The junctional adhesion molecule (JAM) family is a key molecule in a process called transendothelial migration or diapedesis. Here, we report implications of JAM-C in cancer metastasis. We first determined the mRNA expression of JAMs in 19 kinds of cancer cell lines. JAM-C was expressed in most of tumors having potent metastatic properties. Especially in murine K-1735 melanoma cell lines, the highly metastatic sublines (M2 and X21) strongly expressed JAM-C when compared with the poorly metastatic ones (C-10 and C23). Next, we investigated the role of JAM-C in cancer metastasis by using human JAM-C (hJAM-C) gene-transfected HT1080 fibrosarcoma cells. In comparison with mock-transfected HT1080 cells, these cells showed a significant increase in the adhesion to various extracellular substrates and the invasion across a Matrigel TM -coated membrane. The knockdown of hJAM-C using small interfering RNA resulted in the suppression of both the adhesion and the invasion of HT1080 cells, suggesting that endogenous hJAM-C might be involved in tumor metastasis. Finally, we studied the role of hJAM-C in an in vivo experimental metastatic model. The results showed that the overexpression of hJAM-C in HT1080 cells significantly decreased the life spans of the tumorbearing mice. In contrast, the knockdown of hJAM-C in HT1080 cells suppressed the weight gain of the lungs with metastatic colonies. We conclude that the expression of JAM-C promotes metastasis by enhancing both the adhesion of cancer cells to extracellular matrices and the subsequent invasion.Cancer metastasis involves a series of events that include dissociation of malignant cells from a primary site, polarized proteolysis and migration, intravasation into the circulatory system, and adhesion to the vascular endothelium followed by extravasation, invasion, and growth at distant sites (1). Certain cell surface molecules are known to be involved in these processes. For instance, integrins play central roles in regulating cell adhesion, motility, invasion, and angiogenesis (2-4), and matrix metalloproteinases on tumor cells can degrade the extracellular matrix (ECM) 2 (5). In particular, cell adhesion molecules play key roles in tumor adhesion and invasion, resulting in metastasis (6). When compared with normal tissues, malignant tumors are characterized by disrupted tissue architecture and deranged differentiation. Changes in the expression or function of cell adhesion molecules contribute to tumor progression both by altering the adhesion status of the cell and by affecting cell signaling (7). It has been reported that alteration of cell-cell and/or cell-matrix interactions accounts for the ability of cancerous cells to cross tissue boundaries and to disseminate to distant sites. Many adhesion molecules implicated in tumor metastasis have been identified (6), and certain of them belong to the immunoglobulin superfamily (8). Recently, the junctional adhesion molecule (JAM) family, a member of the immunoglobulin superfamily, has become a focus of study in relation to ...
The effects of orally administered sphingomyelin-based liposomes (SM-lipo) on muscle function were investigated in senescence-accelerated mice prone 1 (SAMP1) for the purpose of protection against or treatment of sarcopenia. SM-lipo were prepared by thin lipid-film hydration followed by extrusion. Their spherical shape was observed by transmission electron microscopy. The obtained liposomes were stable in gastric liquid and intestinal fluid models as well as in water. In in vitro tests liposomalization of sphingomyelin significantly increased its transport into human intestinal epithelial Caco-2 cells. In addition, SM-lipo upregulated the proliferation of murine C2C12 myoblasts compared with free sphingomyelin or phosphatidylcholine-based liposomes (PC-lipo). Finally, SM-lipo orally administered to SAMP1 for 10 weeks significantly increased quadriceps femoris weight and extended swimming time until fatigue compared with PC-lipo. In conclusion, these findings indicate that SM-lipo are well absorbed into the body and improve muscle weakness caused by senescence.Key words sarcopenia; sphingomyelin; senescence-accelerated mouse; liposome; muscle Loss of muscle mass induces a progressive decline in physical performance; and it also leads to decrease in quality of life, including increased risk of disability and mortality. 1)This age-related deficit is known as sarcopenia. Sarcopenia is a progressive, insidious process characterized by a 3-8% reduction in lean muscle mass. The etiology of sarcopenia is multi-factorial and involves both intrinsic and extrinsic factors.2,3) Increasing muscle mass is important to prevent sarcopenia. The promising approaches for increasing muscle mass are exercise training and proper nutrition. Exercise training is generally accepted as a useful strategy to increase the number of mitochondria and the expression of mitochondria-associated proteins, as well as to improve the function of mitochondria in muscle.4) Food nutrients such as sphingolipids, leucine, creatine, and whey protein are known to be involved in increasing muscle mass. 5-7)Sphingolipids were first characterized by Thudichum, who studied the chemical constituents of brain tissue; whereupon he named their novel and characteristic "sphingosine" backbone for "the many enigmas it has presented to the inquirer." 8) Most foods contain sphingolipids. Humans on an ordinary Western diet ingest 0.3-0.4 g of sphingolipids per day, of which sphingomyelin in meat, milk, egg products, and soybeans is a large part.9-11) Also, sphingolipids are highly bioactive molecules present mainly in polar lipids of animal origin 9) and the second most abundant polar lipid next to phosphatidylcholine in plasma lipoproteins 12) ; and they are associated with cellular signaling, insulin resistance, metabolic disease, dementia, and so on. 13,14) As a type of sphingolipid, sphingomyelin in mammalian cells is co-localized with cholesterol mainly in the plasma membrane and in lysosomal and Golgi membranes. Dietary supplementation with sphingomyelin combined ...
Purpose We report the treatment results of AVAgamma therapy combining gamma knife (GK) and bevacizumab (Bev) for recurrent glioblastoma. Subjects From August 2013 to July 2022, 56 patients with recurrent glioblastoma treated with AVAgamma therapy as salvage therapy at the time of relapse after initial treatment. When the irradiation volume of GK was 15 ml or less, a single irradiation with a marginal dose of 20 to 26 Gy was performed. More than that received a single marginal dose of 12-15 Gy in two fractions or 8 Gy in three fractions. The mean therapeutic marginal dose was 23.9 Gy. Bev was administered 10 mg / kg or 15 mg / kg 1 to 10 times after GK. Methods Median progression-free survival (mPFS) and median survival (mOS) from AVAgamma treatment, and mOS and 5-year survival rate from initial treatment were compared with historical controls (GK group: 30 patients) who received only GK at the time of recurrence. Results The mPFS from AVAgamma therapy was 6 months, PFS-6m was 39%, OS-6m was 76%, and mOS was 10 months. The mOS from initial treatment was 25 months, which was prolonged compared to 21 months in the GK group (p=0.05). The 5-year survival rate for recurrent glioblastoma was 5% in the GK group and 22% in the AVAgamma group (p=0.04). The 5-year survival rate for glioblastoma with KPS is 70% or more at recurrence was 0% in the GK group and 33% in the AVAgamma group (p=0.017). Discussion Combined use of Bev with GK was considered to provide local control of recurrent lesions and prolong life prognosis in patients with good KPS at the time of recurrence. Conclusion AVAgamma therapy is thought to prolong the survival of recurrent glioblastoma and play an important role as salvage treatment.
BACKGROUND Idiopathic spinal cord herniation (ISCH) is very rare. Some reports have described postoperative ventral cerebrospinal fluid (CSF) collections in patients with ISCH; however, such collections are asymptomatic in most patients, and there is no consensus regarding whether they are part of the natural history or a complication. OBSERVATIONS A 30-year-old man with ISCH underwent direct closure of a duplicated dura mater. Eight months postoperatively, he developed reworsening of right lower limb paresis and new severe right arm pain and paresis. Three-dimensional magnetic resonance imaging revealed ventral CSF collections, which the authors judged as the responsible lesions. The authors initially considered these collections to be present in the epidural space, extradurally compressing the dural sac and resulting in myelopathy. An epidural blood patch failed; however, a CSF drainage test resulted in dramatic improvement. The authors therefore determined that the CSF collections were located in the interdural space, not the epidural space. A lumboperitoneal (LP) shunt was performed to reduce the CSF pressure. The patient’s symptoms improved immediately postoperatively. He had developed no recurrence of symptoms 6 months after surgery. LESSONS Ventral interdural CSF collections after ISCH surgery can cause reworsening of myelopathy and may be cured by a LP shunt to control CSF pressure.
PURPOSE We report the treatment results of AVAgamma therapy combining gamma knife (GK) and bevacizumab for recurrent glioblastoma. SUBJECTS From August 2013 to April 2018, 42 patients (183 lesions) with recurrent glioblastoma treated with AVAgamma therapy as salvage therapy at the time of relapse after initial treatment. The average age is 61.1 years, with 25 men and 17 women. The tumor volume is 100 ml or less, and KPS is 40% or more as the indication of AVAgamma therapy. When the irradiation volume of GK is 15 ml or less, a single irradiation with a boundary dose of 20 Gy was performed, and when the irradiation volume was 15 ml or more, a single irradiation boundary dose was divided into two divided irradiations of 12 to 15 Gy. The mean therapeutic borderline dose was 24 Gy. Bevacizumab was administered 10 mg / kg or 15 mg / kg 1 to 10 times after GK. METHODS Median progression-free survival (mPFS), 6-month progression-free survival (PFS-6m), 6-month survival (OS-6m), median survival (mOS) from treatment with AVAgamma Considered mOS from initial treatment. [Results]: The mPFS from AVAgamma therapy was 5 months, PFS-6m was 37%, OS-6m was 84%, and mOS was 9 months. The mOS from initial treatment were 25 months. In relapsing glioma RPA classification, NABTT CNC class 5 mOS is 5.6 months, class 6 mOS is 6.4 months, but mOS from AVAgamma therapy is 9 months in class 5, 9 months in class 6. The survival time has been extended. DISCUSSION By AVAgamma therapy, it was thought that recurrent lesions were locally controlled and life prognosis was prolonged. CONCLUSION AVAgamma therapy is thought to prolong the survival of recurrent glioblastoma and play an important role as salvage treatment.
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