Squamous cell lung carcinomas: the role of nm23-H1 gene

1997 ◽  
Vol 75 (8) ◽  
pp. 609-613 ◽  
Author(s):  
Maja Herak Bosnar ◽  
Kresimir Pavelić ◽  
Šimun Križanac ◽  
Zoran Slobodnjak ◽  
Jasminka Pavelić
2020 ◽  
Vol 40 (12) ◽  
pp. 6987-6995
Author(s):  
NORBERT NECKEL ◽  
MARCO MICHAEL ◽  
DANIEL TROELTZSCH ◽  
JONAS WÜSTER ◽  
STEFFEN KOERDT ◽  
...  

2019 ◽  
Vol 45 (2) ◽  
pp. e85
Author(s):  
L. Bognar ◽  
S. Bellyei ◽  
I. Hegedus ◽  
K. Gombos ◽  
O.P. Horvath ◽  
...  

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Areeg Elmusrati ◽  
Justin Wang ◽  
Cun-Yu Wang

AbstractHead and neck squamous cell carcinoma (HNSCC), an aggressive malignancy, is characterized by high morbidity and low survival rates with limited therapeutic options outside of regional surgery, conventional cytotoxic chemotherapy, and irradiation. Increasing studies have supported the synergistic role of the tumor microenvironment (TME) in cancer advancement. The immune system, in particular, plays a key role in surveillance against the initiation, development, and progression of HNSCC. The understanding of how neoplastic cells evolve and evade the immune system whether through self-immunogenicity manipulation, or expression of immunosuppressive mediators, provides the foundation for the development of advanced therapies. Furthermore, the crosstalk between cancer cells and the host immune system have a detrimental effect on the TME promoting angiogenesis, proliferation, and metastasis. This review provides a recent insight into the role of the key inflammatory cells infiltrating the TME, with a focus on reviewing immunological principles related to HNSCC, as cancer immunosurveillance and immune escape, including a brief overview of current immunotherapeutic strategies and ongoing clinical trials.


2020 ◽  
Vol 2020 (12) ◽  
Author(s):  
Michael Kmeid ◽  
Breanne Gillie ◽  
Armand Asarian ◽  
Philip Xiao

Abstract Squamous cell carcinomas (SCC) accounts for roughly 20% of lung cancers in the USA. The 2015 World Health Organization classification of lung tumors further categorizes SCC as three subtypes: keratinizing, non-keratinizing and basaloid variant. The non-keratinizing subtype is a poorly differentiated tumor that can present histologically in different ways, and one of which is a rare variant that strongly resembles small cell carcinoma. As a result, histological diagnosis alone is not sufficient to properly diagnose lung carcinomas. Immunohistochemistry has been increasingly used over the past few years to differentiate between lung tumors. The combination of morphological and immunohistochemical staining should be the mainstay for diagnosis of all lung carcinomas as more targeted therapies become more available.


2021 ◽  
Vol 141 (5) ◽  
pp. S12
Author(s):  
M. Gallego Rentero ◽  
M. Gutiérrez-Pérez ◽  
M. Portillo-Esnaola ◽  
M. Mataix ◽  
L. Najera ◽  
...  

Author(s):  
Kuauhyama Luna-Ortiz ◽  
Nancy Reynoso-Noverón ◽  
Luis C. Zacarías-Ramón ◽  
Zelik Luna-Peteuil ◽  
Dorian Y. García-Ortega

2021 ◽  
Vol 20 ◽  
pp. 153473542110316
Author(s):  
Liang Wang ◽  
Lei Xu ◽  
Yu Wang

Cutaneous squamous cell carcinoma (CSCC) is a malignant tumor that originates from keratinocytes in the epidermis or appendage. Traditional Chinese medicine Huaier has anti-tumor activity in various malignancies. Little is known about the role of Huaier in CSCC. Here, we investigated the function of Huaier in CSCC. We treated CSCC cell line (SCL-1 and A431) with a series of concentration gradients of Huaier to examine the half maximal inhibitory concentration (IC50) of Huaier on SCL-1 and A431 cells. The IC50 of Huaier on growth of SCL-1 and A431 cells were 6.96 and 7.57 mg/mL, respectively. Moreover, Huaier reduced the methylation levels of CDKN2A and TP53, and enhanced the expression of CDKN2A and TP53 in SCL-1 and A431 cells in a dosage-dependent manner. The expression of DNA methyltransferase DNMT1 was severely repressed by Huaier treatment in SCL-1 and A431 cells. DNMT1 overexpression enhanced the methylation levels of CDKN2A and TP53, and suppressed the expression of CDKN2A and TP53 in Huaier-treated SCL-1 and A431 cells. Huaier treatment inhibited proliferation, migration, and invasion of SCL-1 and A431 cells. However, inhibition of CDKN2A or TP53 reversed the influence of Huaier treatment on proliferation, migration, and invasion of CSCC cells. In conclusion, our data demonstrate that Huaier inhibits proliferation, migration, and invasion of CSCC cells by regulating DNA methylation of CDKN2A and TP53, thereby attenuating the progression of CSCC. Thus, Huaier extract may act as a drug for treating CSCC.


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