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. 2013 May;15(3):323-7.
doi: 10.1038/aja.2013.40. Epub 2013 Apr 15.

Modelling synergistic interactions between HER2, Sprouty2 and PTEN in driving prostate carcinogenesis

Imran Ahmad  1 , Meiling Gao, Rachana Patel, Hing Y Leung
Affiliations

Modelling synergistic interactions between HER2, Sprouty2 and PTEN in driving prostate carcinogenesis

Imran Ahmad et al. Asian J Androl. 2013 May.
No abstract available

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Figures

Figure 1
Figure 1
Pathway for human PCa progression. Stages of progression are correlated with loss of specific chromosome regions and candidate tumour suppressor genes (modified from Abate-Shen and Shen). Dotted lines signify the uncertainty concerning the individual events regarding the exact stage of their involvements during carcinogenesis. PTEN, phosphatase and tensin homologue; AR, androgen receptor.
Figure 2
Figure 2
Mechanism of tumorigenesis in PB-Cre4: Ptenfl/fl Her2KI mice. PB-Cre4: Ptenfl/fl tumours demonstrate upregulation of the PI3K pathway, which upregulates p53 and leads to a senescent phenotype. In the PB-Cre4: Ptenfl/fl Her2KI tumours, upregulation of the MAPK ‘outweighs' the PI3K upregulation, leading to a proliferative phenotype. When these mice are treated with a MEK1/2 inhibitor, the proliferative phenotype via the MAPK pathway is suppressed and the senesencent phenotype (via the PI3K pathway) predominates. PTEN, phosphatase and tensin homologue.
Figure 3
Figure 3
Enhanced recycling of EGFR/HER2 upon Sprouty2 loss in a PTEN-dependent manner via sequential activation of PI3K/AKT and p38. PTEN, phosphatase and tensin homologue.
Figure 4
Figure 4
Methods of utilisation of tumours generated from GEMMs. Orthografts derived from GEMM tumours can be useful in vivo models to study both primary and metastatic tumour growth and their responses to treatment. GEMM, genetically modified mouse model.
See this image and copyright information in PMC

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