Skin cancer models

2005 ◽  
Vol 2 (1) ◽  
pp. 71-75 ◽  
Author(s):  
Alexandre Nakao Odashiro ◽  
Patricia Rusa Pereira ◽  
Jean-Claude Marshall ◽  
Katyanne Godeiro ◽  
Miguel N. Burnier
Keyword(s):  
2016 ◽  
Vol 233 ◽  
pp. 10-18 ◽  
Author(s):  
Christian Zoschke ◽  
Martina Ulrich ◽  
Michaela Sochorová ◽  
Christopher Wolff ◽  
Kateřina Vávrová ◽  
...  

Life Sciences ◽  
2014 ◽  
Vol 113 (1-2) ◽  
pp. 45-54 ◽  
Author(s):  
Anne Yuqing Yang ◽  
Jong Hun Lee ◽  
Limin Shu ◽  
Chengyue Zhang ◽  
Zheng-Yuan Su ◽  
...  

2016 ◽  
Vol 51 (1) ◽  
pp. 24-35 ◽  
Author(s):  
Giju Thomas ◽  
Bastiaan Tuk ◽  
Ji-Ying Song ◽  
Hoa Truong ◽  
Hans C Gerritsen ◽  
...  

Previous studies have established that 7,12-dimethylbenz(a)anthracene (DMBA) can initiate skin tumourigenesis in conventional furred mouse models by acting on hair follicle stem cells. However, further cancer progression depends on repeated applications of tumour promoter agents. This study evaluated the timeline involved in skin tumourigenesis and progression in immunocompetent hairless SKH1-hr mice with dysfunctional hair follicles using only DMBA with no additional tumour promoter agents. The results showed that topical application of 30 µg (117 nmol) of DMBA over the back and flank regions of the mouse once a week and 15 µg (58.5 nmol) twice a week produced skin tumours after 7–8 weeks. However, by week 14 a heavy benign tumour load required the mice to be euthanized. Lowering the DMBA dose to 15 µg (58.5 nmol) once a week produced tumours more slowly and allowed the mice to be studied for a longer period to week 23. This low-dose DMBA regimen yielded a high percentage of malignant tumours (58.8%) after 23 weekly applications. Additionally DMBA-treated skin showed an increase in mean epidermal thickness in comparison to untreated and acetone-treated skin. Despite the aberrant hair follicles in SKH1-hr mice, this chemically driven skin cancer model in hairless mice can serve as a suitable alternative to the ultraviolet-induced skin cancer models and can be reliably replicated as demonstrated by both the pilot and main experiments.


2020 ◽  
Vol 165 ◽  
pp. 1055-1065 ◽  
Author(s):  
Daniela V. Giacone ◽  
Vanessa F.M.C. Dartora ◽  
Jenyffer K.R. de Matos ◽  
Julia S. Passos ◽  
Daniel A.G. Miranda ◽  
...  

2018 ◽  
Vol 19 (12) ◽  
pp. 3929 ◽  
Author(s):  
Sreeja Sarasamma ◽  
Yu-Heng Lai ◽  
Sung-Tzu Liang ◽  
Kechun Liu ◽  
Chung-Der Hsiao

Animal models play important roles in investigating the pathobiology of cancer, identifying relevant pathways, and developing novel therapeutic tools. Despite rapid progress in the understanding of disease mechanisms and technological advancement in drug discovery, negative trial outcomes are the most frequent incidences during a Phase III trial. Skin cancer is a potential life-threatening disease in humans and might be medically futile when tumors metastasize. This explains the low success rate of melanoma therapy amongst other malignancies. In the past decades, a number of skin cancer models in fish that showed a parallel development to the disease in humans have provided important insights into the fundamental biology of skin cancer and future treatment methods. With the diversity and breadth of advanced molecular genetic tools available in fish biology, fish skin cancer models will continue to be refined and expanded to keep pace with the rapid development of skin cancer research. This review begins with a brief introduction of molecular characteristics of skin cancers, followed by an overview of teleost models that have been used in the last decades in melanoma research. Next, we will detail the importance of the zebrafish (Danio rerio) animal model and other emerging fish models including platyfish (Xiphophorus sp.), and medaka (Oryzias latipes) in future cutaneous malignancy studies. The last part of this review provides the recent development and genome editing applications of skin cancer models in zebrafish and the progress in small molecule screening.


2018 ◽  
Vol 19 (10) ◽  
pp. 3109 ◽  
Author(s):  
Eric Romer ◽  
Anita Thyagarajan ◽  
Smita Krishnamurthy ◽  
Christine Rapp ◽  
Langni Liu ◽  
...  

Platelet-activating factor-receptor (PAF-R) agonists are pleiotropic lipid factors that influence multiple biological processes, including the induction and resolution of inflammation as well as immunosuppression. PAF-R agonists have been shown to modulate tumorigenesis and/or tumor growth in various skin cancer models by suppressing either cutaneous inflammation and/or anti-tumoral adaptive immunity. We have previously shown that a chronic systemic PAF-R agonist administration of mice enhances the growth of subcutaneously implanted melanoma tumors. Conversely, chronic topical applications of a PAF-R agonist suppressed non-melanoma skin cancer (NMSC) in a topical chemical carcinogenesis model (dimethylbenz[a]anthracene/phorbol 12-myristate 13-acetate (DMBA/PMA)) in-part via anti-inflammatory effects. These results indicate that the context of PAF-R agonist exposure via either chronic cutaneous or systemic administration, result in seemingly disparate effects on tumor promotion. To further dissect the contextual role of PAF-R agonism on tumorigenesis, we chronically administered systemic PAF-R agonist, carbamoyl-PAF (CPAF) to mice under a cutaneous chemical carcinogenesis protocol, recently characterized to initiate both NMSC and melanocytic nevus formation that can progress to malignant melanoma. Our results showed that while systemic CPAF did not modulate melanocytic nevus formation, it enhanced the growth of NMSC tumors.


2017 ◽  
Vol 18 ◽  
pp. 302-309 ◽  
Author(s):  
M.S. Soumya ◽  
D. Gayathri Devi ◽  
K.M. Shafeekh ◽  
Suresh Das ◽  
Annie Abraham

2015 ◽  
Vol 21 (9) ◽  
pp. 958-970 ◽  
Author(s):  
Manuel Berning ◽  
Silke Prätzel-Wunder ◽  
Jackie R. Bickenbach ◽  
Petra Boukamp

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