Squamous Cell
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2021 ◽  
Vol 15 (1) ◽  
Author(s):  
M. Nazim Abbas ◽  
Wei Son Tan ◽  
Ganessan Kichenadasse

Abstract Background Sorafenib is an oral multikinase inhibitor that targets Raf serine/threonine receptor tyrosine kinases and inhibits tumor cell growth and angiogenesis. Cutaneous toxicities of sorafenib are common, including cutaneous eruptions (such as truncal erythema and seborrheic-dermatitis-like changes) and hand–foot syndrome. Keratoacanthomas and squamous cell carcinomas have been reported previously; however, we report a case of multiple eruptive keratoacanthomas in the form of Grzybowski syndrome after initiation of sorafenib. Case presentation We report a 63-year-old Caucasian male who developed multiple cutaneous eruptive keratoacanthomas after starting sorafenib 400 mg twice daily. He had a known history of hepatitis-C-related cirrhosis and hepatocellular carcinoma, and previously had actinic keratosis and skin squamous cell carcinoma excision. Approximately two and a half months after starting sorafenib, the patient initially developed two lesions, one on each forearm, and after excision, these lesions demonstrated histological features of squamous cell carcinoma. One month later, the patient presented with approximately 48 new skin lesions of varying size on the back, bilateral upper limbs, and face requiring excisional biopsy of a large number of these lesions. Histopathology showed eruptive invasive keratoacanthomas (Grzybowski syndrome). Sorafenib was temporarily stopped and subsequently restarted at a lower dose. Acitretin 25 mg daily was commenced after few weeks, and no further keratoacanthomas developed during his treatment. Conclusions We report a unique case of sorafenib-associated Grzybowski syndrome. Temporary interruption and dose reduction of sorafenib and use of acitretin appeared to prevent further development of keratoacanthomas.


Author(s):  
Tahereh Nosratzehi ◽  
Ebrahim Alijani ◽  
Neda Hassanpoor

Abstract Objectives The present study aimed to evaluate interleukin-12 (IL-12) and IL-23 in the saliva of patients with oral lichen planus (OLP) and oral squamous cell carcinoma (SCC). Materials and Methods Thirty cases with clinical and histopathological OLP (bilateral lesions, papular and reticular lesions, and Wickham lines) (Group A), 30 with oral SCCs (OSCCs) (Group B), and 30 with no history of oral cancer, other lesions, or lichen planus (Group C) were enrolled at the Department of Oral Medicine School of Dentistry, Zahedan, Iran. The whole unstimulated saliva was collected and the salivary concentration of IL-12 and IL-23 was measured using an enzyme-linked immunosorbent assay in the laboratory. Statistical Analysis Data were analyzed using Kruskal-Wallis, Mann-Whitney tests, and Pearson’s correlation coefficients. Results In the present study, salivary IL-12 and IL-23 levels were higher in OSCC patients than in OLP and healthy individuals. Conclusions The results show that although IL-23 and IL-12 cytokines have an important role in the pathogenesis of chronic immunity and inflammatory diseases, further studies are required to assess matrix metalloproteinase links with tumor invasion.


2021 ◽  
Author(s):  
Shizhang Song ◽  
Bo Jiang ◽  
Sichuan Hou ◽  
Xingang Huang ◽  
Chunmei Li ◽  
...  

Abstract BackgroundSquamous cell carcinoma (SCC) of the prostate is a very rare and highly aggressive tumor, which is insensitive to multiple treatments, prone to metastasis, and has a worse prognosis than adenocarcinoma of the prostate. However, a transformation of prostatic adenocarcinoma into squamous cell carcinoma is rarer and may occur after endocrine or radiotherapy. By now, there are few cases in the world about the transformation from adenocarcinoma into squamous cell carcinoma after treatment. To our knowledge, our case is the first reported in China.Case presentationA 67-year-old man with metastatic adenocarcinoma of the prostate for 2 years, was not suitable for radical prostatectomy due to the disease classified T4N1M1. Endocrine therapy using Luteinizing Hormone-Releasing Hormone (LHRH) analog (leuprorelin) and antiandrogen agent (bicalutamide) was started, and serum prostate-specific antigen (PSA) level gradually decreased to a nadir of 0.04ng/ml. 2 years after treatment, he complained of worsening of lower urinary tract symptoms, and then he underwent transurethral resection of the prostate (TURP). Histopathological examination confirmed most of the tissue areas were accompanied by poorly differentiated keratinizing squamous cell carcinoma. Now, the patient started docetaxel treatment. He has received 2 times of systemic chemotherapy. The patient's current general condition is fair.ConclusionsProstatic adenocarcinoma transformed into squamous cell carcinoma after endocrine therapy is very rare. However, the serum PSA of this tumor is probably normal, PSA and the Gleason grading system are of limited value in the diagnosis of SCC, histopathological can help its diagnosis. The transformation is silent and we cannot know it. The question of whether prostatic adenocarcinoma or SCC of the prostate requires more definitive research to answer.


Author(s):  
Yuanbo Cui ◽  
Chunyan Zhang ◽  
Shanshan Ma ◽  
Zhe Li ◽  
Wenjie Wang ◽  
...  

Abstract Background Long non-coding RNA (LncRNA) controls cell proliferation and plays a significant role in the initiation and progression of esophageal squamous cell carcinoma (ESCC). N6-methyladenosine (m6A) modification now is recognized as a master driver of RNA function to maintain homeostasis in cancer cells. However, how m6A regulates LncRNA function and its role in tumorigenesis of ESCC remain unclear. Methods Multiple ESCC datasets were used to analyze gene expression in tumor tissues and normal tissues. Kaplan-Meier method and the ROC curve were conducted to evaluate the prognostic value and diagnostic value of LINC00022 in ESCC, respectively. Both gain-of-function and loss-of-function experiments were employed to investigate the effects of LINC00022 on ESCC growth in vitro and in vivo. Bioinformatics analysis, colorimetric m6A assay, RIP, MeRIP and co-IP was performed to explore the epigenetic mechanism of LINC00022 up-regulation in ESCC. Results Here we report that m6A demethylation of LncRNA LINC00022 by fat mass and obesity-associated protein (FTO) promotes tumor growth of ESCC in vivo. Clinically, we revealed that LINC00022 was up-regulated in primary ESCC samples and was predictive of poor clinical outcome for ESCC patients. Mechanistically, LINC00022 directly binds to p21 protein and promotes its ubiquitination-mediated degradation, thereby facilitating cell-cycle progression and proliferation. Further, the elevated FTO in ESCC decreased m6A methylation of LINC00022 transcript, leading to the inhibition of LINC00022 decay via the m6A reader YTHDF2. Over-expression of FTO was shown to drive LINC00022-dependent cell proliferation and tumor growth of ESCC. Conclusions Thus, this study demonstrated m6A-mediated epigenetic modification of LncRNA contributes to the tumorigenesis in ESCC and LINC00022, specific target of m6A, serves as a potential biomarker for this malignancy.


DEN Open ◽  
2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Seiichiro Abe ◽  
Yuichiro Hirai ◽  
Takeshi Uozumi ◽  
Mai Ego Makiguchi ◽  
Satoru Nonaka ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Xin Fan ◽  
YangShaobo Ou ◽  
Huijie Liu ◽  
Liangzhen Zhan ◽  
Xingrong Zhu ◽  
...  

Background: Due to the lack of accurate guidance of biomarkers, the treatment of head and neck squamous cell carcinoma (HNSCC) has not been ideal. Ferroptosis plays an important role in tumor suppression and treatment of patients. However, tumor protein p53 (TP53) mutation may promote tumor progression through ferroptosis. Therefore, it is particularly important to mine prognostic-related differentially expressed ferroptosis-related genes (PR-DE-FRGs) in HNSCC to construct a prognostic model for accurately guiding clinical treatment.Methods: First, the HNSCC data obtained from The Cancer Genome Atlas (TCGA) was used to identify PR-DE-FRGs for screening candidate genes to construct a prognostic model. We not only used a variety of methods to verify the accuracy of the model for predicting prognosis but also explored the role of ferroptosis in the development of HNSCC from the perspective of the immune microenvironment and mutation. Finally, we explored the correlation between the prognostic model and clinical treatment and drew a high-precision nomogram to predict the prognosis.Results: Seventeen of the 29 PR-DE-FRGs were selected to construct a prognostic model with good predictive performance. Patients in the low-risk group were found to have a greater number of CD8 + T cells, follicular helper T cells, regulatory T cells, mast cells, T-cell costimulations, and type II interferon responses. A higher tumor mutation burden (TMB) was observed in the low-risk group and was associated with a better prognosis. A higher risk score was found in the TP53 mutation group and was associated with a worse prognosis. The risk score is closely related to the expression of immune checkpoint inhibitors (ICIs)-related genes such as PD-L1 and the IC50 of six chemotherapeutic drugs. The nomogram we constructed performs well in predicting prognosis.Conclusion: Ferroptosis may participate in the progression of HNSCC through the immune microenvironment and TP53 mutation. The model we built can be used as an effective predictor of immunotherapy and chemotherapy effects and prognosis of HNSCC patients.


2021 ◽  
Author(s):  
shanchun hou ◽  
Qi Li ◽  
Wulong Jin ◽  
You Peng ◽  
Sujuan Niu ◽  
...  

Abstract Background: Metformin is the first-line drug for type II diabetes, and recent studies indicate that metformin plays an inhibitory role in multiple cancers. Metformin can also enhance the effect of chemotherapy. Although head and neck squamous cell carcinoma cells are sensitive to metformin, the mechanisms related to the metformin response and the chemosensitization effect have not been fully studied. Results: In this study, we aimed to elucidate the molecular mechanisms of metformin in HNSCC by transcriptome analysis and to reveal the underlying mechanisms of the sensitizing effects of metformin by combined online dataset analysis. mRNA sequencing and functional analysis of HNSCC samples after metformin treatment and functional analysis of mRNAs with opposite metformin-induced effects in chemosensitive versus chemoresistant cells revealed the molecular pathways, mainly the base excision repair pathway, by which this small molecule drug sensitizes HNSCC cells to treatment. Conclusions: These findings indicate that metformin exerts a hypersensitization effect by regulating the BER pathway in tumour cells, reducing their self-repair capacity after chemotherapy-induced DNA damage. In addition, the genes identified by transcriptome analysis are candidates for further investigation into the effector targets of metformin in the inhibition of HNSCC and could be applied to improve the treatment in HNSCC patients who develop resistance after advanced chemotherapy.


2021 ◽  
Author(s):  
shuhan wang ◽  
Xiaoyu Chen ◽  
Xuejie Zhu ◽  
Kehao Lin ◽  
Qixiao Cui ◽  
...  

Abstract To investigate the anti-tumor effect and mechanisms of ailanthone (AIL) in tongue squamous cell carcinoma (TSCC). The viability and apoptotic cell number of TCA8113 and Cal-27 cells declined and increased considerably following AIL. Hoechst 33258 staining revealed chromatin aggregation after exposure to AIL. Along with an accumulation of cleaved caspase-9, caspase-3, and PARP1, Bcl-2/Bax ratio and the levels of caspase-3, caspase-9 and PARP1 reduced after exposure to AIL treatment. Subjecting Cal-27 cells to AIL treatment led to the arrestment of the cell cycle at the G2/M phase. Nevertheless, the cell cycle of AIL-treated TCA8113 cells did not change significantly. Following AIL treatment, a decline in the expression of CDK1 and cyclin B1 was manifested by Western Blot. The p-AKT as well as the expression level of p-PI3K underwent a significant downregulation by AIL in both cells. The outcome furnishes a valuable understanding of the potential applications of AIL in treating TSCC.


2021 ◽  
Author(s):  
Haoyue Xu ◽  
Xiangpu Wang ◽  
Zhien Feng ◽  
Renji Chen ◽  
Zhengxue Han

Abstract Background: Currently, no systematic analysis has been conducted to assess the potential of multiple autophagy-related long non-coding RNAs (lncRNA) to predict the prognosis of head and neck squamous cell carcinoma (HNSCC). we investigated the prognostic potential of autophagy-related long non-coding RNAs (lncRNA) in HNSCC patients. Methods: Patient information and Autophagy-associated genes were obtained from The Cancer Genome Atlas (TCGA) and Human Autophagy data resource. Autophagy-related lncRNAs were determined through Lasso and Cox regression analyses. Then, on the basis of autophagy- related lncRNAs, a risk score and a nomogram were constructed for estimation of prognostic outcomes for HNSCC patients. These models were verified internally using the TCGA and. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used for gene functional analyses. Results: Three autophagy-related lncRNAs (AC002401.4, AC245041.2 and TMEM44-AS1) that are associated with HNSCC were identified. Univariate and multivariate Cox regression analyses revealed that the risk score is an independent prognostic indicator (p ≤ 0.001), with its ability to predict prognosis being higher than that of other clinicopathological indicators (AUC=0.732). Concordance index of the nomogram was 0.712, and AUC values for one-year, three-year and five-year survival rates were 0.730, 0.745 and 0.728, respectively. Internal verifications revealed that this nomogram had a good ability to predict prognosis. Functional analysis showed that the genes were mostly enriched in autophagy and tumor-related cascades. Conclusion: The autophagy-related lncRNAs model can predict the prognosis of patients with HNSCC.Trial registration: Prospective, Observational, Real-world Oral Malignant Tumors Study (POROMS), NCT02395367. Registered 23 March 2015, https://clinicaltrials.gov/ct2/show/NCT02395367


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