Chromobox (CBX) family proteins control chromatin structure and gene expression. However, the functions of CBXs in cancer progression, especially breast cancer, are inadequately studied. We assessed the significance of eight CBX proteins in breast cancer. We performed immunohistochemistry and bioinformatic analysis of data from Oncomine, GEPIA Dataset, bcGenExMiner, Kaplan–Meier Plotter, and cBioPortal. We compared mRNA and protein expression levels of eight CBX proteins between breast tumor and normal tissue. The expression difference of CBX7 was the greatest, and CBX7 was downregulated in breast cancer tissues compared with normal breast tissues. The expression of CBX2 was strongly associated with tumor stage. We further analyzed the association between the eight CBX proteins and the following clinicopathological features: menopause age, estrogen receptor (ER), progesterone receptor (PR) and HER-2 receptor status, nodal status, P53 status, triple-negative status, and the Scarff–Bloom–Richardson grade (SBR) and Nottingham prognostic index (NPI). Survival analysis in the Kaplan–Meier Plotter database showed that the eight CBX proteins were significantly associated with prognosis. Moreover, CBX genes in breast cancer patients had a high net alteration frequency of 57%. There were significant co-expression correlations between the following CBX protein pairs: CBX4 positively with CBX8, CBX6 positively with CBX7, and CBX2 negatively with CBX7. We also analyzed the Gene Ontology enrichment of the CBX proteins, including biological processes, cellular components, and molecular functions. CBX 1/2/3/5/8 may be oncogenes for breast cancer, whereas CBX 6 and 7 may be tumor suppressors for breast cancer. All eight CBX proteins may be predictive for prognosis. Clinical trials are needed to confirm the significance of the eight CBX proteins in breast cancer.

Background: Xanthogranulomatous cholecystitis (XGC) is a rare presentation of chronic cholecystitis, characterized by xanthogranuloma, severe foam cells and fibrosis, and can be an inducement of difficulty in cholecystectomy. The purpose of this study was to review the clinical findings and imageology features of XGC and to optimize the treatment option. Methods: This retrospective study collected clinical symptoms, demographics, imageology, operation records, histopathological findings, and postoperative complications of 100 patients with XGC after evaluating 50005 cholecystectomy specimens between 2009 and 2018 in a single institute. heir clinical symptoms, demographics, imageology, operation records, histopathological findings, and postoperative complications were collected and analyzed. Results: Patients showed various clinical symptoms, ultrasonography was performed in all patients, CT and MRI were further arranged selectively before the operation, but none of the patients were prediagnosed. Fiftytwo patients received open cholecystectomy. Laparoscopic cholecystectomy (LC) was planned in 48 patients within whom 8 cases were converted to open cholecystectomy. No partial cholecystectomy was performed.The intraoperative findings included cholecystolithiasis, choledocholithiasis, thickened gallbladder wall, lesions infiltrating into adjacent tissues, disordered Calot's triangle anatomy, enlarged regional lymph nodes, internal gallbladder fistula, and hepatic abscesses. Frozen-section analysis was performed in 48 patients under the suspicion of gallbladder carcinoma (GBCa), but only 2 cases were finally confirmed. Conclusions:The preoperative diagnosis of XGC was challenging. Open cholecystectomy was the most preferred treatment, and conversion to open was often necessary after LC.

Rationale:Phyllodes tumors (PT) of the breast are rare neoplasm originating from fibroepithelial component. To our knowledge, our report is the first reported case of PT in 2 sisters.Patient concerns:We presented 2 cases of PT of the breast involving in 2 sisters. On physical examination of the younger sister, a firm mass measuring approximately 3 cm in diameter was identified in upper inner quadrant of the right breast. Physical examination of the elder sister revealed a 3 cm lump in upper outer quadrant of the left breast.Diagnoses:Histopathology of the younger sister revealed a malignant PT. The elder sister was diagnosed with borderline PT.Interventions:The younger sister with malignant PT underwent right mastectomy. The elder sister with borderline PT was scheduled for wide resection of the mass in the left breast.Outcomes:After a follow-up of 23 months, no local or distant recurrence was observed.Lessons:Our cases indicate that genetic factor may contribute to the risk of PT of the breast. Markers such as p53 and Ki-67 may have some correlation with PT malignancy.

Background Part of papillary thyroid microcarcinoma (PTMC) has a high risk of tumor invasion and metastasis, which may occur in the regional lymph node metastasis or distant metastasis, severely threatening the life of patients. Invasion and metastasis are tightly involved in the proliferation, migration and invasion in cancer. This study aimed to investigate the role of tescalcin (TESC) in the proliferation, migration and invasion of PTMC. Methods The expressions of TESC in PTMC tissues and cells were detected by immunohistochemistry or qRT-PCR. Then, TPC-1 and BHT101 cells transfected with TESC-RNAi were used for the transcriptome sequencing. The proliferation, apoptosis, migration and invasion of TPC-1 and BHT101 cells were detected by CCK-8, colony formation, flow cytometric assay, transwell migration and scratch test. Moreover, TESC-RNAi transfected TPC-1 and BHT101 cells were subcutaneously injected into mice. Tumor volume and weight were calculated, and the positive rate of Ki-67 was determined by immunohistochemistry. Finally, the levels of c-Fos, ERK1/2 and p-ERK1/2 were determined by western blot. Results The expressions of TESC in PTMC tissues and cell lines were prominently enhanced. Transcriptome sequencing results showed that c-Fos was decreased in TPC-1 and BHT101 cells transfected with TESC-RNAi, which was associated with multiple different signaling pathways including the MAPK signaling pathway. Furthermore, TESC promoted the progress of PTMC by regulating the expression of c-Fos, which might be associated with the ERK signaling pathway. Conclusions TESC promoted the growth and metastasis of PTMC through regulating c-Fos/ERK1/2.

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