Erratum: Chromosomal, epigenetic and microRNA-mediated inactivation of LRP1B, a modulator of the extracellular environment of thyroid cancer cells

Prazeres, Hugo; Torres, Joana; Rodrigues, Fernando; Pinto, M.; Pastoriza, María; Gomes, Diana; Cameselle-Teijeiro, José; Vidal, Anxo; Martins, Tânia; Sobrinho-Simões, Manuel; Soares, Paula

doi:10.1038/onc.2016.143

Cited by 44 publications

(13 citation statements)

References 53 publications

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“…A study suggested that LRP1B inhibits tumor cell growth by increasing Stat3 phosphorylation and p21 C1P1 levels as well as by inactivating the phosphorylation of SRC [25]. Inactivation of LRP1B contributed to tumorigenesis of lung, gastrointestinal, thyroid oral, urothelial, ovarian, and colon cancer [26], [27], [28], [29], [30]. In our study, LRP1B did not show a strongly decreased expression pattern from normal to CIN cervical tissues (Figure 2).…”

Section: Discussionsupporting

confidence: 38%

Cytological Immunostaining of HMGA2, LRP1B, and TP63 as Potential Biomarkers for Triaging Human Papillomavirus-Positive Women

Jiang

Zhu

He³

et al. 2019

Translational Oncology

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Background: Since human papillomavirus (HPV) DNA testing has been promoted as primary screening strategy, the triage method has also evolved from morphological testing to a molecular biomarker detection to improve screening efficiency. In this study, we investigated the performance of three HPV integration hot-spots, HMGA2, LRP1B, and TP63, as potential triage markers in HPV screening tests. Materials and Methods: This cross-sectional study was conducted from November 2016 to December 2017 in the First Affiliated Hospital of Sun Yat-sen University. Immunocytochemistry was carried out using residual cervical cell samples from 121 HPV-positive cases (23 normal, 24 cervical intraepithelial neoplasia (CIN) 1, and 74 CIN2+). Results: Of the 121 cases, 77 showed completely paired for the three biomarkers. In these 77 cases, receiver operating characteristic (ROC) analysis of HMGA2 showed the best potential for detecting CIN2+ among HPV+ cases (sensitivity 70%; specificity 91.89%; AUC 0.839). TP63 was second most effective biomarker (AUC 0.838; sensitivity 80%; specificity 81.08%). In contrast, LRP1B had the smallest AUC (0.801) among the three biomarkers but had the highest sensitivity (90%) and specificity (56.76%). To test the triage value of combining the three biomarkers, logistic regression was conducted followed by ROC comparison analysis. Promisingly, the combination of the three biomarkers gave the largest AUC of 0.951 with 92.5% sensitivity and 89.1% specificity ( P < .0001 compared to liquid-based cytology test by Z -test). Conclusions: A combination of HMGA2, LRP1B, and TP63 as potential biomarkers may be useful for screening during triage of HPV-positive patients, particularly for detecting CIN2 + .

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Section: Discussionsupporting

confidence: 38%

Cytological Immunostaining of HMGA2, LRP1B, and TP63 as Potential Biomarkers for Triaging Human Papillomavirus-Positive Women

Jiang

Zhu

He³

et al. 2019

Translational Oncology

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“…Integration of HBV to LINE1 results in a chimeric HBV-LINE1 transcript, which functions as a hybrid RNA and promotes liver cancer development through Wnt/β-catenin signaling pathway activation [32]. Moreover, it has been well documented that HPV integrations into tumor suppressors contribute to malignant transformation of host cells [44–48]. Therefore, integration of EBV short sequence into the host genome and the consequent disruption of the important host genes for maintaining the biological hemostasis might represent a novel carcinogenic mechanism of EBV, as similar scenarios for HPV and HBV [32, 44, 49, 50].…”

Section: Discussionmentioning

confidence: 99%

Genomic and transcriptomic landscapes of Epstein-Barr virus in extranodal natural killer T-cell lymphoma

et al. 2018

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Extranodal natural killer T-cell lymphoma (nasal type; NKTCL) is an aggressive malignancy strongly associated with Epstein-Barr virus (EBV) infection. However, the role of EBV in NKTCL development is unclear, largely due to the lack of information about EBV genome and transcriptome in NKTCL. Here, using high-throughput sequencing, we obtained whole genome (n = 27) and transcriptome datasets (n = 18) of EBV derived from NKTCL tumor biopsies. We assembled 27 EBV genomes and detected an average of 1,152 single nucleotide variants and 44.8 indels (<50 bp) of EBV per sample. We also identified frequent focal EBV genome deletions and integrated EBV fragments in the host genome. Moreover, Phylogenetic analysis revealed that NKTCL-derived EBVs are closely clustered; transcriptome analysis revealed less activation of both latent and lytic genes and larger amount of T-cell epitope alterations in NKTCL, as compared with other EBV-associated cancers. Furthermore, we observed transcriptional defects of the BARTs miRNA by deletion, and the disruption of host NHEJ1 by integrated EBV fragment, implying novel pathogenic mechanisms of EBV. Taken together, we reported for the first time global mutational and transcriptional profiles of EBV in NKTCL clinical samples, revealing important somatic events of EBV and providing insights to better understanding of EBV’s contribution in tumorigenesis.

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“…Loss of LRP1B , by somatic mutation or gene deletion, could also be involved in these processes. This gene is one of those most frequently deleted in human tumors [27] and its inactivation provokes changes in the tumor environment, conferring increased growth and invasive capacity on cancer cells [28].…”

Section: Discussionmentioning

confidence: 99%

Unraveling transformation of follicular lymphoma to diffuse large B-cell lymphoma

et al. 2019

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Follicular lymphoma (FL) is an indolent but largely incurable disease. Some patients suffer histological transformation to a more aggressive subtype with poorer prognosis. This study aimed to improve our understanding of the genetics underlying FL histological transformation, and to identify genetic drivers or promoters of the transformation by elucidating the differences between FL samples from patients who did and did not transform. We conducted targeted massive parallel sequencing of 22 pre-transformed FL/transformed diffuse large B-cell lymphoma pairs and 20 diagnostic samples from non-transformed FL patients. Additionally, 22 matched samples from 11 transformed FL patients (pre-transformed FL and diffuse large B-cell lymphoma) and 9 non-transformed FLs were studied for copy number variation using SNP arrays. We identified recurrently mutated genes that were enriched at transformation, most notably LRP1B , GNA13 and POU2AF1 , which have roles in B-cell differentiation, GC architecture and migration. Mutations in POU2AF1 might be associated with lower levels of expression, were more frequent in transformed FLs, and seemed to be specific to transformed- compared with de novo- diffuse large B-cell lymphomas. Pre-transformed FLs carried more mutations per sample and had greater subclonal heterogeneity than non-transformed FLs. Finally, we identified four mutated genes in FL samples that differed between patients who did and did not transform: NOTCH2 , DTX1 , UBE2A and HIST1H1E . The presence of mutations in these genes was associated with shorter time to transformation when mutated in the FL biopsies. This information might be useful for identifying patients at higher risk of transformation.

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Erratum: Chromosomal, epigenetic and microRNA-mediated inactivation of LRP1B, a modulator of the extracellular environment of thyroid cancer cells

Cited by 44 publications

References 53 publications

Cytological Immunostaining of HMGA2, LRP1B, and TP63 as Potential Biomarkers for Triaging Human Papillomavirus-Positive Women

Cytological Immunostaining of HMGA2, LRP1B, and TP63 as Potential Biomarkers for Triaging Human Papillomavirus-Positive Women

Genomic and transcriptomic landscapes of Epstein-Barr virus in extranodal natural killer T-cell lymphoma

Unraveling transformation of follicular lymphoma to diffuse large B-cell lymphoma

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