Rhodopsin and Retinoblastoma

Coexpression of Normally Incompatible Developmental Pathways in Retinoblastoma Genesis

“…Initially, the focus was on those features that could be identified by histologic analysis such as the presence of rosettes. With advances in microscopy, histology, and molecular biology, the debate about the retinoblastoma cell of origin has been revisited with a strong predilection toward photoreceptors being the cell of origin (Dickson et al, 1976; Donoso et al, 1985, 1986; Glubrecht et al, 2009; Mirshahi et al, 1986; Ts'o et al, 1970a, 1970b; Vrabec et al, 1989; Xu et al, 2009). However, a number of independent studies suggested that retinoblastomas may also have features of progenitor cells or interneurons such as amacrine cells (Beemer et al, 1984; Donovan et al, 2006; Glubrecht et al, 2009; Johnson et al, 2007; Kyritsis et al, 1984a; Kyritsis et al, 1984b; Kyritsis et al, 1986; Tsokos et al, 1986; Zhong et al, 2007).…”

“…The first attempt to formulate a link between tumor cell features and a specific retinal cell type (i.e., photoreceptors) as the cell of origin was in 1897 with the description of retinoblastoma rosettes (Wintersteiner, 1897). In subsequent decades, this hypothesis was extended to include morphological analysis using transmission electron microscopy (TEM) (Dickson et al, 1976; Ts'o et al, 1970a; Ts'o et al, 1970b), immunohistochemistry (arrestin and rhodopsin) (Donoso et al, 1985, 1986; Mirshahi et al, 1986; Vrabec et al, 1989), and immunofluorescence (Crx and opsin) (Glubrecht et al, 2009; Xu et al, 2009). However, during this same period, data were published suggesting that retinoblastoma may arise from a progenitor cell (Beemer et al, 1984; Donovan et al, 2006; Glubrecht et al, 2009; Kyritsis et al, 1984a, 1984b; Zhong et al, 2007), a glial cell (Daa Schroder, 1987), or an interneuron such as an amacrine cell (Johnson et al, 2007; Kyritsis et al, 1986; Tsokos et al, 1986).…”

Coexpression of Normally Incompatible Developmental Pathways in Retinoblastoma Genesis

“…Initially, the focus was on those features that could be identified by histologic analysis such as the presence of rosettes. With advances in microscopy, histology, and molecular biology, the debate about the retinoblastoma cell of origin has been revisited with a strong predilection toward photoreceptors being the cell of origin (Dickson et al, 1976; Donoso et al, 1985, 1986; Glubrecht et al, 2009; Mirshahi et al, 1986; Ts'o et al, 1970a, 1970b; Vrabec et al, 1989; Xu et al, 2009). However, a number of independent studies suggested that retinoblastomas may also have features of progenitor cells or interneurons such as amacrine cells (Beemer et al, 1984; Donovan et al, 2006; Glubrecht et al, 2009; Johnson et al, 2007; Kyritsis et al, 1984a; Kyritsis et al, 1984b; Kyritsis et al, 1986; Tsokos et al, 1986; Zhong et al, 2007).…”

“…The first attempt to formulate a link between tumor cell features and a specific retinal cell type (i.e., photoreceptors) as the cell of origin was in 1897 with the description of retinoblastoma rosettes (Wintersteiner, 1897). In subsequent decades, this hypothesis was extended to include morphological analysis using transmission electron microscopy (TEM) (Dickson et al, 1976; Ts'o et al, 1970a; Ts'o et al, 1970b), immunohistochemistry (arrestin and rhodopsin) (Donoso et al, 1985, 1986; Mirshahi et al, 1986; Vrabec et al, 1989), and immunofluorescence (Crx and opsin) (Glubrecht et al, 2009; Xu et al, 2009). However, during this same period, data were published suggesting that retinoblastoma may arise from a progenitor cell (Beemer et al, 1984; Donovan et al, 2006; Glubrecht et al, 2009; Kyritsis et al, 1984a, 1984b; Zhong et al, 2007), a glial cell (Daa Schroder, 1987), or an interneuron such as an amacrine cell (Johnson et al, 2007; Kyritsis et al, 1986; Tsokos et al, 1986).…”

Coexpression of Normally Incompatible Developmental Pathways in Retinoblastoma Genesis

“…Initially, the focus was on those features that could be identified by histologic analysis such as the presence of rosettes. With advances in microscopy, histology, and molecular biology, the debate about the retinoblastoma cell of origin has been revisited with a strong predilection toward photoreceptors being the cell of origin (Dickson et al, 1976; Donoso et al, 1985, 1986; Glubrecht et al, 2009; Mirshahi et al, 1986; Ts'o et al, 1970a, 1970b; Vrabec et al, 1989; Xu et al, 2009). However, a number of independent studies suggested that retinoblastomas may also have features of progenitor cells or interneurons such as amacrine cells (Beemer et al, 1984; Donovan et al, 2006; Glubrecht et al, 2009; Johnson et al, 2007; Kyritsis et al, 1984a; Kyritsis et al, 1984b; Kyritsis et al, 1986; Tsokos et al, 1986; Zhong et al, 2007).…”

“…The first attempt to formulate a link between tumor cell features and a specific retinal cell type (i.e., photoreceptors) as the cell of origin was in 1897 with the description of retinoblastoma rosettes (Wintersteiner, 1897). In subsequent decades, this hypothesis was extended to include morphological analysis using transmission electron microscopy (TEM) (Dickson et al, 1976; Ts'o et al, 1970a; Ts'o et al, 1970b), immunohistochemistry (arrestin and rhodopsin) (Donoso et al, 1985, 1986; Mirshahi et al, 1986; Vrabec et al, 1989), and immunofluorescence (Crx and opsin) (Glubrecht et al, 2009; Xu et al, 2009). However, during this same period, data were published suggesting that retinoblastoma may arise from a progenitor cell (Beemer et al, 1984; Donovan et al, 2006; Glubrecht et al, 2009; Kyritsis et al, 1984a, 1984b; Zhong et al, 2007), a glial cell (Daa Schroder, 1987), or an interneuron such as an amacrine cell (Johnson et al, 2007; Kyritsis et al, 1986; Tsokos et al, 1986).…”

Coexpression of Normally Incompatible Developmental Pathways in Retinoblastoma Genesis

“…Initially, the focus was on those features that could be identified by histologic analysis such as the presence of rosettes. With advances in microscopy, histology, and molecular biology, the debate about the retinoblastoma cell of origin has been revisited with a strong predilection toward photoreceptors being the cell of origin (Dickson et al, 1976; Donoso et al, 1985, 1986; Glubrecht et al, 2009; Mirshahi et al, 1986; Ts'o et al, 1970a, 1970b; Vrabec et al, 1989; Xu et al, 2009). However, a number of independent studies suggested that retinoblastomas may also have features of progenitor cells or interneurons such as amacrine cells (Beemer et al, 1984; Donovan et al, 2006; Glubrecht et al, 2009; Johnson et al, 2007; Kyritsis et al, 1984a; Kyritsis et al, 1984b; Kyritsis et al, 1986; Tsokos et al, 1986; Zhong et al, 2007).…”

“…The first attempt to formulate a link between tumor cell features and a specific retinal cell type (i.e., photoreceptors) as the cell of origin was in 1897 with the description of retinoblastoma rosettes (Wintersteiner, 1897). In subsequent decades, this hypothesis was extended to include morphological analysis using transmission electron microscopy (TEM) (Dickson et al, 1976; Ts'o et al, 1970a; Ts'o et al, 1970b), immunohistochemistry (arrestin and rhodopsin) (Donoso et al, 1985, 1986; Mirshahi et al, 1986; Vrabec et al, 1989), and immunofluorescence (Crx and opsin) (Glubrecht et al, 2009; Xu et al, 2009). However, during this same period, data were published suggesting that retinoblastoma may arise from a progenitor cell (Beemer et al, 1984; Donovan et al, 2006; Glubrecht et al, 2009; Kyritsis et al, 1984a, 1984b; Zhong et al, 2007), a glial cell (Daa Schroder, 1987), or an interneuron such as an amacrine cell (Johnson et al, 2007; Kyritsis et al, 1986; Tsokos et al, 1986).…”