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The polymorphic microbiome has been proposed as a new hallmark of cancer. Intratumor microbiome has been revealed to play vital roles in regulating tumor initiation and progression, but the regulatory mechanisms have not been fully uncovered. In this review, we illustrated that similar to other components in the tumor microenvironment, the reside and composition of intratumor microbiome are regulated by tumor cells and the surrounding microenvironment. The intratumor hypoxic, immune suppressive, and highly permeable microenvironment may select certain microbiomes, and tumor cells may directly interact with microbiome via molecular binding or secretions. Conversely, the intratumor microbiomes plays vital roles in regulating tumor initiation and progression via regulating the mutational landscape, the function of genes in tumor cells and modulating the tumor microenvironment, including immunity, inflammation, angiogenesis, stem cell niche, etc. Moreover, intratumor microbiome is regulated by anti‐cancer therapies and actively influences therapy response, which could be a therapeutic target or engineered to be a therapy weapon in the clinic. This review highlights the intratumor microbiome as a vital component in the tumor microenvironment, uncovers potential mutual regulatory mechanisms between the tumor microenvironment and intratumor microbiome, and points out the ongoing research directions and drawbacks of the research area, which should broaden our view of microbiome and enlighten further investigation directions. [ABSTRACT FROM AUTHOR]

Objective: Transoral robotic surgery (TORS) has become an effective treatment for early‐stage oropharyngeal squamous cell carcinomas (OPSCCs). We aimed to analyze the clinical safety and efficacy of TORS for human papilloma virus (HPV)‐positive and HPV‐negative OPSCC in China. Methods: Patients with OPSCC of pT1‐T2 stage who underwent TORS from March 2017 to December 2021 were analyzed. Results: A total of 83 patients (HPV‐positive, n = 25; HPV‐negative, n = 58) were included. The median age of the patients was 57.0 years and 71 were men. The majority of primary tumor sites were palatine tonsils (52, 62.7%) and base of tongues (20, 24.1%). Three patients have a positive margin. A total of 12 (14.5%) patients received tracheotomies, the average duration of tracheostomy tube use was 9.4 days, and nasogastric tube was 14.5 days. No patient had a long‐term tracheotomy. The 3‐year overall survival (OS), disease‐free survival (DFS), and recurrence‐free survival (RFS) for all 83 patients were 89.5%, 80.1%, and 83.3%, respectively. The OS at 3 years between the HPV‐positive group and HPV‐negative group were 100% versus 84.3% (P =.07), while the DFS and RFS between two groups also showed no significant difference. Among multivariate cox regression analysis of all potential risk factors, smoking was the significant risk factors for disease recurrence (P <.05). Conclusion: Transoral robotic surgery achieved encouraging oncologic outcomes and safety in T1‐T2 stage OPSCC treatment, regardless of HPV status. Level of Evidence: 4 [ABSTRACT FROM AUTHOR]

Background: The objective of this study was to investigate the role and molecular mechanism of cyclin‐dependent kinase 5 (CDK5) in regulating the growth of tongue squamous cell carcinoma (TSCC). Methods: The authors used multiple methods to detect the levels of CDK5 expression in samples of TSCC and to explore the relation between CDK5 expression and various clinicopathologic factors. In vivo and in vitro cell experiments were performed to detect the proliferation, invasion, and migration of TSCC cells with CDK5 knockdown or overexpression. These studies verified that CDK5 regulates the occurrence and development of TSCC cells through the microRNA 513c‐5p/cell division cycle 25B pathway. Results: An elevated level of CDK5 expression in TSCC tissues was identified as an independent risk factor affecting TSCC growth and patient prognosis. Patients who had TSCC with low levels of CDK5 expression had a higher survival rate than those with high levels. Knockdown of CDK5 reduced the proliferation, migration, and invasion of TSCC cells both in vitro and in vivo. In addition, the authors observed that CDK5 regulated the growth of TSCC through the microRNA 513c‐5p/cell division cycle C25B pathway. Conclusions: CDK5 functions as an oncogene in TSCC and might serve as a molecular marker for use in the diagnosis and treatment of TSCC. Lay Summary: Tongue squamous cell carcinoma (TSCC) is 1 of the most common malignant tumors of the head and neck, and the survival rate of patients with tongue cancer has been very low.Therefore, it is important to study the molecular mechanism of TSCC progression to identify biomarkers that can be used to improve its clinical diagnosis and treatment.Cyclin‐dependent kinase 5 (CDK5) is an atypical member of the cyclin‐dependent kinase family and is involved in regulating the cell cycle.Changes in the cell cycle are of great significance for the occurrence and development of tumor cells; and, in recent years, increasing evidence has suggested that CDK5 exists in a disordered state in cancer cells.In this study, the authors demonstrate that CDK5 functions as an oncogene in TSCC and might serve as a molecular marker for use in the diagnosis and treatment of TSCC. The role of cyclin‐dependent kinase 5 and its molecular mechanism in regulating the growth of tongue squamous cell carcinoma (TSCC) are investigated. The results indicate that cyclin‐dependent kinase 5 is involved in the occurrence and development of TSCC and could possibly serve as a new prognostic marker and molecular target for treating TSCC. [ABSTRACT FROM AUTHOR]

Systematic analysis of tumor‐infiltrating lymphocytes is essential for the development of new cancer treatments and the prediction of clinical responses to immunotherapy. Immunomodulatory drugs are used for the treatment of oral squamous cell carcinoma (OSCC), depending on immune infiltration profiles of the tumor microenvironment. In this study, we isolated 11,866 single T cells from tumors and paired adjacent normal tissues of three patients with OSCC. Using single‐cell RNA sequencing, we identified 14 distinct T‐cell subpopulations within the tumors and 5 T‐cell subpopulations in the adjacent normal tissues and delineated their developmental trajectories. Exhausted CD8+ T cells and regulatory CD4+ T cells (CD4+ Tregs) were enriched in OSCC tumors, potentially linked to tumor immunosuppression. Programmed death protein 1 (PD‐1) and cytotoxic T lymphocyte‐associated protein 4 (CTLA4) were identified as marker genes in exhausted CD8+ T cells, whereas forkhead box P3 (FOXP3) and CTLA4 were identified as markers of CD4+ Tregs. Furthermore, our data revealed that thymocyte selection‐associated high‐mobility group box (TOX) may be a key regulator of T‐cell dysfunction in the OSCC microenvironment. Overexpression of TOX upregulated expression of genes related to T‐cell dysfunction. In vitro experiments demonstrated that cytotoxic activity and proliferation efficiency of CD8+ T cells overexpressing PD‐1 or TOX were reduced. Notable, the transcription factor PRDM1 was found to transactivate TOX expression via a binding motif in the TOX promoter. Our findings provide valuable insight into the functional states and heterogeneity of T‐cell populations in OSCC that could advance the development of novel therapeutic strategies. [ABSTRACT FROM AUTHOR]

According to our previous study, GOLPH3 is markedly up‐expressed in tongue squamous cell carcinoma (TSCC), which is also associated with poor survival. However, it remains unclear about key upstream and downstream mechanisms of GOLPH3. This study aimed to illuminate new mechanisms modulating GOLPH3 upregulation and promoting TSCC development at the molecular level. Using mass spectrometry and agarose‐streptavidin‐biotin pull‐down analyses, SOX8 (SRY‐Box 8) was identified to be the new protein to bind the GOLPH3 promoter within TSCC cells, which was further verified to be the regulator of GOLPH3 upregulation. The knockdown of SOX8 suppressed the promoter activity of GOLPH3, while secondarily inhibiting TSCC cell proliferation both in vivo and in vitro. Interestingly, GOLPH3 overexpression rescued the SOX8 knockdown‐mediated suppression on TSCC proliferation. Additionally, exogenous over‐expression of SOX8 also activated the activity of promoter as well as GOLPH3 expression, in the meantime of promoting TSCC development. Moreover it was discovered that SOX8 regulated GOLPH3 expression through interacting with TFAP2A. Moreover our results suggested that the SOX8 level was increased within tumor tissue compared with that in para‐cancer normal counterpart, which showed positive correlation with the GOLPH3 level. According to Kaplan‐Meier analyses, TSCC cases having higher SOX8 and GOLPH3 expression were associated with poorer prognostic outcomes. Taken together, this study reveals that SOX8 enhances the TSCC cell growth via the direct transcriptional activation of GOLPH3, which also indicates the potential to use SOX8/GOLPH3 pathway as the treatment target among TSCC patients. [ABSTRACT FROM AUTHOR]

There are many kinds of defects in pipes, which are difficult to detect with a low degree of automation. In this work, a novel omnidirectional vision inspection system for detection of the morphology defects is presented. An active stereo omnidirectional vision sensor is designed to obtain the texture and depth information of the inner wall of the pipeline in real time. The camera motion is estimated and the space location information of the laser points are calculated accordingly. Then, the faster region proposal convolutional neural network (Faster R‐CNN) is applied to train a detection network on their image database of pipe defects. Experimental results demonstrate that system can measure and reconstruct the 3D space of pipe with high quality and the retrained Faster R‐CNN achieves fine detection results in terms of both speed and accuracy. [ABSTRACT FROM AUTHOR]