Prognostic significance of esterase gene expression in multiple myeloma

Abstract Background Esterase enzymes differ in substrate specificity and biological function and may display dysregulated expression in cancer. This study evaluated the biological significance of esterase expression in multiple myeloma (MM). Methods For gene expression profiling and evaluation of genomic variants in the Institute for Molecular Medicine Finland (FIMM) cohort, bone marrow aspirates were obtained from patients with newly diagnosed MM (NDMM) or relapsed/refractory MM (RRMM). CD138+ plasma cells were enriched and used for RNA sequencing and analysis, and to evaluate genomic variation. The Multiple Myeloma Research Foundation (MMRF) Relating Clinical Outcomes in MM to Personal Assessment of Genetic Profile (CoMMpass) dataset was used for validation of the findings from FIMM. Results MM patients (NDMM, n = 56; RRMM, n = 78) provided 171 bone marrow aspirates (NDMM, n = 56; RRMM, n = 115). Specific esterases exhibited relatively high or low expression in MM, and expression of specific esterases (UCHL5, SIAE, ESD, PAFAH1B3, PNPLA4 and PON1) was significantly altered on progression from NDMM to RRMM. High expression of OVCA2, PAFAH1B3, SIAE and USP4, and low expression of PCED1B, were identified as poor prognostic markers (P < 0.05). The MMRF CoMMpass dataset provided validation that higher expression of PAFAH1B3 and SIAE, and lower expression of PCED1B, were associated with poor prognosis. Conclusions Esterase gene expression levels change as patients progress from NDMM to RRMM. High expression of OVCA2, PAFAH1B3, USP4 and SIAE, and low expression of PCED1B, are poor prognostic markers in MM, suggesting a role for these esterases in myeloma biology.

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Clinical Significance of Pim-2 , PD-1 and PD-L1 Expressions in Multiple Myeloma

Blood ◽

10.1182/blood-2018-99-112004 ◽

2018 ◽

Vol 132 (Supplement 1) ◽

pp. 4507-4507

Author(s):

Tingting Zhao ◽

Yu Wu

Keyword(s):

Multiple Myeloma ◽

Bone Marrow ◽

Proportional Hazards ◽

Proportional Hazards Model ◽

Cox Proportional Hazards ◽

Cox Proportional Hazards Model ◽

High Expression ◽

Hazards Model ◽

Early Treatment Response ◽

Low Expression

Abstract Objective The purposes of this study is to investigate the expression of Pim-1 and Pim-2 on macrophages in multiple myeloma (MM) patients; investigate the relationship between co-expression of Pim-1, Pim2 in macrophages and early treatment response and prognosis; investigate the expression of PD-1 and PD-L1 in multiple myeloma; and analyze correlation between the expression of PD-1 and PD-L1 and early treatment response and prognosis, providing preliminary therapeutic evidence for the novel treatment in multiple myeloma. Methods Clinical data and bone marrow biopsy sample of108 patients were selected with newly diagnosed multiple myeloma at West China Hospital of Sichuan University from 2009 to 2014 were collected. Patients that were included were followed up until May 2017. Opal multi-labeling immunohistochemistry of bone marrow was performed, and macrophages were labeled with anti-CD68 antibody in order to detect co-expression of P-im1, P-im2 and macrophages. They were divided into high-expression and low-expression groups according to the degree of their co-expression. Meanwhile detect the expression of PD-1, PD-L1 in MM and they were divided into positive and negative groups. The relationship between the different expression levels of Pim-1 and Pim-2 in macrophages、PD-1、PD-L1 and the early treatment response and prognosis of multiple myeloma were analyzed. The Kaplan-Meier method was used to analyze the influence on disease progression and overall survival in MM patients. The Cox proportional hazards model was used as multivariate analysis used to explore independent risk factors affecting the prognosis of MM patients. Results 1.The median PFS value in high CD68+Pim-1 co-expression group is significantly lower than that of the low expression group(14.0 months vs 24.2 months, Logrank, P=0.0314); the Cox proportional hazards model reveals that the risk of disease progression in high expression of CD68+Pim-1 group is significantly higher than that of the low expression group(risk ratio, 2.22; P=0.04 )Patients with high CD68+Pim-1 expression showed the median survival time is significantly lower than that of the low infiltration group (12.7months vs 37.9months, Logrank, P=0.005); the Cox proportional hazards model reveals that the risk of disease progression in high expression of CD68+Pim-1 group is significantly higher than that of the lower expression group(risk ratio, 4.21; P=0.001 )As for the bone marrow high CD68+Pim-1 expression group ,the median survival time is significantly lower than that of the low infiltration group (18.3 months vs 49.5months, Logrank, P=0.0044); the Cox proportional hazards model reveals that the mortality riskin high expression of CD68+Pim-1 group is significantly higher than that of the lower expression group(risk ratio, 3.64; P=0.01 ).Patients with PD-1 low expression group in bone marrow showed greater response (Complete response/Partial response), while the PD-1 high expression group showed lower response (P=0.013). Conclusion The expression extent of Pim-1 and pim-2 with macrophages in bone marrow are associated with clinical prognosis. The expression extent of pim-2 in MM tumor-associated macrophages display a strong negative correlation to PFS values and the overall survival. The expression extent of pim-1 in MM tumor-associated macrophages display a strong negative correlation to overall survival. Pim-1 and pim-2 are prognostic factors of multiple myeloma. There is a strong negative correlation between expression of PD-1 of bone marrow and the early treatment response. Since the expression degree of PD-1 showed different prognosis in solid tumors and hematological cancer. The evaluation requires combined with other biological indicators Disclosures No relevant conflicts of interest to declare.

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Expression of Coiled-Coil Domain Containing Family mRNA and prognostic value in hepatocellular carcinoma

10.21203/rs.3.rs-153938/v1 ◽

2021 ◽

Author(s):

Sina Zhang ◽

Chen Jin ◽

Yan Yang ◽

Haoqi Li ◽

Jun Ma ◽

...

Keyword(s):

Prognostic Value ◽

Prognostic Markers ◽

Malignant Tumors ◽

Prognostic Significance ◽

Family Members ◽

High Expression ◽

Rank Test ◽

High Expression Group ◽

The Relationship ◽

Low Expression

Abstract Background: The CCDC family plays a significant role in the development and progression of malignant tumors. However, the relationship between CCDC family members and HCC progression is incompletely known. This study used bioinformatics analysis to investigate the expression as well as clinical prognostic value of CCDC family members in HCC and to predict the role of CCDCs family in the development and progression of HCC. Methods: This study utilized the data from two platforms databases to explore the diagnostic value and prognostic significance of CCDC family members by Cox proportional hazards regression analysis, Kaplan-Meier curve and log-rank test, ROC and nomogram diagnostic and prognostic analysis methods. GSEA and tumor microenvironment analysis were employed to investigate the underlying mechanisms and cell-cell interactions of CCDCs family in the development and progression of HCC. The relationship between mutational signatures and CCDCs family were evaluated in HCC patients with somatic mutation. Results: Five CCDC family members (CCDC34, CCDC137, CCDC77, CCDC93 and CCDC21) mRNA expression showed significantly higher in HCC tissues than in normal tissues and high expression levels of these genes predicted poor prognosis in HCC patients. The combined effect analysis of five CCDCs family prognostic markers suggests that the prognosis difference for CCDC family members combination was more significant than that for any individual CCDC family genes. We then developed a risk score model that could predict the prognosis of HCC, and nomogram gene expression was visualized with the probability of predicting the prognosis of HCC by clinical factors. GSEA revealed that, while five CCDCs family combined high expression was associated with increased cell cycle progression and low expression was associated with complement activation pathway. Mutation analysis showed that the combined high expression group had a higher TP53 mutation rate than the combined low expression group, and the high expression group showed higher TMB, which was associated with a better prognosis than high TMB. Conclusions: Our data suggest that the expression of CCDC34, CCDC137, CCDC77, CCDC93 and CCDC21 may be potential prognostic markers in HCC and in combination have a strong interaction and better predictive value for HCC prognosis.

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Abstract 190: Prognostic significance of esterase gene expression in multiple myeloma

10.1158/1538-7445.am2020-190 ◽

2020 ◽

Author(s):

Romika Kumari ◽

M. Mamun Majumder ◽

Juha Lievonen ◽

Raija Silvennoinen ◽

Pekka Anttila ◽

...

Keyword(s):

Gene Expression ◽

Multiple Myeloma ◽

Prognostic Significance ◽

Esterase Gene

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Prognostic significance of magnetic resonance imaging of bone marrow in previously untreated patients with multiple myeloma

Annals of Oncology ◽

10.1093/annonc/mdi362 ◽

2005 ◽

Vol 16 (11) ◽

pp. 1824-1828 ◽

Cited By ~ 76

Author(s):

L.A. Moulopoulos ◽

D. Gika ◽

A. Anagnostopoulos ◽

K. Delasalle ◽

D. Weber ◽

...

Keyword(s):

Magnetic Resonance Imaging ◽

Multiple Myeloma ◽

Bone Marrow ◽

Magnetic Resonance ◽

Prognostic Significance ◽

Resonance Imaging

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Integrating Genetic and Transcriptomic Data to Reveal Pathogenesis and Prognostic Markers of Pancreatic Adenocarcinoma

Frontiers in Genetics ◽

10.3389/fgene.2021.747270 ◽

2021 ◽

Vol 12 ◽

Author(s):

Kaisong Bai ◽

Tong Zhao ◽

Yilong Li ◽

Xinjian Li ◽

Zhantian Zhang ◽

...

Keyword(s):

Gene Expression ◽

Pancreatic Adenocarcinoma ◽

Somatic Mutation ◽

Somatic Mutations ◽

Prognostic Markers ◽

Expression Profiles ◽

Gene Expression Profiles ◽

Genomic Variation ◽

The Cancer Genome Atlas ◽

Driver Genes

Pancreatic adenocarcinoma (PAAD) is one of the deadliest malignancies and mortality for PAAD have remained increasing under the conditions of substantial improvements in mortality for other major cancers. Although multiple of studies exists on PAAD, few studies have dissected the oncogenic mechanisms of PAAD based on genomic variation. In this study, we integrated somatic mutation data and gene expression profiles obtained by high-throughput sequencing to characterize the pathogenesis of PAAD. The mutation profile containing 182 samples with 25,470 somatic mutations was obtained from The Cancer Genome Atlas (TCGA). The mutation landscape was generated and somatic mutations in PAAD were found to have preference for mutation location. The combination of mutation matrix and gene expression profiles identified 31 driver genes that were closely associated with tumor cell invasion and apoptosis. Co-expression networks were constructed based on 461 genes significantly associated with driver genes and the hub gene FAM133A in the network was identified to be associated with tumor metastasis. Further, the cascade relationship of somatic mutation-Long non-coding RNA (lncRNA)-microRNA (miRNA) was constructed to reveal a new mechanism for the involvement of mutations in post-transcriptional regulation. We have also identified prognostic markers that are significantly associated with overall survival (OS) of PAAD patients and constructed a risk score model to identify patients’ survival risk. In summary, our study revealed the pathogenic mechanisms and prognostic markers of PAAD providing theoretical support for the development of precision medicine.

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Multiple Myeloma Cells Alter Adipogenesis, Increase Senescence-Related and Inflammatory Gene Transcript Expression, and Alter Metabolism in Preadipocytes

Frontiers in Oncology ◽

10.3389/fonc.2020.584683 ◽

2021 ◽

Vol 10 ◽

Author(s):

Heather Fairfield ◽

Samantha Costa ◽

Carolyne Falank ◽

Mariah Farrell ◽

Connor S. Murphy ◽

...

Keyword(s):

Gene Expression ◽

Multiple Myeloma ◽

Bone Marrow ◽

Lipid Accumulation ◽

Expression Profiles ◽

Adipogenic Differentiation ◽

Gene Expression Profiles ◽

Mouse Bone Marrow ◽

Gene Transcript ◽

Bone Marrow Mscs

Within the bone marrow microenvironment, mesenchymal stromal cells (MSCs) are an essential precursor to bone marrow adipocytes and osteoblasts. The balance between this progenitor pool and mature cells (adipocytes and osteoblasts) is often skewed by disease and aging. In multiple myeloma (MM), a cancer of the plasma cell that predominantly grows within the bone marrow, as well as other cancers, MSCs, preadipocytes, and adipocytes have been shown to directly support tumor cell survival and proliferation. Increasing evidence supports the idea that MM-associated MSCs are distinct from healthy MSCs, and their gene expression profiles may be predictive of myeloma patient outcomes. Here we directly investigate how MM cells affect the differentiation capacity and gene expression profiles of preadipocytes and bone marrow MSCs. Our studies reveal that MM.1S cells cause a marked decrease in lipid accumulation in differentiating 3T3-L1 cells. Also, MM.1S cells or MM.1S-conditioned media altered gene expression profiles of both 3T3-L1 and mouse bone marrow MSCs. 3T3-L1 cells exposed to MM.1S cells before adipogenic differentiation displayed gene expression changes leading to significantly altered pathways involved in steroid biosynthesis, the cell cycle, and metabolism (oxidative phosphorylation and glycolysis) after adipogenesis. MM.1S cells induced a marked increase in 3T3-L1 expression of MM-supportive genes including Il-6 and Cxcl12 (SDF1), which was confirmed in mouse MSCs by qRT-PCR, suggesting a forward-feedback mechanism. In vitro experiments revealed that indirect MM exposure prior to differentiation drives a senescent-like phenotype in differentiating MSCs, and this trend was confirmed in MM-associated MSCs compared to MSCs from normal donors. In direct co-culture, human mesenchymal stem cells (hMSCs) exposed to MM.1S, RPMI-8226, and OPM-2 prior to and during differentiation, exhibited different levels of lipid accumulation as well as secreted cytokines. Combined, our results suggest that MM cells can inhibit adipogenic differentiation while stimulating expression of the senescence associated secretory phenotype (SASP) and other pro-myeloma molecules. This study provides insight into a novel way in which MM cells manipulate their microenvironment by altering the expression of supportive cytokines and skewing the cellular diversity of the marrow.

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VEGF Specific siRNAs Act Synergistically with Bortezomib and Steroids in Inhibiting VEGF Gene Expression, Proliferation and Induction of Apoptosis in Multiple Myeloma Cells.

Blood ◽

10.1182/blood.v104.11.5266.5266 ◽

2004 ◽

Vol 104 (11) ◽

pp. 5266-5266

Author(s):

Michael Koldehoff ◽

Nina K. Steckel ◽

Rudolf Trenschel ◽

Dietrich W. Beelen ◽

Ahmet H. Elmaagacli

Keyword(s):

Gene Expression ◽

Multiple Myeloma ◽

Bone Marrow ◽

Gene Silencing ◽

Antitumor Agents ◽

Synergistic Effects ◽

Transcriptional Gene Silencing ◽

Vegf Gene ◽

Post Transcriptional Gene Silencing ◽

Induction Of Apoptosis

Abstract Multiple myeloma (MM) is a clonal B-cell malignancy characterized by the accumulation of malignant plasma cells within the bone marrow (BM). Vascular endothelial growth factor (VEGF), a glycoprotein produced by normal and neoplastic cells is an important regulator of physiological and pathological angiogenesis. MM cells secrete VEGF, which promotes production of cytokines in bone marrow stromal cells, as well as migration and proliferation of the tumor cells. Inhibition of VEGF activity or disabling the function of its receptors has been shown to inhibit both tumor growth and spread of metastases in a variety of animal tumor models. RNA interference (RNAi) is rapidly being established as a post-transcriptional gene silencing method and holds promise to specifically inhibit gene expression in mammals. Another novel class of antitumor agents is based on the inhibition of the ubiquitin-proteosomal system which represents the major nonlysosomal pathway through which intracellular proteins are degraded in eukaryotic cells. Bortezomib, a reversible proteosome inhibitor, shows remarkable anticancer activity in various malignant cell types, including MM cells that are resistant to conventional therapies. We studied the effect of transfection with small interfering RNA (siRNA) targeting VEGF in MM cells in terms of proliferation, induction of apoptosis, and cell differentiation. Further, we evaluated if the effects of post-transcriptional gene silencing by VEGF specific siRNA can be augmented by bortezomib and/or steroids in the cell line OPM-2. A mean reduction of VEGF gene expression to 38% as determined by real-time PCR was observed with 0.8 ug VEGF siRNA in OPM-2 cells compared to controls (controls were set up to 100%). Simultaneous administration of bortezomib and siRNA was able to reduce VEGF gene expression down to 23% compared to VEGF siRNA alone demonstrating a synergistic effect of combined bortezomib and siRNA treatment. We found a 2.5-fold increase in induced apoptosis in OPM-2 cells subsequent to VEGF siRNA administration but we saw no additional stimulation of apoptosis after combination of VEGF siRNA with bortezomib and/or steroids. Proliferation in OPM-2 cells was strongly inhibited (about 91%) following combination treatment as opposed to only 62% after administration of VEGF siRNA alone. The transfection of VEGF siRNA in OPM-2 cells had no influence on the expression levels of differentiation markers such as CD38, CD138, CD19, CD34, CD45, and CD7AAD. Our findings suggest that synergistic effects of VEGF siRNA with bortezomib and dexamethason may offer new therapeutic options in the treatment of MM.

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Novel Murine Model To Study Modulation of Genes and Molecular Pathways Induced Following In Vivo Interaction between Multiple Myeloma Cells and Human BM Milieu.

Blood ◽

10.1182/blood.v108.11.3409.3409 ◽

2006 ◽

Vol 108 (11) ◽

pp. 3409-3409

Author(s):

Paola Neri ◽

Pierfrancesco Tassone ◽

Masood Shammas ◽

Mariateresa Fulciniti ◽

Yu-Tzu Tai ◽

...

Keyword(s):

Gene Expression ◽

Multiple Myeloma ◽

Bone Marrow ◽

Cell Growth ◽

Gene Expression Profile ◽

Expression Profile ◽

Murine Model ◽

Cell Signalling

Abstract Interaction between multiple myeloma (MM) cells and the bone marrow (BM) microenvironment plays a critical role in promoting MM cell growth, survival, migration and development of drug resistance. This interaction within the bone marrow milieu is unique and its understanding is important in evaluating effects of novel agents in vitro and in vivo. We here describe a novel murine model that allows us to study the expression changes in vivo in MM cells within the human BM milieu. In this model, the green fluorescent protein (INA-6 GFP+) transduced IL-6-dependent human MM cell line, INA-6, was injected in human bone chip implanted into SCID mice. At different time points the bone chip was retrieved, cells flushed out and GFP+ MM cells were purified by CD138 MACS microbeads. Similar isolation process was used on INA-6 GFP+ cells cultured in vitro and used as control. Total RNA was isolated from these cells and gene expression profile analyzed using the HG-U133 array chip (Affymetrix) and DChip analyzer program. We have identified significant changes in expression of several genes following in vivo interaction between INA-6 and the BM microenvironment. Specifically, we observed up-regulation of genes associated with cytokines (IL-4, IL-8, IGFB 2–5) and chemokines (CCL2, 5, 6, 18, 24, CCR1, 2, 4), implicated in cell-cell signalling. Moreover genes implicated in DNA transcription (V-Fos, V-Jun, V-kit), adhesion (Integrin alpha 2b, 7, cadherin 1 and 11) and cell growth (CDC14, Cyclin G2, ADRA1A) were also up-regulated and genes involved in apoptosis and cell death (p-57, BCL2, TNF1a) were down-regulated. Using the Ingenuity Pathway Analysis the most relevant pathways modulated by the in vivo interaction between MM cells and BMSCs were IL-6, IGF1, TGF-beta and ERK/MAPK-mediated pathways as well as cell-cycle regulation and chemokine signalling. These results are consistent with previously observed in vitro cell signalling studies. Taken together these results highlight the ability of BM microenvironment to modulate the gene expression profile of the MM cells and our ability to in vivo monitor the changes. This model thus provides us with an ability to study in vivo effects of novel agents on expression profile of MM cells in BM milieu, to pre-clinically characterize their activity.

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Metaphase Cytogenetics Adds to Gene Expression Profiling in the Identification of High Risk Multiple Myeloma.

Blood ◽

10.1182/blood.v108.11.114.114 ◽

2006 ◽

Vol 108 (11) ◽

pp. 114-114

Author(s):

Guido Tricot ◽

Fenghuang Zhan ◽

Bart Barlogie ◽

Yongsheng Huang ◽

Jeffrey Sawyer ◽

...

Keyword(s):

Gene Expression ◽

Multiple Myeloma ◽

Gene Expression Profiling ◽

Expression Profiling ◽

Prognostic Significance ◽

Staging System ◽

Treatment Modalities ◽

Prognostic Impact ◽

Newly Diagnosed ◽

Prognostic Information

Abstract The International Staging System (ISS), based on B2-microglobulin and albumin levels at the time of diagnosis, has now generally been adopted as a new prognostic classification system for multiple myeloma (MM). While readily and widely applicable, ISS does not account for genetic disease features, such as metaphase (CA) and interphase fluorescence in situ hybridization (FISH) cytogenetic abnormalities, which when examined in the context of standard prognostic variables, confer higher hazards of relapse and disease-related death. Recently, gene expression profiling (GEP) uncovered the major prognostic significance for outcome of high expression of CKS1B, a gene mapping to an amplicon at chromosome 1q21. We have performed a comprehensive study of CA, FISH, GEP and ISS staging in 351 newly diagnosed MM patients, treated uniformly on Total Therapy 2. We have analyzed outcome based on a combination of high CKS1B by GEP and CA. GEP-based t(11;14) was prognostically favorable, irrespective of expression of CKS1B and, therefore, was removed from the group of patients with high CKS1B expression. After this adjustment, with the combination of both CA and high CKS1B (approximately 10% of all patients) conferred a very poor outcome with only 24% and 40% of such patients being event-free and/surviving at 3 years, compared with 72% and 84% for the others (p values : <.0001). Such patients fared poorly, irrespective of their ISS stage. Similar prognostic information could be gained by combining CA with FISH-defined amplification of 1q21 and t(11;14). Because of their major prognostic impact, all newly diagnosed patients should be tested for these genetic markers. Novel treatment modalities are justified in the small subgroup of such poor prognosis patients, since they derive only a minor benefit from advances in MM therapy. CKS1B Q4 + CA (with no CCND1) vs. Others CKS1B Q4 + CA (with no CCND1) vs. Others

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Clonotypic Bone Marrow-Derived Endothelial Progenitor Cells in Multiple Myeloma.

Blood ◽

10.1182/blood.v108.11.3497.3497 ◽

2006 ◽

Vol 108 (11) ◽

pp. 3497-3497

Author(s):

Marc J. Braunstein ◽

Daniel R. Carrasco ◽

David Kahn ◽

Kumar Sukhdeo ◽

Alexei Protopopov ◽

...

Keyword(s):

Gene Expression ◽

Multiple Myeloma ◽

Bone Marrow ◽

High Resolution ◽

Gene Expression Profiling ◽

Progenitor Cells ◽

Tumor Cells ◽

Endothelial Progenitor Cells ◽

Expression Profiling ◽

Gains And Losses

Abstract In multiple myeloma (MM), bone marrow-derived endothelial progenitor cells (EPCs) contribute to tumor neoangiogenesis and their levels covary with tumor mass and prognosis. Recent X-chromosome inactivation studies in female patients showed that, similar to tumor cells, EPCs are clonally restricted in MM. Genomic profiling of MM using high-resolution array comparative genomic hybridization (aCGH) has been previously utilized to mine the genome and find clinical correlates in MM patients. In this study, clonotypic aspects of bone marrow-derived EPCs and MM cells were investigated using aCGH and expression profiling analysis. Confluent EPCs were outgrown from bone marrow aspirates by adherence to laminin. EPCs were >98% vWF/CD133/KDR+ and <1% CD38+. The laminin-nonadherent bone marrow fraction enriched for tumor cells was >50% CD38+. For aCGH and for gene expression profiling, genomic DNA and total RNA from EPCs and MM cells were hybridized to human oligonucleotide arrays (Agilent Technologies) and human cDNA microarrays (Affymetrix), respectively. High resolution aCGH with segmentation analysis showed that EPCs and MM cells in one of ten cases share identical patterns of chromosomal gains and losses, while another 5 cases shared multiple focal copy number alterations (CNAs) including gains and losses. The genomes of EPCs and MM cells additionally displayed exclusive CNAs, but these were far fewer in EPCs than in MM cells. In 3 patients, EPCs harbored a common 0.6Mb deletion at 1q21 not shared by MM cells. Pertinent genes in this region that could affect proliferation and tumor suppression include N2N, NBPF10, and TXNIP. Validation studies of aCGH findings by other methods are ongoing. Gene expression profiling showed decreased expression of 1q21 region genes (e.g., calgranulin C and lamin A/C). A genome-wide comparison of patients’ MM cells and EPCs, which is focused on their shared genetic characteristics, will be presented.

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