Laparoscopic transabdominal-sacrococcygeal approach for resection of Altman type III sacrococcygeal teratoma in adult women: A case report.

INTRODUCTION: Adult sacrococcygeal teratoma (SCT) is a rare disease that is not easily detected or easily missed, and its treatment is based on surgery, including transabdominal, transsacral, or a combination of both, but there are no clear guidelines for diagnosis and treatment. We share a case of Altman type III SCT in order to provide more reference protocols for the diagnosis and treatment of adult SCT, and more importantly to increase our understanding of different types of SCT cases in adults. PATIENT CONCERNS: Our patient was a 31-year-old adult woman who underwent complete surgical resection of a cystic mature teratoma of the right ovary 8 years ago and is currently 13 months postpartum without menstruation, usually with a feeling of anal bulge, with symptoms such as constipation. DIAGNOSIS: We diagnosed SCT by vaginal ultrasonography, computed tomography and magnetic resonance imaging (MRI); benign tumors were considered in the results of serum tumor markers. INTERVENTIONS: We chose the surgical approach of laparoscopic transabdominal-sacrococcygeal approach to completely remove the patient SCT and coccyx. OUTCOMES: The location of SCT is concealed and the clinical symptoms are not obvious. Vaginal ultrasonography, CT and MRI can not only improve the diagnostic rate of SCT, but also understand the size and mass of SCT, providing an exact basis for clinicians to select the laparoscopic transabdominal-sacrococcygeal approach. CONCLUSION: Our sharing increases the reports of rare cases of teratoma with the same histological findings in different organ tissues of the same patient at different times, whether this occurs incidentally requires more case reports and further basic research; in addition, the laparoscopic transabdominal-sacrococcygeal approach is a safe and effective surgical approach for the treatment of Altman type III SCT in adults; finally, this case reminds us that SCT may not affect pregnancy and pregnancy outcomes and provides a reference for the selection of interventions for SCT with pregnancy.

Prognostic Model Associated with Necroptosis in Colorectal Cancer based on Transcriptomic Analysis and Experimental Validation.

PURPOSE: Numerous studies have emphasised the importance of necroptosis in the malignant progression of colorectal cancer (CRC). However, whether necroptosis-related genes (NRGs) can be used to predict the prognosis of CRC remains to be revealed. METHODS: Patients with CRC were divided into two clusters based on the expression of NRGs, and prognosis was compared between the two clusters. A prognostic model was established based on NRGs, and its predictive efficiency was validated using Kaplan-Meier (K-M) curves, receiver operating characteristic (ROC) curves and a nomogram. Immune infiltration, single-cell and drug sensitivity analyses were used to examine the effects of NRGs on the prognosis of CRC. RESULTS: The prognostic model served as a valid and independent predictor of CRC prognosis. Immune infiltration and single-cell analyses revealed that the unique immune microenvironment of CRC was regulated by NRGs. Drug sensitivity analysis showed that patients in the high- and low-risk groups were sensitive to different drugs. In addition, H2BC18 was found to play an important role in regulating the malignant progression of CRC. CONCLUSION: This study provides novel insights into precision immunotherapy based on NRGs in CRC. The NRG-based prognostic model may help to identify targeted drugs and develop more effective and individualised treatment strategies for patients with CRC.

GADD45α alleviates the CDDP resistance of SK-OV3/cddp cells via redox-mediated DNA damage.

Epithelial ovarian cancer has the highest mortality rate of all malignant ovarian cancer types. Great progress has been made in the treatment of ovarian cancer in recent years. However, drug resistance has led to a low level of 5-year survival rate of epithelial ovarian cancer, and the molecular mechanism of which remains unknown. The aim of the present study was to identify the role of redox status in the cisplatin (CDDP) resistance of ovarian cancer. CDDP-resistant SK-OV3 (SK-OV3/cddp) cells were prepared and their reactive oxygen species and glutathione levels were investigated. The effects of hydrogen peroxide on the CDDP sensitivity of the SK-OV3/cddp cells and their expression levels of the redox-associated protein growth arrest and DNA damage 45a (GADD45α) were also investigated. In addition, the impact of GADD45α overexpression on cell viability was evaluated in vitro and in vivo, and the levels of Ser-139 phosphorylated H2A histone family member X (γ-H2AX), which is associated with DNA damage, were detected. The results suggested that redox status affected the drug resistance of the ovarian cancer cells by increasing the expression of GADD45α. The overexpression of GADD45α reversed the CDDP resistance of the SK-OV3/cddp cells and increased the level of γ-H2AX. In conclusion, GADD45α alleviated the CDDP resistance of SK-OV3/cddp cells via the induction of redox-mediated DNA damage.

Eukaryotic initiation factor 3, subunit C silencing inhibits cell proliferation and promotes apoptosis in human ovarian cancer cells.

Ovarian cancer remains the leading cause of death among all gynaecological cancers, illustrating the urgent need to understand the molecular mechanisms involved in this disease. Eukaryotic initiation factor 3c (EIF3c) plays an important role in protein translation and cancer cell growth and proliferation, but its role in human ovarian cancer is unclear. Our results showed that EIF3c silencing significantly up-regulated 217 and down-regulated 340 genes. Ingenuity Pathway Analysis (IPA) indicated that the top differentially expressed genes are involved in 'Classical Pathways', 'Diseases and Functions' and 'Networks', especially those involved in signalling and cellular growth and proliferation. In addition, eIF3c silencing inhibited cellular proliferation, enhanced apoptosis and regulated the expression of apoptosis-associated proteins. In conclusion, these results indicate that by dysregulating translational initiation, eIF3c plays an important role in the proliferation and survival of human ovarian cancer cells. These results should provide experimental directions for further in-depth studies on important human ovarian cancer cell pathways.

Distribution of human papilloma virus type 16 E6/E7 gene mutation in cervical precancer or cancer: A case control study in Guizhou Province, China.

HPV-16 varies geographically and is correlated with cervical cancer genesis and progression. This study aimed to determine the distribution of HPV-16 E6/E7 genetic variation in patients with invasive cervical cancer or precancer in Guizhou Province, China. A case-control study was designed, and the distribution of HPV-16 E6/E7 genetic variation was compared among women with cervical cancer, precancer, and sexually active without cervical lesion. HPV infection was detected through flow-through hybridization and gene chip techniques to determine the prevalence of HPV 16 E6/E7 genetic variation. Among 90 specimens (30 cervical cancer, 30 precancer, 30 controls), 81 were subjected to HPV-16 E6/E7 gene sequencing. The rates of DNA sequence mutation and amino acid mutation were 76.5% (62/81) and 66.7% (54/81), respectively. Both E6 and E7 genes showed higher mutation rate than their prototypes. The prevalence of E6/E7 mutation significantly differed between the cervical cancer and the controls (P < 0.05) and between the cervical precancer and the controls (P < 0.05). Mutations were simultaneously detected at the E6-D32E (T96A) and E7-M28V (A82G)/L94P (T281C) sites of the amino acid sequence. The most common genetic variation was D32E/M28V/L94P, which accounted for 35.8% of the cases (29/81). D32E/M28V/L94P mutation was higher in the cervical cancer and precancer compared with the prototype. HPV-16 E6/E7 genetic variations, such as D32E/M28V/L94P, are more prevalent in cervical cancer or precancer than those in the controls. The possible correlation between genetic variation and cancerigenesis may be used to design an HPV vaccine for cervical carcinoma.