Comparison study of intraoperative surface acquisition methods on registration accuracy for soft-tissue surgical navigation.

Purpose: To study the difference between rigid registration and nonrigid registration using two forms of digitization (contact and noncontact) in human in vivo liver surgery. Approach: A Conoprobe device attachment and sterilization process was developed to enable prospective noncontact intraoperative acquisition of organ surface data in the operating room (OR). The noncontact Conoprobe digitization method was compared against stylus-based acquisition in the context of image-to-physical registration for image-guided surgical navigation. Data from n=10 patients undergoing liver resection were analyzed under an Institutional Review Board-approved study at Memorial Sloan Kettering Cancer Center. Organ surface coverage of each surface acquisition method was compared. Registration accuracies resulting from the acquisition techniques were compared for (1) rigid registration method (RRM), (2) model-based nonrigid registration method (NRM) using surface data only, and (3) NRM with one subsurface feature (vena cava) from tracked intraoperative ultrasound (NRM-VC). Novel vessel centerline and tumor targets were segmented and compared to their registered preoperative counterparts for accuracy validation. Results: Surface data coverage collected by stylus and Conoprobe were 24.6%±6.4% and 19.6%±5.0%, respectively. The average difference between stylus data and Conoprobe data using NRM was -1.05 mm and using NRM-VC was -1.42 mm, indicating the registrations to Conoprobe data performed worse than to stylus data with both NRM approaches. However, using the stylus and Conoprobe acquisition methods led to significant improvement of NRM-VC over RRM by average differences of 4.48 and 3.66 mm, respectively. Conclusion: The first use of a sterile-field amenable Conoprobe surface acquisition strategy in the OR is reported for open liver surgery. Under clinical conditions, the nonrigid registration significantly outperformed standard-of-care rigid registration, and acquisition by contact-based stylus and noncontact-based Conoprobe produced similar registration results. The accuracy benefits of noncontact surface acquisition with a Conoprobe are likely obscured by inferior data coverage and intrinsic noise within acquisition systems.

Circular RNA hsa_circ_0004277 contributes to malignant phenotype of colorectal cancer by sponging miR-512-5p to upregulate the expression of PTMA.

In recent years, extensive reports have been published concerning the molecular mechanism underlying the occurrence and progression of colorectal cancer. Circular RNAs (circRNAs) have been identified as important modulators in the biological processes of colorectal cancer. Microarray analysis unveiled that differential circ-0004277 expression was identified in tissue samples of colorectal cancer. High circ-0004277 expression was then verified in tissue samples and cell lines of colorectal cancer via qRT-PCR. Kaplan-Meier analysis was used for identifying the association between circ-0004277 expression and the overall survival rate of colorectal cancer patients. A relationship existed between higher circ-0004277 expression and decreased overall survival rate of colorectal cancer patients. From a functional perspective, circ-0004277 knockdown accelerated cell apoptosis and restrained cell proliferation of colorectal cancer. From mechanistic perspective, circ-0004277 upregulated PTMA by sponging miR-512-5p. Rescue assay was used for verifying the roles of the circ-0004277-miR-512-5p-PTMA axis. Both miR-512-5p and PTMA participated in circ-0004277-mediated colorectal cancer cell proliferation based on experiments. In summary, our study showed that circ-0004277 promoted the proliferation of colorectal cancer cells as a miR-512-5p sponge to upregulate the PTMA expression.

Circular RNA PVT1 promotes metastasis via miR-145 sponging in CRC.

Circular RNAs (circRNAs) are a class of covalently closed non-coding RNAs and are widely involved in various cancers including colorectal cancer (CRC). Circular RNA PVT1 (circPVT1) was reported in several malignancies but the role it plays in CRC remains unclear. In our current research, we focused on the expression and function of circPVT1) works in CRC. We found that circPVT1 was upregulated in CRC. Also, we illustrated that the upregulated circPVT1 was closely correlated with poor prognosis and bad clinicopathological features of patients with CRC. Through a loss of function experiment, we showed that a downregulation of circPVT1 suppressed CRC cells metastasis. Through online prediction, we found that circPVT1 had a microRNA response element (MRE) for miR-145. Additionally, we demonstrated that miR-145 was downregulated in CRC. Even further, we showed that miR-145 was involved in circPVT1 mediated facilitation of CRC metastasis. In a further mechanical study, we demonstrated that circPVT1 could target miR-145. Lastly, we revealed that the metastasis-promoting role of circPVT1 in CRC was partially achieved via miR-145 sponging. In brief, the findings of the present study illustrated that circPVT1, working as an oncogene, promotes metastasis via miR-145 sponging in CRC. CircPVT1/miR-145 axial might be a novel point in targeting treatment of CRC.

Paclitaxel reversed trastuzumab resistance via regulating JUN in human gastric cancer cells identified by FAN analysis.

AIM: In this study, we aim to use bioinformatics approach to identify paclitaxel-targeted modulators potentially involved in the process of reversing the trastuzumab resistance. Materials & methods: We extracted data from GSE77346 to identify potential trastuzumab resistance-related genes, used bioinformatics analysis and functional/activity network approach to find genes involved in trastuzumab resistance reversal. RESULTS: We identified hub differentially expressed genes related to trastuzumab resistance, trastuzumab targeting and paclitaxel targeting, respectively. We then found C-Jun may be critical in trastuzumab resistance reversal.  This process may involve transcriptional activation of DUSP1 by JUN, which lead to regulation of DUSP1-related signaling pathways. CONCLUSION: The present study revealed paclitaxel may reverse the trastuzumab resistance by JUN, which possibly in turn regulated DUSP1 and DUSP1-related signaling pathways.