scholarly journals G-CSF-producing renal cell carcinoma characterized by IL-8-induced marked neutrophil infiltration to tumor tissue

Author(s):  
Taiichi Kodaka ◽  
Emiko Ishikawa Sakane ◽  
Hayato Maruoka ◽  
Hiroko Tsunemine ◽  
Hiroshi Akasaka ◽  
...  
2021 ◽  
pp. 1-11
Author(s):  
Zi-Bin Xu ◽  
Mei-Fu Gan ◽  
Hong-Yuan Yu ◽  
Li-Cai Mo ◽  
Yu-Hui Xia ◽  
...  

<b><i>Background:</i></b> Activins and inhibins are structurally related dimeric glycoprotein hormones belonging to the transforming growth factor-β superfamily but whether they are also involved in malignancy is far from clear. No study has reported the expression of INHBE in kidney cancer. The purpose of this study was to examine the expressions of INHBE in the tumor tissue of patients with clear-cell renal cell carcinoma (ccRCC) and to explore the pathologic significance. <b><i>Methods:</i></b> The INHBE mRNA expression in the tumor tissue of ccRCC patients was analyzed by using RNA sequencing data from the TCGA database. To examine the expression of inhibin βE protein, 241 ccRCC patients were recruited and immunohistochemistry was performed on the tumor tissue of these patients along with 39 normal renal samples. The association between the inhibin βE expression level and patient’s clinicopathological indices was evaluated. <b><i>Results:</i></b> In the normal renal tissue, inhibin βE was found to be expressed mainly by renal tubular epithelial cells. In the tumor tissue, inhibin βE was expressed mainly in cancer cells. The expressions of INHBE mRNA and protein in the tumor tissue of ccRCC patients increased significantly compared with those in normal renal samples. There was a significant correlation between the level of inhibin βE in the tumor tissue and tumor grade. Patients with a lower inhibin βE expression in the tumor tissue were found to have a longer overall survival and disease-specific survival. <b><i>Conclusions:</i></b> INHBE might be involved in the pathogenesis of ccRCC and function as a tumor promoter.


Blood ◽  
1986 ◽  
Vol 68 (2) ◽  
pp. 394-399 ◽  
Author(s):  
LR Zacharski ◽  
VA Memoli ◽  
SM Rousseau

Abstract Fibrin was detected by immunospecific techniques associated with both intravascular and extravascular tumor deposits in renal cell carcinoma. In addition, coagulation factors VII and X were demonstrated in intercellular spaces within tumor tissue and adjacent to the surface of tumor cells. Scant accumulation of platelets on intravascular tumor masses was observed. These data suggest that tumor cells in renal cell carcinoma may induce fibrin formation locally by a factor VII-mediated (and thus tissue factor-initiated) pathway of blood coagulation. This mechanism may also account for the hypercoagulable state that exists with this tumor type. We postulate that local fibrin formation may contribute to the growth and spread of this particular type of cancer and that the course of renal cell carcinoma may be ameliorated by anticoagulant therapy.


1991 ◽  
Vol 82 (11) ◽  
pp. 1781-1789 ◽  
Author(s):  
Yasushi Nagase ◽  
Nobuo Moriyama ◽  
Yoshio Hosaka ◽  
Eiji Higashihara ◽  
Isao Murahashi ◽  
...  

2016 ◽  
Vol 31 (1) ◽  
pp. 26-37 ◽  
Author(s):  
Michal Fedorko ◽  
Dalibor Pacik ◽  
Roman Wasserbauer ◽  
Jaroslav Juracek ◽  
Gabriel Varga ◽  
...  

Purpose To provide information about the role of microRNAs in the pathogenesis of renal cell carcinoma (RCC) and their diagnostic and prognostic utility as cancer biomarkers. Methods A literature search was performed in the PubMed and Web of Science databases using the keywords “renal cancer/renal cell carcinoma/kidney cancer” and “miR*/miRNA*/microRNA*”. Articles dealing with the role of miRNAs in the pathogenesis of RCC, diagnostic miRNAs and prognostic miRNAs were separated. Results MiRNAs act both as oncogenes and tumor suppressors. They regulate apoptosis, cell growth, migration, invasion, proliferation, colony formation and angiogenesis through target proteins involved in several signaling pathways, and they are involved in key pathogenetic mechanisms such as hypoxia (HIF/VHL dependent) and epithelial-to-mesenchymal transition. Differentially expressed miRNAs can discriminate either tumor tissue from healthy renal tissue or different RCC subtypes. Circulating miRNAs are promissing as diagnostic biomarkers of RCC. Information about urinary miRNAs associated with RCC is sparse. Detection of a relapse is another implication of diagnostic miRNAs. The expression profiles of several miRNAs correlate with the prognosis of RCC patients. Comparison between primary tumor tissue and metastasis may help identify high-risk primary tumors. Finally, response to target therapy can be estimated thanks to differences in miRNA expression in tissue and serum of therapy-resistant versus therapy-sensitive patients. Conclusions Our understanding of the role of microRNAs in RCC pathogenesis has been increasing dramatically. Identification and validation of their gene targets may have direct impact on developing microRNA-based anticancer therapy. Several microRNAs can serve as diagnostic and prognostic biomarkers.


2021 ◽  
Vol 11 ◽  
Author(s):  
Jing-min Zheng ◽  
Mei-fu Gan ◽  
Hong-yuan Yu ◽  
Lu-xia Ye ◽  
Qing-xin Yu ◽  
...  

KDF1 has been identified as a key regulator of epidermal proliferation and differentiation, but it is unknown whether KDF1 is involved in the pathogenesis of malignancy. No study has reported the expression and function of KDF1 in renal cancer. To explore the pathologic significance of KDF1 in clear cell renal cell carcinoma (ccRCC), the expression level of KDF1 protein in the tumor tissue of ccRCC patients was examined by immunohistochemistry and Western blot while the expression level of KDF1 mRNA was analyzed by using the data from TCGA database. In vitro cell experiments and allogeneic tumor transplantation tests were performed to determine the effects of altered KDF1 expression on the phenotype of ccRCC cells. Both the KDF1 mRNA and protein were found to be decreasingly expressed in the tumor tissue of ccRCC patients when compared with the adjacent non-tumor control tissue. The expression level of KDF1 in the tumor tissue was found to correlate negatively with the tumor grade. Patients with higher KDF1 in the tumor tissue were found to have longer overall survival and disease-specific survival time. KDF1 was shown to be an independent factor influencing the disease-specific survival of the ccRCC patients. Overexpression of KDF1 was found to inhibit the proliferation, migration and invasion of ccRCC cells, which could be reversed by decreasing the expression of KDF1 again. ccRCC cells with KDF1 overexpression were found to produce smaller transgrafted tumors. These results support the idea that KDF1 is involved in ccRCC and may function as a tumor suppressor.


2016 ◽  
Vol 36 (12) ◽  
pp. 6419-6424 ◽  
Author(s):  
ROBERT ILIEV ◽  
MICHAL FEDORKO ◽  
TANA MACHACKOVA ◽  
HANA MLCOCHOVA ◽  
MAREK SVOBODA ◽  
...  

Author(s):  
Michael Lein ◽  
Klaus Jung ◽  
Christian Laube ◽  
Tobias H�bner ◽  
Bjoern Winkelmann ◽  
...  

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