The Effectiveness of Peer Support for Cancer Patients: Potential of activities based on Cancer Philosophy

　　The Objectives of this study is to review various peer support practices of cancer survivors in Japan and to find effective support components. We reviewed the materials on cancer peer support published by the government and research papers on cancer peer support in the fields of psychology and nursing. National peer support activities include training of peer supporters to provide counseling and support by cancer survivors; however, these activities are not very widespread. On the other hand, where peer support activities are carried out effectively, dialogue between the peer who supports cancer patients and the patient receiving the support is on an equal footing. The Cancer Philosophy Clinic Medical Café started by Dr. Okio HINO is one such activity. A medical café has the effect of raising positive emotions and lowering negative emotions, and contribute to cancer education. The perspective of peers supporting and interacting on an equal footing is important for effective peer support activities. In peer support by the government, rather than providing counseling training to those who practice peer support, activities will develop and last longer by creating a relationship in which people can talk freely on the same level as peers

Knockdown of COPA, Identified by Loss-of-Function Screen, Induces Apoptosis and Suppresses Tumor Growth in Mesothelioma Mouse Model

AbstractMalignant mesothelioma is a highly aggressive tumor arising from serosal surfaces of the pleura and is triggered by past exposure to asbestos. Currently, there is no widely accepted treatment for mesothelioma. Development of effective drug treatments for human cancers requires identification of therapeutic molecular targets. We therefore conducted a large-scale functional screening of mesothelioma cells using a genome-wide small interfering RNA library. We determined that knockdown of 39 genes suppressed mesothelioma cell proliferation. At least seven of the 39 genes—COPA, COPB2, EIF3D, POLR2A, PSMA6, RBM8A, and RPL18A—would be involved in anti-apoptotic function. In particular, the COPA protein was highly expressed in some mesothelioma cell lines but not in a pleural mesothelial cell line. COPA knockdown induced apoptosis and suppressed tumor growth in a mesothelioma mouse model. Therefore, COPA may have the potential of a therapeutic target and a new diagnostic marker of mesothelioma

LRRN4 and UPK3B Are Markers of Primary Mesothelial Cells

Mesothelioma is a highly malignant tumor that is primarily caused by occupational or environmental exposure to asbestos fibers. Despite worldwide restrictions on asbestos usage, further cases are expected as diagnosis is typically 20–40 years after exposure. Once diagnosed there is a very poor prognosis with a median survival rate of 9 months. Considering this the development of early pre clinical diagnostic markers may help improve clinical outcomes.Microarray expression arrays on mesothelium and other tissues dissected from mice were used to identify candidate mesothelial lineage markers. Candidates were further tested by qRTPCR and in-situ hybridization across a mouse tissue panel. Two candidate biomarkers with the potential for secretion, uroplakin 3B (UPK3B), and leucine rich repeat neuronal 4 (LRRN4) and one commercialized mesothelioma marker, mesothelin (MSLN) were then chosen for validation across a panel of normal human primary cells, 16 established mesothelioma cell lines, 10 lung cancer lines, and a further set of 8 unrelated cancer cell lines.Within the primary cell panel, LRRN4 was only detected in primary mesothelial cells, but MSLN and UPK3B were also detected in other cell types. MSLN was detected in bronchial epithelial cells and alveolar epithelial cells and UPK3B was detected in retinal pigment epithelial cells and urothelial cells. Testing the cell line panel, MSLN was detected in 15 of the 16 mesothelioma cells lines, whereas LRRN4 was only detected in 8 and UPK3B in 6. Interestingly MSLN levels appear to be upregulated in the mesothelioma lines compared to the primary mesothelial cells, while LRRN4 and UPK3B, are either lost or down-regulated. Despite the higher fraction of mesothelioma lines positive for MSLN, it was also detected at high levels in 2 lung cancer lines and 3 other unrelated cancer lines derived from papillotubular adenocarcinoma, signet ring carcinoma and transitional cell carcinoma

Serine 62 is a phosphorylation site in folliculin, the Birt–Hogg–Dubé gene product

AbstractRecently, it was reported that the product of Birt–Hogg–Dubé syndrome gene (folliculin, FLCN) is directly phosphorylated by 5′-AMP-activated protein kinase (AMPK). In this study, we identified serine 62 (Ser62) as a phosphorylation site in FLCN and generated an anti-phospho-Ser62-FLCN antibody. Our analysis suggests that Ser62 phosphorylation is indirectly up-regulated by AMPK and that another residue is directly phosphorylated by AMPK. By binding with FLCN-interacting proteins (FNIP1 and FNIP2/FNIPL), Ser62 phosphorylation is increased. A phospho-mimic mutation at Ser62 enhanced the formation of the FLCN–AMPK complex. These results suggest that function(s) of FLCN–AMPK–FNIP complex is regulated by Ser62 phosphorylation.Structured summaryMINT-7298145, MINT-7298166: Flcn (uniprotkb:Q76JQ2) physically interacts (MI:0915) with AMPK alpha 1 (uniprotkb:P54645) by anti tag coimmunoprecipitation (MI:0007)MINT-7298267: AMPK alpha 1 (uniprotkb:Q13131) phosphorylates (MI:0217) tsc2 (uniprotkb:P49816) by protein kinase assay (MI:0424)MINT-7298182: FNIP1 (uniprotkb:Q8TF40) physically interacts (MI:0915) with Flcn (uniprotkb:Q76JQ2) by anti tag coimmunoprecipitation (MI:0007)MINT-7298132: AMPK alpha 1 (uniprotkb:Q13131) phosphorylates (MI:0217) Flcn (uniprotkb:Q76JQ2) by protein kinase assay (MI:0424)MINT-7298229: FNIPL (uniprotkb:Q9P278) physically interacts (MI:0915) with Flcn (uniprotkb:Q76JQ2) by anti tag coimmunoprecipitation (MI:0007

Persistent activation of Nrf2 through p62 in hepatocellular carcinoma cells

Impaired autophagy stabilizes p62 and promotes tumorigenesis through activation of the Nrf2 transcription factor

HZE RADIATION EFFECT FOR HEREDITARY RETINAL CARCINOMAS

Cancer is a heritable disorder of somatic cells. The Eker rat is well characterized as an animal model for dominantly inherited cancer. All of the Eker rats develop renal carcinomas (RC) approximately 1 year after birth. According to Mendelian laws of inheritance, this occurrence suggests the existence of a single responsible gene. Tuberous sclerosis complex (Tsc2) gene encoding a tumor suppressor protein, are the responsible factor for the RC. We have investigated the effects of space radiation on carcinogenesis and analyzed RBE ratio of tumor induction, in which we compared the effects of heavy-ion (C-290MeV/u,Fe-500MeV/u) exposure and X-ray exposure. Pregnant rats were irradiated by carbon-ions, iron-ions and X-rays by 0.5Gy, 1Gy, 2Gy and 3Gy individually on 19th day of gestation. These rats were sacrificed at age of 8 weeks, and organ weight and tumor genesis were measured. Thymus, Lung, Liver, Spleen weight were not different at 1Gy, but decreased by 50% at 3Gy irradiation. Kidney, Brain, Testis were radiation sensitive organs of which weight were decreased by 40% at 1Gy and by 80% at 3Gy. The number of hereditary renal carcinomas per one cross section of kidney were 3.7(1Gy), 42.0(3Gy) in the case of X-ray exposure, and 4. (1Gy) and 54.1(3Gy) by carbon ion exposure, and 14.5(1Gy) and 49.6(2Gy) by iron ion exposure. The Dose-response relationship on radiation-induced carcinoma was clearly fitted by LQ model. The RBE were observed as 1.1 for carbon-ions, and 1.6 for iron ions.3rd International Workshop on Space Radiation Resarc