Publications by authors named "S Q Qu"

1,919 Publications

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[The relationship between symptom burden and hematologic responses after treatment with interferon/hydroxyurea in patients with polycythemia vera].

Zhonghua Xue Ye Xue Za Zhi 2021 Aug;42(8):635-641

State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China.

To explore the relationship between symptom burden and hematologic responses after treatment with interferon and/or hydroxyurea in patients with polycythemia vera (PV) . Hematologic responses after continuous treatment with interferon and/or hydroxyurea for six months were evaluated in 190 patients with PV using the Myeloproliferative Neoplasm Symptom Assessment Form Total Symptom Score (MPN-10 score) . In all patients, the PV diagnosis was based on the 2016 World Health Organization diagnostic definitions. The study cohort comprised 93 (48.9% ) male and 97 (51.1% ) female patients. The median age at the time of MPN-10 assessment was 60 (32-82) years. The median MPN-10 score of the entire cohort was 9 (range, 0-67) . The median MPN-10 score of patients treated with interferon plus hydroxyurea (=27) was 11 (0-67) , which was significantly higher than those of patients treated with interferon only (=64) (6[0-56], =0.019) or hydroxyurea only (=99) (9[0-64], =0.047) , whereas the median MPN-10 score was not significantly different between those treated with interferon only and hydroxyurea only (=0.421) . The rate of severe symptom burden (i.e., any single symptom burden score ≥ 7 and/or total score ≥ 44) was 28.9% (55/190) in the entire cohort, whereas the rate of severe symptom burden was not significantly different among the interferon only (23.4% ) , hydroxyurea only (29.3% ) , and interferon plus hydroxyurea (40.7% ) groups (>0.05 for all two-group comparisons) . When evaluating MPN-10 score, 37.4% (71/190) of the patients achieved complete hematologic remission (CHR) . Only 28.9% (55/190) patients had adequate disease control, defined as CHR without severe symptom burden. Reasons for inadequate disease control were evaluating blood counts alone, severe symptom burden alone, and evaluating blood counts accompanied with severe symptom burden in 42.1% (80/190) , 8.4% (16/190) , and 20.5% (39/190) of the patients, respectively. Compared to the patients with a platelet count ≤ 400×10(9)/L, those with a platelet count > 400×10(9)/L had a significantly higher rate of severe symptom burden (40.8% [20/49] 24.8% [35/141], =0.044) and a higher median MPN-10 score (14[0-67] 7[0-56], =0.038) . Platelet count > 400×10(9)/L was associated with an increased risk of severe symptom burden (hazard ratio, 2.089; 95% confidence interval, 1.052-4.147, =0.035) . Symptoms related to disease after treatment with interferon and/or hydroxyurea were rather universal in patients with PV. Some patients still experienced severe symptom burden despite achieving CHR. Platelet count > 400×10(9)/L was associated with an increased risk of severe symptom burden in patients with PV treated with interferon and/or hydroxyurea.
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http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2021.08.004DOI Listing
August 2021

Long intergenic non-protein coding RNA 02570 promotes nasopharyngeal carcinoma progression by adsorbing microRNA miR-4649-3p thereby upregulating both sterol regulatory element binding protein 1, and fatty acid synthase.

Bioengineered 2021 Dec;12(1):7119-7130

Department of Otolaryngology & Head and Neck, The People's Hospital of Guangxi Zhuang Autonomous Region, Guangxi Academy of Medical Sciences, Nanning City, P.R. China.

Our previous studies have elucidated a possible connection between long intergenic non-protein coding RNA 2570 (LINC02570) and nasopharyngeal carcinoma (NPC). However, the precise mechanism by which LINC02570 promotes NPC remains unknown. We used quantitative polymerase chain reaction (qPCR) to detect LINC02570 expression in nasopharyngeal cell lines, NPC tissues, and chronic rhinitis tissues. Subcellular LINC02570 localization was confirmed by fluorescence hybridization (FISH). The effects of LINC02570 stable knockdown and overexpression on viabillity, proliferation, migration, and invasion were analyzed using 3-(4,5-Dimethyl-2-Thiazolyl)-2,5-Diphenyl-2-H-Tetrazolium bromide (MTT), a colorimetric focus-formation assay, a wound healing assay, and transwell assays. RNA crosstalk analysis predicted microRNA-4649-3p (miR-4649-3p) binding to LINC02570 or sterol regulatory element binding transcription factor 1 (SREBF1). A dual luciferase reporter assay was used to confirm potential interactions. Sterol regulatory element binding protein 1 (SREBP1) and fatty acid synthase (FASN) expression were detected by western blotting. The results suggest that LINC02570 is upregulated in late clinical stage NPC patients, and promotes NPC progression by adsorbing miR-4649-3p to up-regulate SREBP1 and FASN. This study elucidates a potential chemotherapeutic target involved in lipid metabolism in NPC.
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http://dx.doi.org/10.1080/21655979.2021.1979317DOI Listing
December 2021

Overexpression of miR-132-3p contributes to neuronal protection in in vitro and in vivo models of Alzheimer's disease.

Behav Brain Res 2021 Sep 15:113584. Epub 2021 Sep 15.

Central Laboratory, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, Guangdong, 528300, China; Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address:

One of the neuropathological hallmarks of Alzheimer's disease (AD) is accumulation and deposition of amyloid-beta (Aβ) plaques in the hippocampus. Recently, microRNAs (miRNAs), have been demonstrated to play an essential role in AD. We have previously demonstrated that miR-132-3p exerts neuroprotection via regulating histone deacetylase 3 (HDAC3) in a mouse model of AD. In the present study, we further unveiled neuroprotective roles of miR-132-3p in transgenic amyloid precursor protein/presenilin 1 (APP/PS1) mice compared with those in age-matched wild-type C57BL/6 mice. Lentiviral-mediated inhibition or overexpression of miR-132-3p in the hippocampus of APP/PS1 mice was used to explore the contributions of hippocampal miR-132-3p in spatial memory, amyloid burden, apoptosis, and the number of hippocampal cells in a mouse model of AD. Overexpression of hippocampal miR-132-3p ameliorated spatial memory deficits in the Morris water maze, reduced both Aβ accumulation and apoptosis, and promoted the numbers of hippocampal cells in the brains of APP/PS1 mice. Furthermore, trichostatin A (TSA) promoted the expression of miR-132-3p in Aβ-burdened neurons while increasing the expression levels of synaptic proteins. Taken together, our results suggest that miR-132-3p may represent a promising therapeutic target for the treatment of AD.
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http://dx.doi.org/10.1016/j.bbr.2021.113584DOI Listing
September 2021

Iron deficiency in JAK2 exon12 and JAK2-V617F mutated polycythemia vera.

Blood Cancer J 2021 Sep 17;11(9):154. Epub 2021 Sep 17.

State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.

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http://dx.doi.org/10.1038/s41408-021-00552-xDOI Listing
September 2021

Molecular Subtypes of Primary Small Cell Lung Cancer Tumors and Their Associations with Neuroendocrine and Therapeutic Markers.

J Thorac Oncol 2021 Sep 14. Epub 2021 Sep 14.

Thoracic Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health. Electronic address:

Introduction: A new molecular subtype classification was recently proposed for small cell lung cancer (SCLC). It is necessary to validate it in primary SCLC tumors by immunohistochemical (IHC) staining and define its clinical relevance.

Methods: We used IHC to assess four subtype markers (ASCL1, NEUROD1, POU2F3, and YAP1) in 194 cores from 146 primary SCLC tumors. The profiles of tumor-associated CD3 and CD8 T-cells, MYC paralogs, schlafen-11, and synaptophysin were compared between different subtypes. Validation was performed using publicly available RNA sequencing data of SCLC.

Results: ASCL1, NEUROD1, POU2F3, and YAP1 were the dominant molecular subtypes in 78.2%, 5.6%, 7%, and 2.8% of the tumors, respectively; and 6.3% of the tumors were negative for all four subtype markers. Notably, three cases were uniquely positive for YAP1. Significant intratumoral heterogeneity was observed, with 17.6% and 2.8% of the tumors being positive for two and three subtype markers, respectively. The non-ASCL1/NEUROD1 tumors had more CD8 T-cells and manifested more frequently an 'inflamed' immunophenotype. L-MYC and MYC were more commonly associated with ASCL1/NEUROD1 subtypes and non-ASCL1/NEUROD1 subtypes, respectively. Schlafen-11 expression was absent in 40% of the tumors, especially those negative for the four subtype markers. Synaptophysin was commonly expressed in the ASCL1 and NEUROD1 subtypes and was associated with less tumor-associated CD8 T-cells and a 'desert' immunophenotype.

Conclusions: We validated the new molecular subtype classification in primary SCLC tumors by IHC and identified several intriguing associations between subtypes and therapeutic markers. The new subtype classification may potentially assist treatment decisions in SCLC.
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http://dx.doi.org/10.1016/j.jtho.2021.08.763DOI Listing
September 2021
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