A Giant Borderline Phyllodes Tumor of Breast With Skin Ulceration Leading to Non-Insular Tumorigenic Hypoglycemia: A Case Report and Literature Review.

Phyllodes tumor (PT) is a special type of breast tumors, including three types: malignant, borderline, and benign. Most of these tumors form unilateral disease and can rapidly increase in size. The occurrence of axillary lymph node metastasis is rare. Tumor-associated hypoglycemia can be divided into non-islet cell tumor and insulinoma. In non-islet cell tumor hypoglycemia (NICTH), a considerable high molecular weight form of insulin like growth factor 2 (IGF-2) is formed, which abnormally binds to insulin receptors in the tissues and causes hypoglycemia. Breast phyllodes tumors with NICTH are rare and first reported in 1983. Surgical resection is the main treatment and hypoglycemia symptoms usually resolve after surgery. Nevertheless, prior to surgery, intravenous glucose infusion is used to maintain blood glucose levels. A female patient presented with a rapidly growing breast mass and was diagnosed with a phyllodes tumor with NICTH at our hospital in August 2020; she was successfully treated through surgical resection. We reviewed the relevant literature to investigate and analyze the relationship between NICTH and phyllodes tumors, as well as optimize its diagnosis and treatment.

Expert consensus workshop report: Guidelines for thermal ablation of thyroid tumors (2019 edition).

As a treatment option for cancer, thermal ablation has satisfactory effects on many types of solid tumors (such as liver and renal cancers). However, its clinical applications for the treatment of thyroid nodules and metastatic cervical lymph nodes are still under debate both in China and abroad. In 2015, the "Zhejiang Expert consensus on thermal ablation for thyroid benign nodules, microcarcinoma, and metastatic cervical lymph nodes (2015 edition)," was released by the Thyroid Cancer Committee of Zhejiang Anti-Cancer Association, China. To further standardize the application of thermal ablation for thyroid tumors, the Thyroid Tumor Ablation Experts Group of Chinese Medical Doctor Association has organized many seminars and finally produced a consensus to formulate the "Expert consensus workshop report: Guidelines for thermal ablation of thyroid tumors (2019 edition)."

Inflammatory myofibroblastic tumor of the neck with thyroid invasion: a case report and literature review.

Inflammatory myofibroblast tumor (IMT) is a unique intermediate soft tissue tumor, comprising myofibroblasts/fibroblasts, with infiltrating plasma cells, lymphocytes, and/or eosinophils. IMT, first reported in 1939 in the lung or pleura, is most common in children or adolescents and in the lungs; however, it can also occur in other tissues. The exact etiology and pathogenesis of IMT are yet to be clarified. Virus-induced trauma, surgery, autoimmune etiology, inflammation, infection, and abnormal responses to long-standing exogenous stimuli in the body, dominated by myofibroblast proliferation, can lead to IMT development. Most patients with IMT have masses, with or without physical manifestations, including fever, weight loss, and various clinical laboratory abnormalities. Surgical resection is the main treatment. IMT is not common in the head and neck region, and additional thyroid involvement is rare. A male patient presented a rapidly growing neck mass was treated and diagnosed with IMT in the neck and thyroid involvement in our hospital in September 2018 by successful surgical resection. Follow-up for 6 months showed no recurrence or metastasis. We review the etiology, clinical features, pathological features, treatment, and prognosis of IMT, with the aim of improving the diagnosis and treatment of this condition in the head and neck region.

Therapy With Carboplatin and Anti-PD-1 Antibodies Before Surgery Demonstrates Sustainable Anti-Tumor Effects for Secondary Cancers in Mice With Triple-Negative Breast Cancer.

Patients with triple-negative breast cancer (TNBC) suffer an unfavorable prognosis. Carboplatin (CBDCA) as a cytotoxic reagent has been widely administered to patients with cancer including TNBC. Programmed cell death protein 1 (PD-1) is an immune checkpoint, blockade of which unleashes T cell functions that kill cancer cells. However, the efficacy of CBDCA combined with anti-PD-1 antibodies in TNBC has not been determined. Patient-derived xenografts (PDX) were implanted to immune-deficient mice. Three mouse TNBC cell lines (4T1, EMT6, and E0771) were seeded to immune-competent mice. Tumor volumes and survival rates were monitored. CBDCA and anti-PD-1 antibodies were administered by intra-peritoneal injection at designated time points. Total CD8+ T cells, memory CD8+ T cells, and CD103+ dendritic cells (DC) in the tumor were measured by flow cytometry. Tumor-specific CD8+ T cells were quantified by the ELISpot assay. Administration of CBDCA to PDX-bearing mice induced increased levels of tumor cell necrosis and reduced tumor size. Treatment with CBDCA and anti-PD-1 antibodies reduced TNBC tumor volumes and slightly improved survival rates. More importantly, therapy with CBDCA and anti-PD-1 antibodies before surgery showed a remarkably improved, sustainable protection against a secondary tumor after surgery by a CD8+- T-cell-dependent manner, which required CCL4 expressed in the tumor and subsequently CD103+ DC recruited to the tumor microenvironment. Immunochemotherapy with CBDCA and anti-PD-1 antibodies before surgery improves the outcome of a secondary tumor after surgery via increasing the number of tumor-specific CD8+ T cells in the tumor microenvironment of murine TNBC. These results highlight the possibility to utilize this regimen in clinical practice.

Roxatidine inhibits fibrosis by inhibiting NF­κB and MAPK signaling in macrophages sensing breast implant surface materials.

Capsular contracture is an important complication after silicone mammary implant surgery. Fibroblasts and macrophages play critical roles in the pathogenesis of capsular contracture, making these two cell types therapeutic targets. It has been reported that inhibiting histamine receptors results attenuates fibrosis, but the role of roxatidine (a histamine receptor 2 inhibitor) in preventing fibrosis caused by breast implant materials remains unknown. The aim of the present study was to assess the hypothesis that roxatidine might have a prophylactic effect in capsular contracture induced by implant material. Inflammation induced by breast implant materials was mimicked by co­culturing macrophages or fibroblasts with these materials in vitro. Capsular contracture was modeled in mice by planting breast implant materials in a subcutaneous pocket. Roxatidine was added in the culture medium or administered to mice bearing breast implant materials. By co­culturing macrophages or fibroblasts with common breast implant materials (micro­textured or smooth breast implants), the present study demonstrated that macrophages respond to these materials by producing pro­inflammatory cytokines, a process that was abolished by addition of roxatidine to the culture medium. Although fibroblasts did not respond to implant surface materials in the same way as macrophages, the conditioned media of macrophages induced proliferation of fibroblasts. Mechanistically, administration of roxatidine inhibited activation of NF­κB and p38/mitogen­activated protein kinase (MAPK) signaling in macrophages. Furthermore, treatment with roxatidine in implant­bearing mice reduced serum concentrations of transforming growth factor­ß and the abundance of fibroblasts around the implant. The present study concluded that roxatidine plays an important role in preventing fibrosis by inhibiting activation of NF­κB and p38/MAPK signaling in macrophages.

Long noncoding RNA SBF2-AS1 promotes colorectal cancer proliferation and invasion by inhibiting miR-619-5p activity and facilitating HDAC3 expression.

Evidence, demonstrating long noncoding RNAs (lncRNAs) as critical players in cancer, remains to increase. lncRNA SBF2-AS1 was reported to be involved in several cancers, such as hepatocellular carcinoma. However, the role of SBF2-AS1 in colorectal cancer (CRC) is unknown. We showed lncRNA SBF2-AS1 expression was growing in CRC samples, especially in advanced cases. Accordingly, SBF2-AS1 possesses higher expression in CRC cell lines than in normal cell line. Moreover, SBF2-AS1 high expression indicated a low survival rate. Functionally, SBF2-AS1 knockdown suppressed the proliferation, migration, and invasion of CRC cells. In terms of mechanism, SBF2-AS1 upregulation restrained the activity of miR-619-5p and led to overexpression of HDAC3. Importantly, downregulation of miR-619-5p or HDAC3 overexpression reversed SBF2-AS1-silencing-caused suppression on proliferation and metastasis. Summarily, our findings elucidated a crucial role of SBF2-AS1 as a miR-619-5p sponge, shedding novel light on lncRNA-related prognostics.

C-C motif chemokine ligand 5 (CCL5) levels in gastric cancer patient sera predict occult peritoneal metastasis and a poorer prognosis.

Gastric cancer is one of the most common cancers and the third leading cause of cancer death worldwide. A number of chemokines and cytokines play important roles in the progress of gastric cancer. The roles of C-C motif chemokine ligand 5 (CCL5) in gastric cancer remain unclear. Here, we retrospectively report an analysis of 105 patients with gastric cancer. Increased levels of CCL5 in circulation were correlated with more advanced T and N stages, poorly- or un-differentiated histological types, peritoneal metastasis, higher rates of residual tumor, and shorter survivals. Patients in the CCL5 High Group had stronger CCL5 immunohistochemistry (IHC) staining in tumor beds. Circulating CCL5 concentrations before surgery are a good biomarker for occult peritoneal metastasis. Elevated levels of serum CCL5, along with strong IHC CCL5 staining and poorly- or un-differentiated cancer are predictors for poorer outcomes. In conclusion, increased serum levels of CCL5 can be used to predict peritoneal dissemination and a poorer prognosis.

Interleukin (IL)-4 -590C>T polymorphism is not associated with the susceptibility of gastric cancer: An updated meta-analysis.

Gastric cancer (GC) is a common cancer affecting patients around the world. The pathogenesis of gastric cancer has not been understood completely. Genetic mutations and the inflammation induced by Helicobacter pylori (HP) seem to play important roles. The cytokine Interleukin-4 (IL-4) has effects in inflammation, allergies and cancer including GC. The association of IL-4 -590 C>T polymorphism and gastric cancer has been studied in different populations with inconsistent results. Here, we report this meta-analysis showing that the polymorphism of IL-4 -590C>T might not be associated with the GC susceptibility in both Asian and Caucasian populations.

The early diagnostic value of C-reactive protein for anastomotic leakage post radical gastrectomy for esophagogastric junction carcinoma: A retrospective study of 97 patients.

BACKGROUND/AIMS: The incidence of esophagogastric junction (EGJ) carcinoma has increased worldwide. The only curable strategy for EGJ carcinoma is surgery, whereas anastomotic leakage is the major complication after operations. We aimed to test whether the serum levels of C-reactive protein have the diagnostic value for anastomotic leakage after surgery for EGJ carcinoma. METHODS: In this study, we analyzed the values of CRP before and 5 continuous days after surgery in 97 EGJ carcinoma patients who received surgery as the initial treatment. The levels of CRP in the groups of EGJ patients with or without anastomotic leakage were compared. RESULTS: The CRP levels of patients with anastomotic leakage elevated faster and remained higher compared patients without anastomotic leakage. The CRP value at Day 2 after radical surgery for EGJ carcinoma patients has the early diagnostic value for anastomotic leakage. The cut-off value of CRP for anastomotic leakage at Day 2 is 177 mg/l with the sensitivity of 0.9 and specificity of 0.95 (P < 0.0001). CONCLUSION: Surgical EGJ carcinoma patients with elevated CRP at Day 2 after surgery should be excluded the possibility of anastomotic leakage.

Heme oxygenase-1 modulates thrombomodulin and activated protein C levels to attenuate lung injury in cecal ligation and puncture-induced acute lung injury mice.

Acute lung injury (ALI) is often associated with sepsis and is the most common cause of acute respiratory failure. The authors evaluated the role of the heme oxygenase (HO)/carbon monoxide (CO) system on lung injury in a cecal ligation and puncture (CLP)-induced mouse model of ALI. The authors established CLP-induced ALI in C57BL/6 mice. They pretreated CLP-induced mice with HO-1 inducer (hemin) or HO-1 inhibitor (Zn protoporphyrin [Znpp]) and determined various lung injury parameters including partial pressure of arterial oxygen, thrombosis, edema, and plasma malondialdehyde (MDA), and myeloperoxidase (MPO) level. Enzyme-linked immunosorbent assay (ELISA) was performed to measure plasma thrombomodulin (TM) and activated protein C (APC) levels. TM and HO-1 expression in lung tissue was evaluated by immunofluorescence staining and Western blotting. Survival rate was also monitored. CLP-induced ALI was associated with decreased partial pressure of arterial oxygen, and increased thrombosis, edema, and plasma MDA, and MPO level. Plasma TM was significantly up-regulated, whereas cell surface TM in lung tissue was significantly decreased in the CLP group compared to the sham animals. Pretreatment with hemin caused up-regulation of HO-1 expression and improved partial pressure of arterial oxygen. Hemin pretreatment also caused a significant decrease in plasma TM along with increased cell surface TM expression in lung tissue, suggesting attenuation of lung injury. Survival data showed that no difference for survival between CLP animals pretreated with hemin or Znpp. Taken together, HO-1 exerts its protective effects on CLP-induced ALI via regulating cell surface TM and APC expression and modulating blood coagulation.