Triple-negative breast cancer (TNBC) is an aggressive subset of breast carcinomas that lack expression of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2). Unlike other breast cancer subtypes, targeted therapy is presently unavailable for patients with TNBC. In spite of initial responses to chemotherapy, drug resistance tends to develop rapidly and the prognosis of metastatic TNBC is poor. Hence, there is an urgent need for novel-targeted treatment methods or development of safe and effective alternatives with recognized mechanism(s) of action. AMP-activated protein kinase (AMPK), an energy sensor, can regulate protein and lipid metabolism responding to alterations in energy supply. In the past 10 years, interest in AMPK has increased widely since it appeared as an attractive targeting molecule for cancer therapy. There has been a deep understanding of the possible role of abnormal AMPK signaling pathways in the regulation of growth and survival and the development of drug resistance in TNBC. The increasing popularity of using AMPK regulators for TNBC-targeted therapy is supported by a considerable development in ascertaining the molecular pathways implicated. This review highlights the available evidence for AMPK-targeted anti-TNBC activity of various agents or treatment strategies, with special attention placed on recent preclinical and clinical advances in the manipulation of AMPK in TNBC. The elaborative analysis of these AMPK-related signaling pathways will have a noteworthy impact on the development of AMPK regulators, resulting in efficacious treatments for this lethal disease.

Idiopathic granulomatous lobular matitis (IGLM) is a rare non-specific inflammatory disease of the breast. Although IGLM is completely benign, it is easily confused with cancer due to progressive breast lump with firmly unilateral and discrete mass, nipple retraction and sinus formation. Patients with IGLM are usually associated with inflammation of the overlying skin. This study aimed to investigate the clinical characteristics of IGLM, treatment options and prognosis. From January 2010 to February 2015, 75 IGLM patients in our hospital were included, with an average age of 35.9 ± 10.0 (range 21-61) years. Most of them were parous. The main clinical characteristic was the presence of a large, irregular and painful mass. Hypoechoic lobulated, irregular tubular or oval shaped masses were detected by breast gland ultrasound. Ill-defined mass, enlarged axillary lymph nodes, asymmetric density, and architectural distortion were found by breast molybdenum palladium X-ray. Diagnosis of IGLM was confirmed with histological examination. The majority (60/75) of the IGLM patients received surgical treatment, including lumpectomy, abscess drainage or mastectomy. Antibiotics were used after surgery. The disease recurred in three patients during the follow-up period. Our study suggested that IGLM diagnosis more depends on CNB and postoperative histopathological examination, and surgery and symptomatic treatment can completely remove the lesions, in order to cure the disease.

Breast cancer has a high incidence worldwide. The results of substantial studis reveal that inflammation plays an important role in the initiation, development, and aggressiveness of many malignancies. The use of celecoxib, a novel NSAID, is repetitively associated with the reduced risk of the occurrence and progression of a number of types of cancer, particularly breast cancer. This observation is also substantiated by various meta-analyses. Clinical trials have been implemented on integration treatment of celecoxib and shown encouraging results. Celecoxib could be treated as a potential candidate for antitumor agent. There are, nonetheless, some unaddressed questions concerning the precise mechanism underlying the anticancer effect of celecoxib as well as its activity against different types of cancer. In this review, we discuss different mechanisms of anticancer effect of celecoxib as well as preclinical/clinical results signifying this beneficial effect.

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