Oncotarget

BUFFALO, NY- May 19, 2022 – A new research paper was published in Volume 13 of Oncotarget, entitled, “CancerOmicsNet: a multi-omics network-based approach to anti-cancer drug profiling.”

Researchers from Louisiana State University developed CancerOmicsNet—a graph neural network model to predict the growth rate of a cancer cell line after drug treatment.

“CancerOmicsNet is more advanced than many deep learning techniques operating in the Euclidean space [47], because it extracts knowledge directly from biological networks providing a more adequate representation of complex diseases such as cancer.”

CancerOmicsNet integrates multiple heterogeneous data, such as biological networks, genomics, inhibitor profiling, and gene-disease associations, into a unified graph structure. This novel method utilizes compact, cancer-specific networks constructed from protein-protein interactions, differential gene expression, disease-gene association, and drug inhibition data.

“In order to evaluate the performance of CancerOmicsNet, we conducted a cross-validation at the tissue level by removing from model training all cell lines originating from a particular tissue and then analyzing the accuracy for these cell lines.”

In this study, the researchers carefully evaluated the generalizability of CancerOmicsNet in a series of cross-validation benchmarks against different tumor tissues. Encouragingly, the cross-validated accuracy of CancerOmicsNet at the tissue level was significantly higher than those measured for other approaches on the same data.

“The performance of CancerOmicsNet, properly cross-validated at the tissue level, is 0.83 in terms of the area under the receiver operating characteristics, which is notably higher than those measured for other approaches.”

The researchers specify that the applicability of CancerOmicsNet is presently limited to kinase inhibitors, while alternative methods are applicable to other classes of therapeutics as well.

“Overall, CancerOmicsNet offers a high performance and the desired generalizability in the prediction of the effect of kinase-targeted therapies on the cancer cell growth.”

DOI: https://doi.org/10.18632/oncotarget.28234

Correspondence to: Michal Brylinski – Email: [email protected]

Keywords: cancer growth rate, kinase inhibitors, differential gene expression, gene-disease association, cancer-specific networks

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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Listen to a blog summary of a trending research paper published by Oncotarget, entitled, "Proteomic analysis reveals dual requirement for Grb2 and PLCγ1 interactions for BCR-FGFR1-Driven 8p11 cell proliferation."

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Chromosomes are found in the nucleus of cells and consist of proteins and tightly coiled strands of DNA. During cell division, chromosomal translocations can occur while the chromosomes are being copied. This type of mutation can mean that an entire chromosome has moved to another location, or that a chromosome has broken, usually into two pieces, and moved to another site. Some translocations are harmless, but others can lead to aberrant cell proliferation and cancer.

“Over the last half century, chromosomal translocations encoding functional oncogenic proteins have been identified as drivers of multiple cancers, and account for 20% of all malignant neoplasms [1, 2].”

For example, the t(8;22)(p11;q11) chromosomal translocation leads to the initiation of an oncogenic fusion protein called the Breakpoint Cluster Region Fibroblast Growth Factor Receptor 1 (BCR-FGFR1). BCR-FGFR1 is a single driver of 8p11 myeloproliferative syndrome, which is also known as stem cell leukemia/lymphoma (SCLL).

“Stem cell leukemia/lymphoma (SCLL) exhibits distinct clinical and pathological features characterized by chromosomal translocations involving the FGFR1 gene at chromosome 8p11.”

In a trending new study, researchers from the University of California San Diego and Sanford Burnham Prebys Medical Discovery Institute examined mutations in PLCγ1 and Grb2 binding sites individually and when combined together in a double mutant within BCR-FGFR1. On May 11, 2022, the research paper was published in Oncotarget and entitled, “Proteomic analysis reveals dual requirement for Grb2 and PLCγ1 interactions for BCR-FGFR1-Driven 8p11 cell proliferation.”

Full blog - https://www.oncotarget.org/2022/05/12/trending-with-impact-dual-requirement-in-stem-cell-leukemia-lymphoma/

DOI - https://doi.org/10.18632/oncotarget.28228

Correspondence to - Daniel J. Donoghue - [email protected]

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Keywords - oncogenic fusion protein, chromosomal translocation, protein interactome, phosphoproteome, stem cell leukemia/lymphoma

About Oncotarget

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

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BUFFALO, NY-May 16, 2022 – Impact Journals (based out of Buffalo, New York) is an international open-access publisher of journals in the field of biomedical sciences. Impact Journals is on a mission to provide scientists with the opportunity to share exceptional discoveries, offer services that enable rapid dissemination of results, and present vital findings from the many fields of biomedical science. This mission cannot be accomplished without following strong ethical standards.

Scientific integrity is a crucial component of scholarly publishing. At Impact Journals, a growing industry of digital technologies, tools, and ideas are constantly being added to a robust scientific integrity process. The Impact Journals Scientific Integrity Process is built around six main components:

1-Presence of ethics statements

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4-Elimination of Plagiarism

5-Image Forensics Service

6-If a problem arises post-publication, Impact Journals conducts investigations following COPE guidelines in cooperation with the authors and their affiliated institution.

During the 12:00pm Industry Breakout Session on June 1, Impact Journals will be presenting its full scientific integrity process at the 2022 Society for Scholarly Publishing (SSP) Annual Meeting at the Sheraton Grand Chicago Riverwalk in Chicago, Illinois.

More about Impact Journals:

Impact Journals is an open-access publisher, focusing on topics surrounding cancer research, all fields of aging research, and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Our goal is life without disease.

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Dr. Mark Woodford, Assistant Professor at the Department of Urology, SUNY Upstate Medical University, Syracuse, NY, describes his experience publishing the meeting report, “Seventh BHD international symposium: recent scientific and clinical advancement,” with Oncotarget.

DOI - https://doi.org/10.18632/oncotarget.28176

Correspondence to - Mehdi Mollapour - [email protected]

Abstract

The 7th Birt-Hogg-Dubé (BHD) International Symposium convened virtually in October 2021. The meeting attracted more than 200 participants internationally and highlighted recent findings in a variety of areas, including genetic insight and molecular understanding of BHD syndrome, structure and function of the tumor suppressor Folliculin (FLCN), therapeutic and clinical advances as well as patients’ experiences living with this malady.

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Keywords - Birt-Hogg-Dubé syndrome, folliculin, FLCN, tuberous sclerosis complex, LDHA

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Listen to a blog summary of a research paper published by Oncotarget in Volume 13, entitled, "Bladder cancer survival in patients with NOD2 or CDKN2A variants.”

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Genitourinary cancers are a group of cancers that affect components of the urinary tract, including the bladder and kidneys. Worldwide, bladder and kidney cancer impact men at disproportionately higher rates than women. While incidence and mortality rates of bladder cancer in most western European countries have been consistently decreasing, some countries in the region, such as Poland, have seen an increase. Bladder cancer is the 4th most common malignancy in Polish men and the 14th most common malignancy in Polish women. There is currently a need to identify more effective bladder cancer biomarkers and therapeutic targets to develop new effective treatments that improve patient outcomes.

“The association between the NOD2 c.3020insC allele and CDKN2A missense variant c.442G>A (p.P.A148T) and survival of patients with bladder or kidney cancer remains controversial.”

In April of 2022, researchers from Pomeranian Medical University, University of Newcastle and NSW Health Pathology published the first larger-scale study in Poland to describe the clinical characteristics and survival of bladder cancer patients and kidney cancer patients associated with variants in NOD2 and CDKN2A. Their research paper was published in Oncotarget on April 22, 2022, and entitled, “Bladder cancer survival in patients with NOD2 or CDKN2A variants.”

Full blog - https://www.impactjournals.com/journals/blog/oncotarget/gene-variants-investigated-in-polish-bladder-and-kidney-cancer/

DOI - https://doi.org/10.18632/oncotarget.28226

Correspondence to - Elżbieta Złowocka-Perłowska - [email protected]

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Keywords - bladder cancer, kidney cancer, NOD2, CDKN2A, survival

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Listen to a blog summary of a trending research paper published by Oncotarget in Volume 13, entitled, "Real-world survival analysis by tumor mutational burden in non-small cell lung cancer: a multisite U.S. study."

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While a high tumor mutational burden (TMB) may seem unfavorable in the midst of battling non-small cell lung cancer (NSCLC), a higher TMB has been associated with a higher number of neoantigens. The presence of more neoantigens can potentially elicit a stronger immune response. Therefore, TMB may be a viable biomarker of tumor response to immunotherapeutic agents. However, the definitions, parameters and units used to measure high- and low-TMB have been inconsistent over the years. Today, the consensus unit for reporting TMB has shifted to mutations per megabase (mut/Mb). The common cut-off for high- vs. low-TMB from tissue samples is >10 mut/Mb in NSCLC.

“Despite inconsistencies with TMB definition and reporting over time, high TMB has consistently been associated with improved clinical benefit among patients receiving immunotherapy for NSCLC [22].”

Researchers—from University of Utah, University of Minnesota Duluth, Huntsman Cancer Institute, H. Lee Moffitt Cancer Center and Research Institute, Baptist Health Medical Group, MetroHealth Medical Center, Rutgers Cancer Institute of New Jersey, University of Southern California, Saint Luke’s Cancer Institute, University of Kentucky, and Bristol Myers Squibb—used the newest consensus unit and common cut-off parameters for TMB expression to measure TMB’s relationship to treatment response and survival outcomes among metastatic NSCLC patients. Their trending research paper was published in Oncotarget’s Volume 13 on January 31, 2022, and entitled, “Real-world survival analysis by tumor mutational burden in non-small cell lung cancer: a multisite U.S. study.”

“The purpose of this study is to evaluate clinical outcomes by TMB among NSCLC patients treated with immunotherapy containing regimens in the first-line setting.”

Full blog - https://www.oncotarget.org/2022/04/21/trending-with-impact-analysis-of-mutational-burden-in-nsclc/

DOI - https://doi.org/10.18632/oncotarget.28178

Correspondence to - Connor Willis - [email protected]

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Press release - https://www.oncotarget.com/news/pr/oncotarget-mutational-burden-in-lung-cancer-studied-in-multisite-cohort/

Keywords - lung neoplasma, tumor biomarkers, immunotherapy

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BUFFALO, NY-April 25, 2022 – A new research paper, entitled, “Real-world survival analysis by tumor mutational burden in non-small cell lung cancer: a multisite U.S. study,” was published in Oncotarget on January 31, 2022, by researchers from University of Utah, University of Minnesota Duluth, Huntsman Cancer Institute, H. Lee Moffitt Cancer Center and Research Institute, Baptist Health Medical Group, MetroHealth Medical Center, Rutgers Cancer Institute of New Jersey, University of Southern California, Saint Luke’s Cancer Institute, University of Kentucky, and Bristol Myers Squibb.

This multidisciplinary research team analyzed tumor mutational burden (TMB) among a large cohort of patients who had been diagnosed with stage IV non-small cell lung cancer (NSCLC). The cohort included 667 patients recruited from nine different academic and community cancer centers across the United States.

“The purpose of this study is to evaluate clinical outcomes by TMB among NSCLC patients treated with immunotherapy containing regimens in the first-line setting.” (Source, 2022)

While having a high TMB may sound unfavorable, a higher TMB has been associated with a higher number of neoantigens. The presence of a greater number of neoantigens may potentiate a stronger immune response. Thus, TMB may be a viable biomarker of tumor response to immuno-oncology agents.

“Based on the results in this study and prior research, TMB along with other biomarkers, such as PD-L1, may help identify patients more likely to benefit from first-line immunotherapy.” (Source, 2022)

Results of the study confirmed the association between a higher TMB and smoking history. However, the study did not show an association between TMB and sex, age or tumor histology. The team found that, among patients treated with first-line immunotherapy, TMB levels greater than or equal to 10 mutations per megabase were significantly associated with improved overall survival and progression-free survival.

DOI: https://doi.org/10.18632/oncotarget.28178

Corresponding author: Connor Willis – [email protected]

Video: https://youtu.be/Q5JI4L6Moq0

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Dr. Stanley Lipkowitz and Dr. Yoshimi Endo Greer from the Women’s Malignancies Branch at the National Cancer Institute discuss a research paper they co-authored that was published by Oncotarget in 2018, entitled, "ONC201 kills breast cancer cells in vitro by targeting mitochondria."

DOI - https://doi.org/10.18632/oncotarget.24862

Correspondence to - [email protected]

Abstract

We report a novel mechanism of action of ONC201 as a mitochondria-targeting drug in cancer cells. ONC201 was originally identified as a small molecule that induces transcription of TNF-related apoptosis-inducing ligand (TRAIL) and subsequently kills cancer cells by activating TRAIL death receptors. In this study, we examined ONC201 toxicity on multiple human breast and endometrial cancer cell lines. ONC201 attenuated cell viability in all cancer cell lines tested. Unexpectedly, ONC201 toxicity was not dependent on either TRAIL receptors nor caspases. Time-lapse live cell imaging revealed that ONC201 induces cell membrane ballooning followed by rupture, distinct from the morphology of cells undergoing apoptosis. Further investigation found that ONC201 induces phosphorylation of AMP-dependent kinase and ATP loss. Cytotoxicity and ATP depletion were significantly enhanced in the absence of glucose, suggesting that ONC201 targets mitochondrial respiration. Further analysis indicated that ONC201 indirectly inhibits mitochondrial respiration. Confocal and electron microscopic analysis demonstrated that ONC201 triggers mitochondrial structural damage and functional impairment. Moreover, ONC201 decreased mitochondrial DNA (mtDNA). RNAseq analysis revealed that ONC201 suppresses expression of multiple mtDNA-encoded genes and nuclear-encoded mitochondrial genes involved in oxidative phosphorylation and other mitochondrial functions. Importantly, fumarate hydratase deficient cancer cells and multiple cancer cell lines with reduced amounts of mtDNA were resistant to ONC201. These results indicate that cells not dependent on mitochondrial respiration are ONC201-resistant. Our data demonstrate that ONC201 kills cancer cells by disrupting mitochondrial function and further suggests that cancer cells that are dependent on glycolysis will be resistant to ONC201.

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Press release - https://www.oncotarget.com/index.php?journal=oncotarget&page=news&op=press&item=onc201-kills-breast-cancer-cells-in-vitro-by-targeting-mitochondria

Keywords - ONC201, breast cancer, mitochondria

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Listen to a blog summary of a recent research paper published in Volume 13, entitled, "A novel group of genes that cause endocrine resistance in breast cancer identified by dynamic gene expression analysis."

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Hormones can cause tumor growth in some subtypes of breast cancer. Endocrine therapy, also known as hormone therapy, is a type of cancer treatment that removes or blocks the hormones which fuel breast cancer growth. This treatment is often given as adjuvant therapy after breast cancer surgery to lower the risk of cancer reoccurrence. In some cases, endocrine therapy may be used as a first-line treatment for hormone receptor-positive breast cancers, such as estrogen receptor-positive (ER-positive) breast cancers. However, ER-positive tumors frequently become unresponsive to endocrine therapy, and tumor regrowth can occur after treatment. The underlying causes of endocrine resistance are mostly undetermined.

“Endocrine therapies have been successful at improving cancer outcomes; however, the development of endocrine resistance, or resistance to inhibition of ER actions, remains a roadblock in breast cancer treatment.”

Recently, researchers—from UTHealth Houston, University of Chicago, University of Texas MD Anderson Cancer Center, and the University of Houston—used a new statistical and computational pipeline method of analysis to study the dynamic behavior of gene expression during the development of endocrine resistance in breast cancer. Their trending research paper published in Oncotarget on April 06, 2022, is entitled, “A novel group of genes that cause endocrine resistance in breast cancer identified by dynamic gene expression analysis.”

Full blog - https://www.oncotarget.org/2022/04/14/trending-with-impact-genes-identified-in-endocrine-therapy-resistance/

DOI - https://doi.org/10.18632/oncotarget.28225

Correspondence to - Michihisa Umetani - [email protected], and Vahed Maroufy - [email protected]

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Keywords - breast cancer, triple negative breast cancer, gene expression profiling, endocrine resistance, gene clustering

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Jonathan Kelber and Francesca Sanchez from the Department of Biology, California State University Northridge, Northridge CA, discuss a research paper they co-authored for Oncotarget in 2019, entitled, "Secretomes from metastatic breast cancer cells, enriched for a prognostically unfavorable LCN2 axis, induce anti-inflammatory MSC actions and a tumor-supportive premetastatic lung."

DOI - https://doi.org/10.18632/oncotarget.26903

Correspondence to - [email protected]

Abstract

Cancer metastasis is responsible for the clear majority of cancer-related deaths. Survival and expansion of cancer cells at secondary sites requires that these premetastatic microenvironments be primed by primary tumor cells and their secreted factors. Efforts to date have been limited by immune-deficient in vivo models and/or the need for finely-tuned analysis time points that reduce contributions from early-disseminating cancer cells. In this regard, we developed a tumor cell-free syngeneic breast cancer model for characterizing tumor cell secretome-mediated reprogramming of premetastatic tissues. We demonstrate that secretomes from metastatic breast cancer cells differentially regulate the lung and brain, promoting a tumor-supportive lung microenvironment with both elevated CD73 expression and decreased TNFα expression. Using in vitro models of CD73-positive mesenchymal stem cells (MSCs) and macrophages/monocytes, we tested whether MSCs can mediate anti-inflammatory effects of metastatic breast cancer cells. Notably, conditioned media from metastatic Py230 cells reprogrammed the secretomes of MSCs toward an anti-inflammatory state. Mining transcriptome data from Py8119 and Py230 cells revealed a lipocalin 2 (LCN2) axis that is selectively expressed in the metastatic Py230 cells, predicts poor breast cancer patient survival and is elevated in circulating serum of mice chronically treated with conditioned media from Py230 cells. Taken together, these results establish the utility of an immune-competent tumor cell-free model for characterizing the mechanisms of breast cancer cell priming of the premetastatic niche, demonstrate that MSCs can mediate the anti-inflammatory effects of metastatic breast cancer cells and substantiate LCN2 as a promising therapeutic target for blocking breast cancer progression.

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Press release - https://www.oncotarget.com/index.php?journal=oncotarget&page=news&op=press&item=secretomes-from-metastatic-breast-cancer-cells-enriched-for-a-prognostically-unfavorable-lcn2-axis-induce-anti-inflammatory-msc-actions-and-a-tumor-supportive-premetastatic-lung

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Keywords - premetastatic niche, tumor microenvironment, metastasis, breast cancer secretomes, LCN2

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