patients had new-onset diabetes with mean Hb A1c of 9.1% on DKA presentation and persistent elevations over time.

Two patients who tested positive for glutamic acid decarboxylase antibodies presented with DKA at 20 and 106 days from first anti-PD-1 administration whereas patients who were autoantibody negative had DKA more than a year later.

The case series suggests that monitoring glycemia in patients on PD-1 inhibitors is not predictive for diabetes occurrence.

Dr. Sandip Pravin Patel from The Division of Hematology-Oncology in the Department of Medicine at The University of California San Diego said, "Cancer immunotherapy has broadened in clinical use over the last decade with FDA approval for treatment of various malignancies including melanoma, non-small cell lung cancer (NSCLC), renal cell carcinoma, urothelial carcinoma, head, and neck carcinomas, cutaneous squamous cell cancer, microsatellite unstable tumors, and Hodgkin's lymphoma."

Autoimmune type 1 diabetes is generally associated with positive autoantibodies to islet proteins including glutamic acid decarboxylase, insulin, insulinoma-associated antigen-2, zinc transporter 8, and islet cells.

However, only a subset of patients who acquire type 1 diabetes is found to have autoantibodies and specific HLA alleles, making these biomarkers poor predictors of diabetes incidence.

Given the rarity of type 1 diabetes as an ir AE, the authors sought to characterize the real-world diagnosis, management, and sequelae of patients who developed this ir AE in the context of their immune checkpoint blockade.

This Oncotarget paper highlights the rapid kinetics of type 1 diabetes in patients on checkpoint inhibitors.

Type 1 diabetes presented as DKA for all patients in this series and all but one patient had a new diagnosis of diabetes, without antecedent laboratory or imaging findings.

The Patel Research Team concluded in their Oncotarget Research Paper that their case series illustrates the rare incidence of immunotherapy-induced type 1 diabetes and describes the rapid course of this disease in patients.

Regardless of whether or not patients remain on checkpoint inhibitors, those with immunotherapy-induced diabetes are at risk for hyperglycemia and recurrent DKA. Surveillance of glycemia or Hb A1c does not predict diabetes but does have a role after type 1 diabetes arises as glycemia fluctuates and elevated Hb A1c levels persist.

Furthermore, GAD antibodies are present in about half of patients who develop type 1 diabetes after immunotherapy, warranting additional investigations into whether this is all association and a marker of immune attack.

Given the absence of prescient laboratory or imaging findings in patients who develop type 1 diabetes on anti-PD-1 therapy, patients should be counseled on the symptoms of hyperglycemia which include polyuria, polydipsia, abdominal pain, nausea and emesis and seek medical attention immediately.

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DOI - https://doi.org/10.18632/oncotarget.27665

Full text - https://www.oncotarget.com/article/27665/text/

Correspondence to - Sandip Pravin Patel - [email protected]

Keywords - type 1 diabetes, diabetic ketoacidosis (DKA), immune-related adverse event (irAE), immunotherapy, PD-1 inhibitors

About Oncotarget

Oncotarget is a weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

Volume 11, Issue 28 of Oncotarget features "Genetic analysis of the cooperative tumorigenic effects of targeted deletions of tumor suppressors Rb1, Trp53, Men1, and Pten in neuroendocrine tumors in mice" by Xu et, al. which reported that the authors examined whether the TSGs Rb1, Trp53, Pten, and Men1 have cooperative effects in suppressing neuroendocrine tumors in mice.

By monitoring growth and examining the histopathology of the pituitary and pancreas in these mice, the authors demonstrated that pRB had the strongest cooperative function with PTEN in suppressing Pit NETs and had strong cooperative function with Menin and TRP53, respectively, in suppressing Pit NETs and Pan NETs. TRP53 had weak cooperative function with PTEN in suppressing pituitary lesions.

Collectively, the data indicated that pRB and PTEN pathways play significant roles in suppressing Pit NETs, while the Menin-mediated pathway plays a significant role in suppressing Pan NETs. Understanding the molecular mechanisms of these genes and pathways on NETs will help us understand the molecular mechanisms of neuroendocrine tumorigenesis and develop effective preclinical murine models for NET therapeutics to improve clinical outcomes in humans.

Dr. Eugenia Y. Xu from Rutgers and Princeton University as well as Dr. Daniel A. Notterman from Princeton University said, "Human pituitary neuroendocrine tumors (PitNETs) are the third most common intracranial neoplasms and represent approximately 10–25% of all primary intracranial tumors."

Additionally, in rare cases, RB1 has been found with epigenetic mutations in the promoter region in Pit NETs suggesting that inactivation of the RB pathway contributes to the development of Pit NETs. Compound mice with concomitant deletions of Men1 and Pten develop Pit NETs and Pan NETs and mice with p18–/– Pten+/– mutations develop Pit NETs, suggesting that PTEN plays a role in pituitary and pancreatic islet tumorigenesis.

However, Men1 deletion mice develop pars distalis prolactinomas and Rb1 deletion mice develop pars intermedia tumors of the pituitary, suggesting that the functions of Menin and pRB may not fully overlap.

Here they investigate the question of whether Men1 and Rb1 have cooperative tumorigenic effects on NETs using tissue-specific double homozygous deletions of Men1 and Rb1 in mice.

The Oncotarget authors report that the characterization of Pit NETs and Pan NETs with double homozygous deletions of TSGs and illustrate that pRB has the strongest cooperative function with PTEN in suppressing Pit NETs and has a strong cooperative function with Menin and TRP53, respectively, in suppressing Pit NETs and Pan NETs in mice.

The Xu/Notterman Research Team concluded in their Oncotarget Research Paper, "our data clearly demonstrate that TSGs Rb1, Pten, Men1, and Trp53 have distinct tissue specificity in neuroendocrine tumorigenesis in mouse and likely in man. The mouse models here and deletion of these TSGs in MIP-Cre mice will help further our understanding the molecular function of these TSGs and their pathways in PitNET and PanNET pathogenesis, which will help develop targeted novel therapeutic options in treating human patients."

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DOI - https://doi.org/10.18632/oncotarget.27660

Full text - https://www.oncotarget.com/article/27660/text/

Correspondence to - Eugenia Y. Xu - [email protected] and Daniel A. Notterman - [email protected]

Keywords - neuroendocrine tumors, RB1, Trp53, PTEN, Men1

About Oncotarget

Oncotarget is a weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology.