The prognosis for patients with refractory soft-tissue sarcoma (STS) is dismal. Anlotinib has previously shown antitumor activity on STS in preclinical and phase I studies. Patients 18 years and older, progressing after anthracycline-based chemotherapy, naïve from angiogenesis inhibitors, with at least one measurable lesion according to RECIST 1.1, were enrolled. The main subtypes eligible were undifferentiated pleomorphic sarcoma (UPS), liposarcoma (LPS), leiomyosarcoma (LMS), synovial sarcoma (SS), fibrosarcoma (FS), alveolar soft-part sarcoma (ASPS), and clear cell sarcoma (CCS). Participants were treated with anlotinib. The primary endpoint was progression-free rate at 12 weeks (PFR). A total of 166 patients were included in the final analysis. Overall, the PFR was 68%, and objective response rate was 13% (95% confidence interval, 7.6%-18%). The median progression-free survival (PFS) and overall survival (OS) were 5.6 and 12 months, respectively. The PFR, median PFS and OS were: 58%, 4.1 and 11 months for UPS ( = 19); 63%, 5.6 and 13 months for LPS ( = 13); 75%, 11 and 15 months for LMS ( = 26); 75%, 7.7 and 12 months for SS ( = 47); 81%, 5.6 and 12 months for FS ( = 18); 77%, 21 and not reached for ASPS ( = 13); 54%, 11 and 16 months for CCS ( = 7); and 44%, 2.8 and 8.8 months for other sarcoma ( = 23), respectively. The most common clinically significant grade 3 or higher adverse events were hypertension (4.8%), triglyceride elevation (3.6%), and pneumothorax (2.4%). No treatment-related death occurred. Anlotinib showed antitumor activity in several STS entities. The toxicity was manageable. .
The ultimate goal of phototherapy based on nanoparticles, such as photothermal therapy (PTT) which generates heat and photodynamic therapy (PDT) which not only generates reactive oxygen species (ROS) but also induces a variety of anti-tumor immunity, is to kill tumors. In addition, due to strong efficacy in clinical treatment with minimal invasion and negligible side effects, it has received extensive attention and research in recent years. In this paper, the generations of nanomaterials in PTT and PDT are described separately. In clinical application, according to the different combination pathway of nanoparticles, it can be used to treat different diseases such as tumors, melanoma, rheumatoid and so on. In this paper, the mechanism of pathological treatment is described in detail in terms of inducing apoptosis of cancer cells by ROS produced by PDT, immunogenic cell death to provoke the maturation of dendritic cells, which in turn activate production of CD4+ T cells, CD8+T cells and memory T cells, as well as inhibiting heat shock protein (HSPs), STAT3 signal pathway and so on.
A recent study reported that Botulinum toxin type A (BTXA) could inhibit the growth of hypertrophic scars and improve their appearance. However, the mechanism of BTXA’s action on hypertrophic scars is still unknown. Some in vitro studies had shown BTXA could alleviate hypertrophic scars by acting on the biological behavior of fibroblasts, but there are few in vivo experiments, especially animal model experiments, supporting these findings. The aim of the study reported herein was to investigate the effect of BTXA on collagen deposition on hypertrophic scars in a rabbit ear model and partially clarify the mechanism of BTXA on the hypertrophy of scars. The rabbit hypertrophic scar model was used and eight rabbits were employed. BTXA was injected into the hypertrophic scar tissue of one ear; and the other ear in the same rabbit was the control without BTXA injection. The scar thickness and deposition of collagen was examined through immune histochemistry including haematoxylin and eosin (H&E) and Masson trichrome staining. The thicknesses of hypertrophic scars in the BTXA treatment group were obviously lower than in the control groups (P < 0.01). H&E and Masson staining showed that collagen fibers were stained blue. Compared with the treatment group, the collagen fibers were thicker and the arrangement of collagen fibers were disordered in the control group. This study used the rabbit ear model of hypertrophic scars to assess the effects of BTXA on scar hypertrophy. The application of BTXA may be useful for inhibiting hypertrophic scars.
BackgroundMDM4 is the important negative regulator of the tumor suppressor protein p53, which is overexpressed in various human cancers. This study evaluates the MDM4 expression in patients with gastric adenocarcinoma (GTAC) at the mRNA and protein levels and examines relationships among MDM4 expression, clinicopathological features, and prognosis.ResultsThe qRT-PCR and the Western blot analysis showed that the MDM4 expression level was high in GTACN+ but not in GTACN−. The high expression level of MDM4 was significantly associated with age (P = 0.047), lymph node metastasis (LNM) (P < 0.001), pathological stage (P < 0.001), differentiation status (P = 0.001), and preoperative serum CA19-9 level (P < 0.001). Moreover, the survival analysis showed that Borrmann type, depth of invasion, LNM, and preoperative serum CA19-9 level were independent prognostic factors. The univariate analysis revealed that MDM4 expression influenced GTAC prognosis. Furthermore, the influence of overall prognosis relies on whether or not the high MDM4 expression level could lead to LNM.Materials and MethodsWe investigated MDM4 expression in primary GTAC and paired normal gastric tissues (30 pairs) through qRT-PCR and Western blot analyses. We also performed immunohistochemistry analysis on 336 paraffin-embedded GTAC specimens and 33 matched normal specimens.ConclusionsMDM4 expression may result in LMN of GTAC. High MDM4 expression levels are associated with LMN of GTAC and influence the prognosis of patients with GTAC.
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