Head and neck squamous cell carcinoma in non-smoking and non-drinking patients with multiple tumors: etiologic significance of p53 and Ki-67 in non-tumorous epithelium

2008 ◽  
Vol 37 (9) ◽  
pp. 549-554 ◽  
Author(s):  
F. Farshadpour ◽  
G. J. Hordijk ◽  
R. Koole ◽  
P. J. Slootweg
Head & Neck ◽  
2011 ◽  
Vol 33 (2) ◽  
pp. 267-273 ◽  
Author(s):  
Claude A. Fischer ◽  
Minoa Jung ◽  
Inti Zlobec ◽  
Edith Green ◽  
Claudio Storck ◽  
...  

2019 ◽  
Vol 276 (4) ◽  
pp. 1221-1229 ◽  
Author(s):  
Toshiya Maebayashi ◽  
Naoya Ishibashi ◽  
Takuya Aizawa ◽  
Masakuni Sakaguchi ◽  
Tsutomu Saito ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4952
Author(s):  
Cristina Mir ◽  
Yoelsis Garcia-Mayea ◽  
Laia Garcia ◽  
Pol Herrero ◽  
Nuria Canela ◽  
...  

To characterize the mechanisms that govern chemoresistance, we performed a comparative proteomic study analyzing head and neck squamous cell carcinoma (HNSCC) cells: CCL-138 (parental), CCL-138-R (cisplatin-resistant), and cancer stem cells (CSCs). Syntenin-1 (SDCBP) was upregulated in CCL-138-R cells and CSCs over parental cells. SDCBP depletion sensitized biopsy-derived and established HNSCC cell lines to cisplatin (CDDP) and reduced CSC markers, Src activation being the main SDCBP downstream target. In mice, SDCBP-depleted cells formed tumors with decreased mitosis, Ki-67 positivity, and metastasis over controls. Moreover, the fusocellular pattern of CCL-138-R cell-derived tumors reverted to a more epithelial morphology upon SDCBP silencing. Importantly, SDCBP expression was associated with Src activation, poor differentiated tumor grade, advanced tumor stage, and shorter survival rates in a series of 382 HNSCC patients. Our results reveal that SDCBP might be a promising therapeutic target for effectively eliminating CSCs and CDDP resistance.


Oral Oncology ◽  
2004 ◽  
Vol 40 (7) ◽  
pp. 688-696 ◽  
Author(s):  
Sabrina D Silva ◽  
Michelle Agostini ◽  
Inês N Nishimoto ◽  
Ricardo D Coletta ◽  
Fábio A Alves ◽  
...  

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