A panel of glycoproteins as candidate biomarkers for early diagnosis and treatment evaluation of B-cell acute lymphoblastic leukemia

Cavalcante, Márcio de Souza; Romero, José Camilo Torres; Lobo, Marina Duarte Pinto; Moreno, Frederico Bruno Mendes Batista; Bezerra, Leonardo Primo; Lima, Diego Silva; Matos, Jesamar C.; Moreira, Renato de Azevedo; Monteiro-Moreira, Ana Cristina de Oliveira

doi:10.1186/s40364-016-0055-6

Cited by 44 publications

(42 citation statements)

References 53 publications

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“…4 ). For example, a set of three complement related genes—complement C3, α-2 macroglobulin and the complement lysis inhibitor SP-40/clusterin (CLU)—that have been implicated in various cancers including gliomas ( Reis et al, 2018 ; Saratsis et al, 2014 ; Shinoura et al, 1994 ; Suman et al, 2016 ) were present in this group, and interestingly, these three proteins have been recently shown to form a network of related biomarkers in B-ALL ( Cavalcante et al, 2016 ). One tumor contained a cluster of highly mutated genes ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Detection and benchmarking of somatic mutations in cancer genomes using RNA-seq data

Coudray

Battenhouse

Bücher

et al. 2018

PeerJ

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To detect functional somatic mutations in tumor samples, whole-exome sequencing (WES) is often used for its reliability and relative low cost. RNA-seq, while generally used to measure gene expression, can potentially also be used for identification of somatic mutations. However there has been little systematic evaluation of the utility of RNA-seq for identifying somatic mutations. Here, we develop and evaluate a pipeline for processing RNA-seq data from glioblastoma multiforme (GBM) tumors in order to identify somatic mutations. The pipeline entails the use of the STAR aligner 2-pass procedure jointly with MuTect2 from genome analysis toolkit (GATK) to detect somatic variants. Variants identified from RNA-seq data were evaluated by comparison against the COSMIC and dbSNP databases, and also compared to somatic variants identified by exome sequencing. We also estimated the putative functional impact of coding variants in the most frequently mutated genes in GBM. Interestingly, variants identified by RNA-seq alone showed better representation of GBM-related mutations cataloged by COSMIC. RNA-seq-only data substantially outperformed the ability of WES to reveal potentially new somatic mutations in known GBM-related pathways, and allowed us to build a high-quality set of somatic mutations common to exome and RNA-seq calls. Using RNA-seq data in parallel with WES data to detect somatic mutations in cancer genomes can thus broaden the scope of discoveries and lend additional support to somatic variants identified by exome sequencing alone.

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Section: Resultsmentioning

confidence: 99%

Detection and benchmarking of somatic mutations in cancer genomes using RNA-seq data

Coudray

Battenhouse

Bücher

et al. 2018

PeerJ

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“…Glycoproteins play key roles in inflammatory and pathological processes [5][6][7][8][9]. Thus, it is not surprising that investigation of the clinical utility of assays that measure inflammatory glycoproteins has received much attention [10][11][12][13]. Besides the clinical information that can be gleaned by quantifying circulating levels of glycoproteins, it is now clear that measurements based on the glycan structures of circulating proteins represent another avenue for improving diagnosis, prognosis and risk prediction of common inflammatory disorders [4,7,[13][14][15][16][17][18][19].…”

Section: Introductionmentioning

confidence: 99%

Inflammatory glycoproteins in cardiometabolic disorders, autoimmune diseases and cancer

Connelly

Gruppen

Otvos

et al. 2016

Clinica Chimica Acta

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The physiological function initially attributed to the oligosaccharide moieties or glycans on inflammatory glycoproteins was to improve protein stability. However, it is now clear that glycans play a prominent role in glycoprotein structure and function and in some cases contribute to disease states. In fact, glycan processing contributes to pathogenicity not only in autoimmune disorders but also in atherosclerotic cardiovascular disease, diabetes and malignancy. While most clinical laboratory tests measure circulating levels of inflammatory proteins, newly developed diagnostic and prognostic tests are harvesting the information that can be gleaned by measuring the amount or structure of the attached glycans, which may be unique to individuals as well as various diseases. As such, these newer glycan-based tests may provide future means for more personalized approaches to patient stratification and improved patient care. Here we will discuss recent progress in high-throughput laboratory methods for glycomics (i.e. the study of glycan structures) and glycoprotein quantification by methods such as mass spectrometry and nuclear magnetic resonance spectroscopy. We will also review the clinical utility of glycoprotein and glycan measurements in the prediction of common low-grade inflammatory disorders including cardiovascular disease, diabetes and cancer, as well as for monitoring autoimmune disease activity.

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“…In MM, RECQ1 was found to be significantly overexpressed and associated with poor prognosis in patients. Moreover, this RECQ1 overexpression protected the MM cells from cytotoxicity mediated by the standard of care agents melphalan and bortezomib [ 73 , 74 ].…”

Section: Deregulation Of the Cell Cycle In Multiple Myelomamentioning

confidence: 99%

The therapeutic potential of cell cycle targeting in multiple myeloma

Maes

Veirman

et al. 2017

Oncotarget

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Proper cell cycle progression through the interphase and mitosis is regulated by coordinated activation of important cell cycle proteins (including cyclin-dependent kinases and mitotic kinases) and several checkpoint pathways. Aberrant activity of these cell cycle proteins and checkpoint pathways results in deregulation of cell cycle progression, which is one of the key hallmarks of cancer. Consequently, intensive research on targeting these cell cycle regulatory proteins identified several candidate small molecule inhibitors that are able to induce cell cycle arrest and even apoptosis in cancer cells. Importantly, several of these cell cycle regulatory proteins have also been proposed as therapeutic targets in the plasma cell malignancy multiple myeloma (MM). Despite the enormous progress in the treatment of MM the past 5 years, MM still remains most often incurable due to the development of drug resistance. Deregulated expression of the cyclins D is observed in virtually all myeloma patients, emphasizing the potential therapeutic interest of cyclin-dependent kinase inhibitors in MM. Furthermore, other targets have also been identified in MM, such as microtubules, kinesin motor proteins, aurora kinases, polo-like kinases and the anaphase promoting complex/cyclosome. This review will provide an overview of the cell cycle proteins and checkpoint pathways deregulated in MM and discuss the therapeutic potential of targeting proteins or protein complexes involved in cell cycle control in MM.

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A panel of glycoproteins as candidate biomarkers for early diagnosis and treatment evaluation of B-cell acute lymphoblastic leukemia

Cited by 44 publications

References 53 publications

Detection and benchmarking of somatic mutations in cancer genomes using RNA-seq data

Detection and benchmarking of somatic mutations in cancer genomes using RNA-seq data

Inflammatory glycoproteins in cardiometabolic disorders, autoimmune diseases and cancer

The therapeutic potential of cell cycle targeting in multiple myeloma

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