Oncotarget

BUFFALO, NY- September 25, 2023 – A new research paper was published in Oncotarget's Volume 14 on September 22, 2023, entitled, “Transcriptomic analysis identifies four novel receptors potentially linking endometrial cancer with polycystic ovary syndrome and generates a transcriptomic atlas.”

Polycystic Ovary Syndrome (PCOS) is associated with a 3 to 4-fold increased risk of endometrial cancer (EC), but molecular mechanisms are unclear. Upregulation of the IGF1 gene in PCOS endometrium may increase EC risk, but this is uncertain. In this new study, researchers Fatma Alqutami, Mahmood Hachim, Charlie Hodgman, and William Atiomo from the Mohammed Bin Rashid University of Medicine and Health Sciences and the University of Nottingham aimed to investigate links between EC and PCOS, by analyzing publicly available transcriptomic data.

“The original aim of this study was to investigate the links between EC and PCOS, by analysing publicly available transcriptomic data and investigate IGF-1 and IGFBP gene expression in the endometrium of women with PCOS and EC compared with normal endometrium.”

The NCBI Gene Expression Omnibus was used to identify relevant studies. Differentially expressed genes (DEGs) were identified and analyzed using Metascape to identify pathways of interest. PCOS DEGs that encode proteins secreted into blood were identified using the Human Protein Atlas blood protein database.

EC DEGs that are cellular receptors were identified using EcoTyper. These were intersected to identify which EC receptors interact with PCOS secreted proteins. Seven receptors were identified in EC but only PTPRF, ITGA2, ITGA3, and ITGB4 genes were expressed on epithelial cells. Pathway enrichment of these genes showed that the major and common pathway involved was that of the PI3K-AKT signaling pathway which was consistent with a link between PCOS and EC. However, IGF1 was down regulated in PCOS and EC.

“Our conclusions at this stage do not support a link between IGF-1 and IGFBP genes in PCOS and EC. However, we have identified four novel receptors which may underpin the risk of EC in PCOS, and we believe our findings provide sufficient evidence to form the basis for a transcriptomic atlas to underpin future research into the links between PCOS and EC and the molecular mechanisms underpinning both diseases.”

DOI - https://doi.org/10.18632/oncotarget.28513

Correspondence to - William Atiomo - [email protected]

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Keywords - cancer, polycystic ovary syndrome, endometrial cancer, transcriptomics, IGF1, in-silico

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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Multiple myeloma (MM) is a type of blood cancer that affects plasma cells, which are responsible for producing antibodies. MM is characterized by the accumulation of abnormal plasma cells in the bone marrow, leading to bone damage, kidney failure, anemia, and increased susceptibility to infections. MM is a heterogeneous disease with different subtypes and genetic mutations that affect the prognosis and response to treatment. Therefore, there is a need for new biomarkers and therapeutic targets that can improve the outcomes of MM patients.

One of the potential targets that has recently emerged is the fatty acid binding protein (FABP) family. FABPs are proteins that bind and transport fatty acids, which are essential for energy production, cell signaling and membrane synthesis. FABPs are expressed in various tissues and organs, and have different roles depending on their location and type. There are nine members of the FABP family, but FABP5 seems to be the most relevant for MM.

In a recent editorial paper, researchers Heather Fairfield and Michaela R. Reagan from Maine Health Institute for Research, University of Maine and Tufts University School of Medicine summarized previous findings from their 2023 study and the current evidence on the role of FABPs in MM. On June 19, 2023, their editorial was published in Oncotarget, entitled, “The hope for targeting fatty acid binding proteins in multiple myeloma.”

Full blog - https://www.oncotarget.org/2023/09/21/targeting-fatty-acid-binding-proteins-in-multiple-myeloma/

Paper DOI - https://doi.org/10.18632/oncotarget.28437

Correspondence to - Michaela R. Reagan - [email protected]

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Keywords - cancer, multiple myeloma, FABPs, fatty acid binding proteins, immunoncology, pre-clinical discovery

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BUFFALO, NY- September 20, 2023 – A new editorial paper was published in Oncotarget's Volume 14 on September 15, 2023, entitled, “Potential repurposing of DPP4 inhibitors for target therapy resistance in renal cell carcinoma.”

In their new editorial, researchers Kuniko Horie and Satoshi Inoue from Saitama Medical University and Tokyo Metropolitan Institute for Geriatrics and Gerontology discuss renal cell carcinoma (RCC) — a major adult kidney cancer, which is often incidentally discovered as an asymptomatic disease on imaging in the developed countries. RCC has the most fatal disease among urological cancers, as a recent 5-year relative survival rate in the U.S. (2009–2015) is less than 80%. While RCC is known as a cancer resistant to chemo- and radio-therapies, the prognosis of RCC has been remarkably improved after the clinical application of tyrosine kinase inhibitors (TKIs) and immunotherapy.

The rationale for the efficacy of TKIs in RCC is mainly based on the angiogenetic status, particularly in clear cell RCC (ccRCC) that is the most common type of RCC (70–75% of RCC), in which the loss of function mutation of Von Hippel-Lindau (VHL) tumor suppressor gene activates hypoxia inducible factor (HIF) and vascular endothelial growth factor (VEGF) pathways. The first-line TKIs that predominantly target VEGF receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) (e.g., sunitinib and sorafenib) have been clinically used since late 2000s, and the second-line TKIs such as cabozantinib, which targets more receptor tyrosine kinases including MET and TAM kinases as well as VEGFR, have been further applied to the treatment of advanced RCC since early 2010s in which the first-line TKIs are ineffective.

“In our recent study, we established a panel of patient-derived ccRCC spheroid cultures with the enhancement of cancer stemness gene signature including DPP4 [9]. Focusing on TKI sunitinib sensitivity, we demonstrated that DPP4 inhibition increased sunitinib efficacy in DPP4-high RCC spheroids and DPP4 was upregulated in sunitinib-resistant RCC cells.”

DOI - https://doi.org/10.18632/oncotarget.28463

Correspondence to - Satoshi Inoue - [email protected]

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Keywords - cancer, renal cell carcinoma (RCC), tyrosine kinase inhibitor (TKI), Dipeptidyl peptidase IV (DPP4), drug resistance, drug repurposing

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BUFFALO, NY- September 19, 2023 – A new research paper was published in Oncotarget's Volume 14 on September 15, 2023, entitled, “Real time ex vivo chemosensitivity assay for pancreatic adenocarcinoma.”

Patient-derived organoids (PDOs) and xenografts (PDXs) have been extensively studied for drug-screening. However, their usage is limited due to lengthy establishment time, high engraftment failure rates and different tumor microenvironment from original tumors. In this new study, researchers Dae Won Kim, Francisca Beato, Youngchul Kim, Alexandra F. Tassielli, Ruifan Dai, Jason W. Denbo, Pamela J. Hodul, Mokenge P. Malafa, and Jason B. Fleming from Moffitt Cancer Center developed real time-live tissue sensitivity assay (RT-LTSA) using fresh tumor samples to overcome these limitations.

“To overcome the major hurdles of the PDX-based assay, we developed real time LTSA (RT-LTSA) using fresh tumor samples. In this study, we report a reliable and reproducible RT-LTSA with resected fresh tumor samples to predict patients’ clinical response to chemotherapy in pancreatic cancer.”

Tissue slices from resected pancreatic cancer samples were placed in 96-well plates, and the slices were treated with chemotherapeutic agents. The correlation between the chemo-sensitivity of tissue slices and each patient’s clinical outcome was analyzed. The viability and tumor microenvironment of the tissue slices were well-preserved over 5 days. The drug sensitivity assay results were available within 5 days after tissue collection.

While all 4 patients who received RT-LTSA sensitive adjuvant regimens did not develop recurrence, 7 of 8 patients who received resistant adjuvant regimens developed recurrence. The researchers observed significantly improved disease-free survival in the patients who received RT-LTSA sensitive adjuvant regimens (median: not reached versus 10.6 months, P = 0.02) compared with the patient who received resistant regimens. A significant negative correlation between RT-LTSA value and relapse-free survival was observed (Somer’s D: −0.58; P = 0.016).

“RT-LTSA which maintains the tumor microenvironment and architecture as found in patients may reflect clinical outcome and could be used as a personalized strategy for pancreatic adenocarcinoma. Further, studies are warranted to verify the findings.”

DOI - https://doi.org/10.18632/oncotarget.28508

Correspondence to - Jason B. Fleming - [email protected]

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Keywords - cancer, pancreatic cancer, sensitivity assay, chemotherapy

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A new editorial paper was published in Oncotarget's Volume 14 on July 7, 2023, entitled, “Systemic treatment for brain metastasis in HER2- positive advanced breast cancer: what have we learned so far?”

In their new editorial, researchers Marta Vaz Batista, José Perez-Gracia, Inês Eiriz, Maria Gion, Antonio Llombart, Sofia Braga, and Javier Cortés from Medica Scientia Innovation Research (MEDSIR) and Hospital Professor Doutor Fernando Fonseca discuss new drugs available for breast cancer (BC) patients with brain metastasis (BM). The better survival of Human Epidermal growth factor receptor-type 2 positive (HER2+) BC patients unmasked the biological predilection of this BC subtype for development of BM.

Indeed, central nervous system (CNS) is a frequent metastatic site for HER2+ advanced BC patients. Over the last years, new therapeutic strategies targeting the HER2 protein have been introduced for systemic treatment of HER2+ BC - either tyrosine kinase inhibitors, monoclonal antibodies, or antibody-drug conjugates. Patients with BMs have a poorer outcome, compared with patients without BMs, but their prognosis is also improving with the introduction of new anti HER2+ - targeted therapies.

“Our group has been working in the DEBBRAH trial, using trastuzumab deruxtecan for different settings of CNS involvement: stable or progressing BM and/or leptomeningeal carcinomatosis.”

The team included patients with HER2+ and HER2-low BC. Activity of trastuzumab-deruxtecan in patients with HER2+ BC and untreated or progressing after local therapy BMs also has been shown in another phase II trial.

“The final results are yet to be reported, but so far, we observed intracranial responses in HER2+ BC patients [7].”

Read the full editorial: DOI: https://doi.org/10.18632/oncotarget.28435

Correspondence to: Marta Vaz Batista - [email protected]

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Keywords - cancer, brain metastasis, HER2+ breast cancer

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A new editorial paper was published in Oncotarget's Volume 14 on May 26, 2023, entitled, “Latest updates on MET targeted therapy for EXON 14 mutations in lung cancer.”

In their new editorial, researchers Mira Al Jaberi, Wolfgang Clough and Samir Dalia from Mercy Hospital discuss the MET gene. Several alterations in the MET gene were identified as targetable oncogenic changes leading to non-small cell lung cancer (NSCLC). These include genomic amplifications, exon 14 skipping mutations and fusion.

Capmatinib has been considered as a first-line treatment for patients with NSCLC carrying a MET exon 14 skipping mutation since May 2020 by the USFDA. A study newly published in early 2023 showed that Crizotinib, a tyrosine kinase inhibitor, was also effective for MET fusions, which occur rarely in 0.2–0.3% of patients with lung cancer. A major challenge arising after the introduction of tyrosine kinase inhibitors is limited clinical benefit, which is due to primary and potential secondary acquired drug resistance.

“A major challenge arising after the introduction of tyrosine kinase inhibitors is limited clinical benefit, which is due to primary and potential secondary acquired drug resistance [4, 5].”

Several structurally different MET tyrosine kinase inhibitors (TKIs) have been developed or are under clinical evaluation. TKIs are categorized into type I TKIs (type Ia: crizotinib; type Ib: savolitinib, capmatinib) and type II TKIs (cabozantinib, glesatinib, merestinib). Combination therapy reduces resistance and enhances clinical outcomes.

“These clinical trials along with others will show us if other MET inhibitors or combination therapy may be better than the current standard of care.”

DOI - https://doi.org/10.18632/oncotarget.28419

Correspondence to - Samir Dalia - [email protected]

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Keywords - cancer, non small cell lung cancer, MET mutation, targeted therapy, precision medicine

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How can we understand the role of genetic variations in cancer development and treatment? This is one of the most challenging and important questions in modern biology and medicine. A new editorial paper, by researchers Jun S. Song and Mohith Manjunath from the University of Illinois at Urbana-Champaign, offers a novel discussion involving computational methods to address this question. On August 30, 2023, their editorial was published in Oncotarget, entitled, "Predicting the molecular functions of regulatory genetic variants associated with cancer." 

In this editorial, the authors review recent advances and challenges in identifying and characterizing the functional effects of genetic variants that affect gene regulation, such as enhancers, promoters, and transcription factors. These variants, also known as expression quantitative trait loci (eQTLs), can modulate the expression levels of genes and influence various cellular processes and phenotypes, including cancer susceptibility and response to therapy.

The authors propose a framework for predicting the molecular functions of eQTLs based on their genomic context, epigenetic marks, chromatin accessibility, and three-dimensional interactions. They also discuss how to integrate multiple types of data and methods to improve the accuracy and interpretability of the predictions. Furthermore, they highlight the potential applications and implications of their approach for cancer research and precision medicine.

“A promising approach to address these challenges is to integrate genomic, epigenomic, transcriptomic and machine learning methods to identify functional genetic variants and characterize their mode of action in regulating target genes.”

Full blog - https://www.oncotarget.org/2023/09/07/predicting-functions-of-cancer-associated-genetic-variants/

Editorial DOI - https://doi.org/10.18632/oncotarget.28451

Correspondence to - Jun S. Song - [email protected]

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Keywords - cancer, genome-wide association studies, cancer risk, regulatory variants, functional genomics

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A new editorial paper was published in Oncotarget's Volume 14 on August 30, 2023, entitled, “Subpopulations of AIB1 isoform-expressing breast cancer cells enable invasion and metastasis.”

In their new editorial, researchers Amber J. Kiliti, Ghada M. Sharif, Anton Wellstein, and Anna T. Riegel from Georgetown University Medical Center discuss potential mechanisms of breast cancer invasion and metastasis. Genetic and epigenetic events drive individual tumor cells to proliferate and expand into a heterogeneous mixture of cells that evade immune surveillance, acquire the ability to invade the vasculature and spread as metastatic seeds to distant sites. Organ metastasis contributes to more than 90% of all cancer-related deaths.

“The model of Darwinian evolution explains the stepwise selection of cancer cells capable of invasion and metastatic spread and an extensive body of work supports that cancer cell-autonomous features match the selected cancer cell ‘seed’ with the appropriate ‘soil’ of the target organ.”

However, this concept was challenged in a recent paper in Cancer Research. Sharif et al. observed that a subclonal population of cells in a heterogeneous tumor can significantly alter the growth characteristics, invasiveness and metastasis of an entire tumor through cell-cell crosstalk. These functionally relevant cell subpopulations are difficult to detect through bulk analysis though their presence may influence disease outcome and efficacy of treatments.

“In their paper, Sharif et al. detailed how expression of a splice isoform of the transcriptional coregulator and oncogene Amplified In Breast Cancer 1 (AIB1) in a small subpopulation of cells can lead to increased tumor growth and invasion of surrounding tissues by ductal carcinoma in situ (DCIS) cells.”

DOI - https://doi.org/10.18632/oncotarget.28452

Correspondence to - Anna T. Riegel - [email protected]

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Keywords - cancer, AIB1, AIB1Δ4, breast cancer, invasion, metastasis

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A new research paper was published in Oncotarget's Volume 14 on August 30, 2023, entitled, “Analytic validation of NeXT Dx™, a comprehensive genomic profiling assay.”

In this new research paper, researchers from Personalis, Inc. describe the analytic validation of NeXT Dx, a comprehensive genomic profiling assay to aid therapy and clinical trial selection for patients diagnosed with solid tumor cancers.

“The NeXT Dx clinical report currently provides the ordering clinician with information from 401 cancer-related genes on clinically relevant mutations, as well as related drug response associations and a curated list of clinical trials that may be applicable to the patient.”

Proprietary methods were utilized to perform whole exome and whole transcriptome sequencing for detection of single nucleotide variants (SNVs), insertions/deletions (indels), copy number alterations (CNAs), and gene fusions, and determination of tumor mutation burden and microsatellite instability. Variant calling is enhanced by sequencing a patient-specific normal sample from, for example, a blood specimen. This provides highly accurate somatic variant calls as well as the incidental reporting of pathogenic and likely pathogenic germline alterations. Fusion detection via RNA sequencing provides more extensive and accurate fusion calling compared to DNA-based tests.

NeXT Dx features the proprietary Accuracy and Content Enhanced technology, developed to optimize sequencing and provide more uniform coverage across the exome. The exome was validated at a median sequencing depth of >500x. While variants from 401 cancer-associated genes are currently reported from the assay, the exome/transcriptome assay is broadly validated to enable reporting of additional variants as they become clinically relevant. NeXT Dx demonstrated analytic sensitivities as follows: SNVs (99.4%), indels (98.2%), CNAs (98.0%), and fusions (95.8%). The overall analytic specificity was >99.0%.

“By more comprehensively characterizing the molecular characteristics of each patient’s tumor, NeXT Dx provides personalized recommendations critical to clinical decision-making with respect to current FDA-approved drug-variant specific treatments and evolving treatment opportunities via enrollment in clinical trials.”

DOI - https://doi.org/10.18632/oncotarget.28490

Correspondence to - Richard Chen - [email protected]

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Keywords - cancer, comprehensive genomic profiling, whole exome sequencing, whole transcriptome sequencing, tumor-normal, precision medicine

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A new research perspective was published in Oncotarget's Volume 14 on April 14, 2023, entitled, “Adopted neoplastic cells and the consequences of their existence.”

In this research perspective, researcher Yuri Lazebnik from Lerna Consulting begins by explaining a view that guides the bulk of cancer research and oncology: each neoplastic cell in a tumor is a genetic offspring of another neoplastic cell.

“Yet, analyzing tumors from transplant patients has revealed that some normal migratory cells adopt the phenotype of neoplastic cells without acquiring their genome, thus becoming what I suggest to call adopted neoplastic cells.”

This commentary reviews the evidence for the existence of adopted neoplastic cells, outlines the consequences of their presence, and discusses what kind of cells can be adopted, how and why.

“Finally, as experiments with humans can go only that far, and fortunately so, testing the hypotheses we have discussed will require experimental systems, such as human tumor explants which have been explored to reveal intercellular bridging [129, 130] and chimeric animals designed to monitor cell fate, cell fusion, and component transfer [206].”

DOI - https://doi.org/10.18632/oncotarget.28408

Correspondence to - Yuri Lazebnik - [email protected]

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Keywords - cancer, tumor microenvironment, horizontal oncogenesis, intercellular bridges, cell fusion, cell repair

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