Photodynamic therapy (PDT) is an established therapeutic method, first approved by the FDA for certain kinds of cancer in 1998. There are also increasing data to show that a related procedure, sonodynamic therapy (SDT), is a promising new modality for cancer treatment. Here, the authors report clinical results in 3 advanced refractory breast cancer patients who were treated using a combination of sonodynamic and photodynamic therapy (SPDT), along with conventional therapies. All 3 patients had pathologically proven metastatic breast carcinoma. These widely disseminated carcinomas had ultimately failed to respond to conventional therapy. A new sensitizing agent, Sonoflora 1™ (SF1) was administered sublingually; then, after a 24-hour delay, patients were treated with a combination of light and ultrasound. All patients had significant partial or complete responses. SPDT is a promising new therapeutic combination for the treatment of breast cancer.
SHP2 mediates the activities of multiple receptor tyrosine kinase signaling and its function in endothelial processes has been explored extensively. However, genetic studies on the role of SHP2 in tumor angiogenesis have not been conducted. Here, we show that SHP2 is activated in tumor endothelia. Shp2 deletion and pharmacological inhibition reduce tumor growth and microvascular density in multiple mouse tumor models. Shp2 deletion also leads to tumor vascular normalization, indicated by increased pericyte coverage and vessel perfusion. SHP2 inefficiency impairs endothelial cell proliferation, migration, and tubulogenesis through downregulating the expression of proangiogenic SRY-Box transcription factor 7 (SOX7), whose re-expression restores endothelial function in SHP2-knockdown cells and tumor growth, angiogenesis, and vascular abnormalization in Shp2-deleted mice. SHP2 stabilizes apoptosis signal-regulating kinase 1 (ASK1), which regulates SOX7 expression mediated by c-Jun. Our studies suggest SHP2 in tumor associated endothelial cells is a promising anti-angiogenic target for cancer therapy.
Background: Apical hypertrophic cardiomyopathy (AHCM) is a relatively rare form of hypertrophic cardiomyopathy (HCM), originally described in Japan and later in the West. Limited information is available on this disease in China. Hypothesis: This study was designed to describe clinical features and prognoses of patients with AHCM in China. Methods: A retrospective study of 208 consecutive patients with AHCM examined at FuWai Hospital was performed. Clinical features, mortality, and cardiovascular morbidity were analyzed. Results: The 208 patients with AHCM represented 16.0% of all HCM patients. Among them, 64.4% were pure form and 35.6% were mixed form. Compared with the pure group, the mixed group had a significantly larger left atrial diameter and thicker apical thickness. One hundred ninety-nine patients had a mean follow-up of 8.0 ± 3.5 years, cardiovascular mortality was 1.0%, and annual cardiovascular mortality was 0.1%. The 2 cardiovascular deaths were both mixed form. The probability of survival was 97.0 ± 2% at 10 years. Of the patients, 17.8% had 1 or more cardiovascular events. The probability of survival without morbid events at 10 years was 77 ± 4%. Three independent predictors of cardiovascular morbidity were identified: age at diagnosis ≥60 years, left atrial diameter ≥36 mm, and New York Heart Association class ≥III at baseline. Conclusions:The prevalence of AHCM is relatively high, and it has a benign prognosis in China. However, 17.8% of patients may develop cardiovascular events. It is important to distinguish the 2 phenotypes of AHCM; the mixed form is less common but more serious than the pure form.
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