Preliminary study of in vivo autofluorescence of nasopharyngeal carcinoma and normal tissue

Autofluorescence spectral signals were measured in vivo from 85 nasopharyngeal carcinoma lesions and 131 normal tissue sites of 59 subjects during routine nasal endoscopy. Diagnostic algorithms based on principal component analysis and the ratio of the spectral signals between multiple-wavelength bands were developed for classifying the autofluorescence spectra. Performances of the algorithms were evaluated using the cross-validation method. The principal component analysis based algorithms using information from the entire fluorescence spectrum can differentiate nasopharyngeal carcinoma lesions from normal tissue with 95% sensitivity and 93% specificity. With 94% sensitivity, the specificities of multiple-wavelength ratio algorithms are about 83%. The results demonstrate that light-induced autofluorescence endoscopy with principal component analysis algorithms can provide accurate diagnostic information for the detection of nasopharyngeal carcinoma in vivo and may be potentially used in clinical practice combined with the routine white-light endoscopy procedure.

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Faculty Opinions recommendation of T cells expressing a LMP1-specific chimeric antigen receptor mediate antitumor effects against LMP1-positive nasopharyngeal carcinoma cells in vitro and in vivo.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.726300140.793517243 ◽

2016 ◽

Author(s):

Bruce Brockstein

Keyword(s):

T Cells ◽

Nasopharyngeal Carcinoma ◽

Chimeric Antigen Receptor ◽

Antigen Receptor ◽

Carcinoma Cells ◽

Antitumor Effects

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In vivo Monitoring of Oxygen Levels in Human Brain Tumor Between Fractionated Radiotherapy Using Oxygen-enhanced MR Imaging

Current Medical Imaging Formerly Current Medical Imaging Reviews ◽

10.2174/1573405614666180925144814 ◽

2020 ◽

Vol 16 (4) ◽

pp. 427-432

Author(s):

Junchao Qian ◽

Xiang Yu ◽

Bingbing Li ◽

Zhenle Fei ◽

Xiang Huang ◽

...

Keyword(s):

Mr Imaging ◽

Tumor Cells ◽

Normal Tissue ◽

Oxygen Level ◽

Tissue Oxygen ◽

Human Brain Tumor ◽

Fractionated Radiotherapy ◽

Oxygen Levels ◽

Oxygen Breathing

Background:: It was known that the response of tumor cells to radiation is closely related to tissue oxygen level and fractionated radiotherapy allows reoxygenation of hypoxic tumor cells. Non-invasive mapping of tissue oxygen level may hold great importance in clinic. Objective: The aim of this study is to evaluate the role of oxygen-enhanced MR imaging in the detection of tissue oxygen levels between fractionated radiotherapy. Methods: A cohort of 10 patients with brain metastasis was recruited. Quantitative oxygen enhanced MR imaging was performed prior to, 30 minutes and 22 hours after first fractionated radiotherapy. Results: The ΔR1 (the difference of longitudinal relaxivity between 100% oxygen breathing and air breathing) increased in the ipsilateral tumor site and normal tissue by 242% and 152%, respectively, 30 minutes after first fractionated radiation compared to pre-radiation levels. Significant recovery of ΔR1 in the contralateral normal tissue (p < 0.05) was observed 22 hours compared to 30 minutes after radiation levels. Conclusion: R1-based oxygen-enhanced MR imaging may provide a sensitive endogenous marker for oxygen changes in the brain tissue between fractionated radiotherapy.

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HDAC4 promotes nasopharyngeal carcinoma progression and serves as a therapeutic target

Cell Death and Disease ◽

10.1038/s41419-021-03417-0 ◽

2021 ◽

Vol 12 (2) ◽

Author(s):

Chun Cheng ◽

Jun Yang ◽

Si-Wei Li ◽

Guofu Huang ◽

Chenxi Li ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Tumor Growth ◽

Therapeutic Target ◽

Histone Deacetylases ◽

Migration And Invasion ◽

Poor Overall Survival ◽

Mesenchymal Transition ◽

E Cadherin

AbstractHistone deacetylases (HDACs) are involved in tumor progression, and some have been successfully targeted for cancer therapy. The expression of histone deacetylase 4 (HDAC4), a class IIa HDAC, was upregulated in our previous microarray screen. However, the role of HDAC4 dysregulation and mechanisms underlying tumor growth and metastasis in nasopharyngeal carcinoma (NPC) remain elusive. Here, we first confirmed that the HDAC4 levels in primary and metastatic NPC tissues were significantly increased compared with those in normal nasopharyngeal epithelial tissues and found that high HDAC4 expression predicted a poor overall survival (OS) and progression-free survival (PFS). Functionally, HDAC4 accelerated cell cycle G1/S transition and induced the epithelial-to-mesenchymal transition to promote NPC cell proliferation, migration, and invasion in vitro, as well as tumor growth and lung metastasis in vivo. Intriguingly, knockdown of N-CoR abolished the effects of HDAC4 on the invasion and migration abilities of NPC cells. Mechanistically, HDAC3/4 binds to the E-cadherin promoter to repress E-cadherin transcription. We also showed that the HDAC4 inhibitor tasquinimod suppresses tumor growth in NPC. Thus, HDAC4 may be a potential diagnostic marker and therapeutic target in patients with NPC.

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Partial Decellularization for Segmental Tracheal Scaffold Tissue Engineering: A Preliminary Study in Rabbits

Biomolecules ◽

10.3390/biom11060866 ◽

2021 ◽

Vol 11 (6) ◽

pp. 866

Author(s):

Luong Huu Dang ◽

Yuan Tseng ◽

How Tseng ◽

Shih-Han Hung

Keyword(s):

Mechanical Stability ◽

Vital Staining ◽

Potential Method ◽

Term Survival ◽

Long Term Survival ◽

Cartilage Cells ◽

Preliminary Study ◽

Epithelial Layers

In this study, we developed a new procedure for the rapid partial decellularization of the harvested trachea. Partial decellularization was performed using a combination of detergent and sonication to completely remove the epithelial layers outside of the cartilage ring. The post-decellularized tracheal segments were assessed with vital staining, which showed that the core cartilage cells remarkably remained intact while the cells outside of the cartilage were no longer viable. The ability of the decellularized tracheal segments to evade immune rejection was evaluated through heterotopic implantation of the segments into the chest muscle of rabbits without any immunosuppressive therapy, which demonstrated no evidence of severe rejection or tissue necrosis under H&E staining, as well as the mechanical stability under stress-pressure testing. Finally, orthotopic transplantation of partially decellularized trachea with no immunosuppression treatment resulted in 2 months of survival in two rabbits and one long-term survival (2 years) in one rabbit. Through evaluations of posttransplantation histology and endoscopy, we confirmed that our partial decellularization method could be a potential method of producing low-immunogenic cartilage scaffolds with viable, functional core cartilage cells that can achieve long-term survival after in vivo transplantation.

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Cancer-associated fibroblasts promote the survival of irradiated nasopharyngeal carcinoma cells via the NF-κB pathway

Journal of Experimental & Clinical Cancer Research ◽

10.1186/s13046-021-01878-x ◽

2021 ◽

Vol 40 (1) ◽

Cited By ~ 1

Author(s):

Weiqiang Huang ◽

Longshan Zhang ◽

Mi Yang ◽

Xixi Wu ◽

Xiaoqing Wang ◽

...

Keyword(s):

Dna Damage ◽

Nasopharyngeal Carcinoma ◽

Enrichment Analysis ◽

Underlying Mechanism ◽

Gene Set Enrichment Analysis ◽

Cancer Associated Fibroblasts ◽

Western Blot Assay ◽

Damage Level ◽

Radiation Resistant

Abstract Background Irradiation has emerged as a valid tool for nasopharyngeal carcinoma (NPC) in situ treatment; however, NPC derived from tissues treated with irradiation is a main cause cancer-related death. The purpose of this study is to uncover the underlying mechanism regarding tumor growth after irradiation and provided potential therapeutic strategy. Methods Fibroblasts were extracted from fresh NPC tissue and normal nasopharyngeal mucosa. Immunohistochemistry was conducted to measure the expression of α-SMA and FAP. Cytokines were detected by protein array chip and identified by real-time PCR. CCK-8 assay was used to detect cell proliferation. Radiation-resistant (IRR) 5-8F cell line was established and colony assay was performed to evaluate tumor cell growth after irradiation. Signaling pathways were acquired via gene set enrichment analysis (GSEA). Comet assay and γ-H2AX foci assay were used to measure DNA damage level. Protein expression was detected by western blot assay. In vivo experiment was performed subcutaneously. Results We found that radiation-resistant NPC tissues were constantly infiltrated with a greater number of cancer-associated fibroblasts (CAFs) compared to radiosensitive NPC tissues. Further research revealed that CAFs induced the formation of radioresistance and promoted NPC cell survival following irradiation via the IL-8/NF-κB pathway to reduce irradiation-induced DNA damage. Treatment with Tranilast, a CAF inhibitor, restricted the survival of CAF-induced NPC cells and attenuated the of radioresistance properties. Conclusions Together, these data demonstrate that CAFs can promote the survival of irradiated NPC cells via the NF-κB pathway and induce radioresistance that can be interrupted by Tranilast, suggesting the potential value of Tranilast in sensitizing NPC cells to irradiation.

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The Radiation-Induced Regenerative Response of Adult Tissue-Specific Stem Cells: Models and Signaling Pathways

Cancers ◽

10.3390/cancers13040855 ◽

2021 ◽

Vol 13 (4) ◽

pp. 855

Author(s):

Paola Serrano Martinez ◽

Lorena Giuranno ◽

Marc Vooijs ◽

Robert P. Coppes

Keyword(s):

Signaling Pathways ◽

Progenitor Cells ◽

Tissue Regeneration ◽

Normal Tissue ◽

Cellular Response ◽

Adult Tissue ◽

Tissue Specific ◽

Radiation Induced

Radiotherapy is involved in the treatment of many cancers, but damage induced to the surrounding normal tissue is often inevitable. Evidence suggests that the maintenance of homeostasis and regeneration of the normal tissue is driven by specific adult tissue stem/progenitor cells. These tasks involve the input from several signaling pathways. Irradiation also targets these stem/progenitor cells, triggering a cellular response aimed at achieving tissue regeneration. Here we discuss the currently used in vitro and in vivo models and the involved specific tissue stem/progenitor cell signaling pathways to study the response to irradiation. The combination of the use of complex in vitro models that offer high in vivo resemblance and lineage tracing models, which address organ complexity constitute potential tools for the study of the stem/progenitor cellular response post-irradiation. The Notch, Wnt, Hippo, Hedgehog, and autophagy signaling pathways have been found as crucial for driving stem/progenitor radiation-induced tissue regeneration. We review how these signaling pathways drive the response of solid tissue-specific stem/progenitor cells to radiotherapy and the used models to address this.

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EBV-LMP1 promotes radioresistance by inducing protective autophagy through BNIP3 in nasopharyngeal carcinoma

Cell Death and Disease ◽

10.1038/s41419-021-03639-2 ◽

2021 ◽

Vol 12 (4) ◽

Author(s):

San Xu ◽

Zhuan Zhou ◽

Xingzhi Peng ◽

Xuxiu Tao ◽

Peijun Zhou ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Crucial Role ◽

Epstein Barr Virus ◽

Interacting Protein ◽

Multiple Tumors ◽

Barr Virus ◽

Signaling Axis ◽

Epstein Barr ◽

Adenovirus E1b

AbstractStudies have indicated that dysfunction of autophagy is involved in the initiation and progression of multiple tumors and their chemoradiotherapy. Epstein–Barr virus (EBV) is a lymphotropic human gamma herpes virus that has been implicated in the pathogenesis of nasopharyngeal carcinoma (NPC). EBV encoded latent membrane protein1 (LMP1) exhibits the properties of a classical oncoprotein. In previous studies, we experimentally demonstrated that LMP1 could increase the radioresistance of NPC. However, how LMP1 contributes to the radioresistance in NPC is still not clear. In the present study, we found that LMP1 could enhance autophagy by upregulating the expression of BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3). Knockdown of BNIP3 could increase the apoptosis and decrease the radioresistance mediated by protective autophagy in LMP1-positive NPC cells. The data showed that increased BNIP3 expression is mediated by LMP1 through the ERK/HIF1α signaling axis, and LMP1 promotes the binding of BNIP3 to Beclin1 and competitively reduces the binding of Bcl-2 to Beclin1, thus upregulating autophagy. Furthermore, knockdown of BNIP3 can reduce the radioresistance promoted by protective autophagy in vivo. These data clearly indicated that, through BNIP3, LMP1 induced autophagy, which has a crucial role in the protection of LMP1-positive NPC cells against irradiation. It provides a new basis and potential target for elucidating LMP1-mediated radioresistance.

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