Malignant Melanoma of Uvea

Sobin, L. H.; Gospodarowicz, M.K.; Wittekind, Ch.

doi:10.1002/9780471420194.tnmc50

Cited by 272 publications

(329 citation statements)

References 0 publications

Supporting

Mentioning

324

Contrasting

Unclassified

Order By: Relevance

“…Histological and clinicopathological evaluations were performed in accord with the Japanese Classification of Esophageal Cancer proposed by the Japan Esophageal Society along with the TNM classification of the Union for International Cancer Control. 17,18 Immunohistochemistry Immunohistochemistry was performed with labeled streptavidin biotinylated antibody method as previously described. 15 Specific rabbit polyclonal antibody against growth differentiation factor 15 (GDF15) (HPA011191, 1:50; Sigma-Aldrich, Munich, Germany), specific mouse monoclonal antibodies against CD68 (Kp-1, 1:100; DakoCytomation, Glostrup, Denmark), CD163 (10D6, 1:100; Novocastra, Newcastle upon Tyne, UK), and CD204 (SRA-E5, 1:50; Trans Genic, Kobe, Japan) were used for the primary reaction.…”

Section: Macrophage Culturesmentioning

confidence: 99%

GDF15 derived from both tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression via Akt and Erk pathways

Urakawa

Utsunomiya

Nishio

et al. 2015

Laboratory Investigation

View full text Add to dashboard Cite

Tumor-associated macrophages (TAMs) are known to be involved in the progression, angiogenesis, and motility of various cancers. We previously reported the association between an increased number of infiltrating TAMs with tumor progression and poor prognosis in esophageal squamous cell carcinomas (ESCCs). To study the roles of TAMs in ESCC, we first exposed peripheral blood monocyte (PBMo)-derived macrophages from healthy volunteers to conditioned media of TE series human ESCC cell line (TECM) and confirmed the induction of the expression of the M2 macrophage marker CD204 and the protumorigenic factors interleukin (IL)-10, VEGFA, and MMPs. Next, we compared gene expression profiles between PBModerived macrophages stimulated with or without TECM by cDNA microarray and focused on growth differentiation factor 15 (GDF15) among the highly expressed genes including IL-6, IL-8, and CXCL1. Our immunohistochemical study of 70 surgically resected ESCCs revealed that GDF15 was present not only in cancer cells but also in macrophages. The high expression of GDF15 in the ESCCs was significantly correlated with several more malignant phenotypes including vessel invasion, lymph node metastasis, and clinical stages. Patients with high GDF15 expression showed significantly poorer disease-free survival (P = 0.011) and overall survival (P = 0.041). We also found that recombinant human GDF15 promotes cell proliferation and the phosphorylation of both Akt and Erk1/2 in ESCC cell lines in vitro. These results indicate that GDF15 is secreted by both TAMs and cancer cells in the tumor microenvironment and is associated with aberrant growth and a poor prognosis in human ESCC.

show abstract

Section: Macrophage Culturesmentioning

confidence: 99%

GDF15 derived from both tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression via Akt and Erk pathways

Urakawa

Utsunomiya

Nishio

et al. 2015

Laboratory Investigation

View full text Add to dashboard Cite

show abstract

“…The number of metastatic sites was defined as the total number of sites described above that were involved by metastases. The primary diseases of patients with NPC were staged according to the seventh edition of the TNM staging system [21].…”

Section: Definitions and Groupingmentioning

confidence: 99%

M1 Stage Subdivision and Treatment Outcome of Patients With Bone-Only Metastasis of Nasopharyngeal Carcinoma

et al. 2015

View full text Add to dashboard Cite

Background. The current M1 stage in nasopharyngeal carcinoma (NPC) does not differentiate patients based on metastatic site and number of metastases. This study aims to subdivide the M1 stage of NPC patients with bone-only metastases and to identify the patients who may benefit from combined chemoradiotherapy (CRT). Methods. Between 1998 and 2007, 312 patients diagnosed with bone-only metastasis at Sun Yat-sen University Cancer Center were enrolled.Various possible subdivisions of M1 stage were considered, including by the time order of metastasis (synchronous vs. metachronous), involvement of specific bone metastatic site, the number of metastatic sites, and the number of metastases. The correlation of the subdivisions of M1 stage with overall survival (OS) was determined by Cox regression. Results. The median OS was 23.4 months. Patients with more than three metastatic sites had significantly poorer OS than patients with three or fewer metastatic sites (16.2 vs. 32.4

show abstract

“…Histological diagnosis was made in accordance with the World Health Organization classification 15. All the tumors were graded on the basis of previously described criteria16 and classified according to the pathological Tumor‐Node‐Metastasis (TNM) classification 17. Clinicopathological parameters of CIMP‐negative and CIMP‐positive patients are summarized in Table 1.…”

Section: Methodsmentioning

confidence: 99%

Alterations of the spindle checkpoint pathway in clinicopathologically aggressive CpG island methylator phenotype clear cell renal cell carcinomas

Arai¹,

Gotoh²,

Tian³

et al. 2015

Intl Journal of Cancer

View full text Add to dashboard Cite

CpG‐island methylator phenotype (CIMP)‐positive clear cell renal cell carcinomas (RCCs) are characterized by accumulation of DNA hypermethylation of CpG islands, clinicopathological aggressiveness and poor patient outcome. The aim of this study was to clarify the molecular pathways participating in CIMP‐positive renal carcinogenesis. Genome (whole‐exome and copy number), transcriptome and proteome (two‐dimensional image converted analysis of liquid chromatography‐mass spectrometry) analyses were performed using tissue specimens of 87 CIMP‐negative and 14 CIMP‐positive clear cell RCCs and corresponding specimens of non‐cancerous renal cortex. Genes encoding microtubule‐associated proteins, such as DNAH2, DNAH5, DNAH10, RP1 and HAUS8, showed a 10% or higher incidence of genetic aberrations (non‐synonymous single‐nucleotide mutations and insertions/deletions) in CIMP‐positive RCCs, whereas CIMP‐negative RCCs lacked distinct genetic characteristics. MetaCore pathway analysis of CIMP‐positive RCCs revealed that alterations of mRNA or protein expression were significantly accumulated in six pathways, all participating in the spindle checkpoint, including the “The metaphase checkpoint (p = 1.427 × 10−6),” “Role of Anaphase Promoting Complex in cell cycle regulation (p = 7.444 × 10−6)” and “Spindle assembly and chromosome separation (p = 9.260 × 10−6)” pathways. Quantitative RT‐PCR analysis revealed that mRNA expression levels for genes included in such pathways, i.e., AURKA, AURKB, BIRC5, BUB1, CDC20, NEK2 and SPC25, were significantly higher in CIMP‐positive than in CIMP‐negative RCCs. All CIMP‐positive RCCs showed overexpression of Aurora kinases, AURKA and AURKB, and this overexpression was mainly attributable to increased copy number. These data suggest that abnormalities of the spindle checkpoint pathway participate in CIMP‐positive renal carcinogenesis, and that AURKA and AURKB may be potential therapeutic targets in more aggressive CIMP‐positive RCCs.

show abstract

Malignant Melanoma of Uvea

Cited by 272 publications

References 0 publications

GDF15 derived from both tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression via Akt and Erk pathways

GDF15 derived from both tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression via Akt and Erk pathways

M1 Stage Subdivision and Treatment Outcome of Patients With Bone-Only Metastasis of Nasopharyngeal Carcinoma

Alterations of the spindle checkpoint pathway in clinicopathologically aggressive CpG island methylator phenotype clear cell renal cell carcinomas

Contact Info

Product

Resources

About