The incidence of traumatic neuroma is extremely low, especially in those patients with breast cancer after mastectomy. There are only 10 cases reported in the literature. We report a patient who developed a palpable nodular mass near the mastectomy scar. The result of excisional biopsy was traumatic neuroma. Review of the literature reveal 10 cases with breast cancer of traumatic neuromas after mastectomy. Traumatic neuroma is a benign lesion and a reparative response of the nerve to injury, either direct/indirect trauma or chronic inflammation. Benign lesions as traumatic neuromas are more rarely seen after mastectomy. However, in order to manage patients' treatment, the most critical problem is to distinguish it from recurrent breast carcinoma. Although assistant examination methods such as ultrasound and computed tomography are valuable to a certain extent, the final diagnosis can only be confirmed on pathologic examination.
Due to the substantial limitation of study population, Spindle cell sarcoma (SCS) was unexplored comprehensively. In this study, we investigated the clinical characteristics and disease specific prognostic factors of SCS. 3299 SCS cases were identified and extracted from Surveillance, Epidemiology, and End Results (SEER) database (1973–2017). White people account for 79.1% with median age of 57 years without predominance in any gender. Significant disease specific survival (DSS) and overall survival (OS) were found differentiated in age, T stage, N stage, M stage, AJCC stage, SEER historic stage, tumor locations, surgery, and pathologic grade. In the multivariate Cox analysis, the age >64 years (for DSS, P < 0.001 and for OS, P < 0.001; Reference age ≤64 years), AJCC stage III (for DSS, P = 0.006 and for OS, P = 0.04; Reference: AJCC stage I), and non-surgical treatment (for DSS, P < 0.001 and for OS, P < 0.001; Reference: surgery) were independently associated with worse DSS and OS. In brief, our study demonstrated that SCS mostly found in white people at fifth to seventh decades of life without gender predilection. The patient’s age, AJCC stage, tumor location and surgery were independent prognostic indicators for both DSS and OS of SCS.
Emerging evidence shows that ring finger protein 144A (RNF144A), a poorly characterized member of the Ring‐between‐Ring (RBR) family of E3 ubiquitin ligases, is a potential tumor suppressor gene. However, its regulatory mechanism in breast cancer remains undefined. Here, we report that RNF144A promoter contains a putative CpG island and the methylation levels of RNF144A promoter are higher in primary breast tumors than those in normal breast tissues. Consistently, RNF144A promoter methylation levels are associated with its transcriptional silencing in breast cancer cells, and treatment with DNA methylation inhibitor 5‐Aza‐2‐deoxycytidine (AZA) reactivates RNF144A expression in cells with RNF144A promoter hypermethylation. Furthermore, genetic knockdown or pharmacological inhibition of endogenous methyl‐CpG‐binding domain 4 (MBD4) results in increased RNF144A expression. These findings suggest that RNF144A is epigenetically silenced in breast cancer cells by promoter hypermethylation and MBD4.
Background: To investigate the expression of S1 RNA binding domain 1 (SRBD1) in non-small cell lung cancer tissue and the effects of SRBD1 silencing on the biological behaviors of human non-small cell lung cancer cells, and to explore the molecular mechanism of SRBD1functions in human non-small cell lung cancer cells. Methods: Expressions of SRBD1 in human non-small cell lung cancer tissues and cell lines were examined by immunostaining and RT-PCR. shRNAs of SRBD1 were chemically synthesized and transfected into A549 and NCI-H1299 cells by lentivirus. Cell proliferation was assayed by cell counting, MTT and clone formation. Cell apoptosis was assayed by flow cytometry. Tumorigenicity was assessed by cell injection into BALB/c athymic nude mouse. Gene chip analysis was employed to explore genomic changes in A549 cells. Potential classical signaling pathways, upstream regulators and gene interaction networks were analyzed by Ingenuity Pathway Analysis, and verified by western blot analysis.Results: SRBD1 was specifically expressed in human squamous cell carcinoma and highly expressed in lung cancer cell lines, NCI-H1299, A549 and NCI-H1975. SRBD1 directed-shRNA (shSRBD1) effectively reduced the expression of SRBD1 in A549 and NCI-H1299 cells. SRBD1 silencing inhibited cell proliferation, and promoted cell apoptosis in non-small cell lung cancer cells, and suppressed tumorigenesis in a nude mouse model. In addition, we found silencing of SRBD1 expression resulted in marked changes in gene expression in A549 cells. Besides, in shSRBD1 group, the protein levels of EPS 15, IGF1R, MYC, PYCR1 and HNRNPA0 were downregulated, and the expressions of several classical factors involved in the growth and apoptosis of cancer cells were also decreased.
Conclusions:We found that SRBD1 were specifically expressed in non-small cell lung cancer tissue.Silencing of SRBD1 inhibits cell growth and promotes cell apoptosis in non-small cell lung cancer cells, and suppresses tumorigenesis in vivo, suggesting that SRBD1 may be a new diagnostic indicator and therapeutic target of non-small cell lung cancer.
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