The objective of this study was to investigate the clinical characteristics and surgical modality of plasma cell mastitis (PCM). A total of 93 breasts of 91 female patients with PCM from June 2003 to June 2010 (unilateral in 89 patients and bilateral in two patients) were investigated in this study. All breasts were divided into two groups: the direct excision group (DE group) received focused excision and nipple retraction correction; and the incision drainage group (ID group) received these procedures only in the event of failing at least two incision drainages. Clinical characteristics, extent of excision, and prognosis were compared between two groups. There were 53 breasts in the DE group and 40 breasts in the ID group. No significant differences were noted in the number of retracted nipples and abscesses in the first visit or extent of disease between two groups ( P > 0.05). However, during surgery, 3.85 ± 0.97 abscesses per breast were detectable in the ID group, which was significantly higher than 1.21 ± 0.06 abscesses per breast in the DE group. The ID group had significantly higher inflammation and excised extent compared with the DE group ( P < 0.05). Hospitalization time was 179.60 ± 14.8 days in the ID group, which was significantly higher than 22.49 ± 1.93 days in the DE group ( P < 0.05). Bacterial culture was negative for pus of 39 non-rupturing abscesses. Congenital nipple retraction may be the primary cause of PCM. Early and complete focused excision and nipple retraction correction are effective treatment methods.
Triple negative breast cancer (TNBC) is a highly aggressive cancer and lack of targeting therapies. It is believed that the breast cancer stem cells (BCSCs) are responsible for the aggressive characteristics of TNBC. Hence, developing BCSC-targeting agents may provide new therapeutic strategies for the patients. Huaier polysaccharide (HP), an active ingredient extracted from the mushroom
Murr, has been widely used in clinical anti-cancer treatments in China. Here we demonstrated that HP could target BCSCs in TNBC cells, resulting in decreased mammosphere formation, downregulated expression of stem-related genes and reduced proportion of aldehyde dehydrogenase positive cells
and inhibited xenograft tumor formation
. Mechanically, HP markedly reduced the expression of estrogen receptor α-36 (ERα-36), a recently identified subtype of estrogen receptor α, and attenuated ERα-36-mediated activation of AKT/β-catenin signaling in ERα-36
TNBC cells. This study provides a new insight into the mechanism of HP on BCSC-targeting therapy and new ideas for comprehensive treatment strategies for TNBC.
BackgroundBreast conservation therapy (BCS) after neoadjuvant chemotherapy (NCT) can improve patients’ quality of life. Currently used intraoperative examination for negative margins may not be sufficient to detect microresidual foci, which are a risk factor for local recurrence. This study was conducted to investigate the shrinking pattern of breast cancer and residual tumors as a risk factor for BCS after NCT.MethodsNinety women with stage II or III invasive ductal carcinoma who achieved partial response after NCT with paclitaxel and epirubicin were enrolled. All patients had undergone modified radical mastectomy. One-half of the surgical specimens were subjected to subserial sectioning. Pathological changes of tumor bed and pericancerous tissues were examined with an optical microscope. The levels of estrogen receptors, progesterone receptors and HER2 were analyzed by immnohistochemical staining.ResultsThe residual tumors were classified into three types according to their microscopic morphology: solitary lesion, multifocal and patchlike lesions, and main residual tumor with satellite lesions. Type I residual tumors were found in 55 patients (61%), type II in 30 patients (33%) and type III in 5 patients (6%). Types II and III were often associated with larger primary tumors. The types of residual tumors were not correlated with the status of hormone receptors or HER2.ConclusionThree types of residual tumors were observed after NCT. The solitary residual tumor is most common, but main residual tumors with satellite lesions are most likely to cause local recurrence after BCS. Subserial sectioning would improve the identification of microfoci and patient survival after BCS.
The role of Wilms' tumor 1 (WT1) in breast cancer and the relationship between WT1 expression and clinicopathological factors, molecular subtypes and prognosis of breast cancer patients have not been clarified to date. We used publicly available microarray datasets of 266 early breast cancer patients to perform bioinformatics analysis on the relationship between WT1 mRNA expression and breast cancer. Results showed that WT1 mRNA expression was correlated with higher histological grades, ER-negative and basal-like and ERBB2 molecular subtypes in breast cancer. With regard to disease-free survival analysis, the WT1 high expression group showed worse prognosis than the low expression group in univariate analysis, and WT1 was demonstrated to be an independent prognostic indicator in multivariate analysis. This study confirms an oncogenic role of WT1 and demonstrates a possible relation between WT1 and progression of breast cancer.
Acute pancreatitis is an inflammatory disorder of the pancreas associated with substantial morbidity and mortality, which is characterized by a rapid depletion of glutathione (GSH). Cysthionine-β-synthase (CBS) is a key coenzyme in GSH synthesis, and its deficiency is related to a variety of clinical diseases. However, whether CBS is involved in the pathogenesis of acute pancreatitis remains unclear. First, we found that CBS was downregulated in both in vivo and in vitro AP models. The pancreatic damage and acinar cell necrosis related to CBS deficiency were significantly improved by VB 12, which stimulated clearance of reactive oxygen species (ROS) by conserving GSH. Furthermore, EX-527 (a specific inhibitor of SIRT1) exposure counteracted the protective effect of VB 12 by promoting oxidative stress and aggravating mitochondrial damage without influencing CBS, indicating that vitamin B12 regulates SIRT1 to improve pancreatical damage by activating CBS. In conclusion, we found that VB 12 protected acute pancreatitis associated with oxidative stress via CBS/SIRT1 pathway.
Platelets play a central role in hemostasis and thrombosis, regulating the occurrence and development of thrombotic diseases, including ischemic stroke. Programmed death ligand 1 (PD-L1) has recently been detected in platelet, while the function of PD-L1 in platelets remain elusive. Our data reveal a novel mechanism for the role of PD-L1 on platelet activation and arterial thrombosis. PD-L1 knockout does not affect platelet morphology, count, and mean volume under homeostasis and without risk of bleeding, which inhibits platelet activation by suppressing outside-in-activation of integrin by downregulating the Caspase-3/GSDME pathway. Platelet adoptive transfer experiments demonstrate that PD-L1 knockout inhibits thrombosis. And the absence of PD-L1 improves ischemic stroke severity and increases mice survival. Immunohistochemical staining of the internal structure of the thrombus proves that PD-L1 enhances the seriousness of the thrombus by inhibiting platelet activation. This work reveals a regulatory role of PD-L1 on platelet activation and thrombosis while providing novel platelet intervention strategies to prevent thrombosis.
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