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The C134W (402 C > G) FOXL2 mutation is absent in ovarian gynandroblastoma

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The C134W (402 C > G) FOXL2 mutation is absent in ovarian gynandroblastoma : insights into the genesis of an unusual tumour. / Oparka, Richard; Cassidy, Andrew; Reilly, Stephanie; Stenhouse, Alasdair; McCluggage, W. Glenn; Herrington, C. Simon.

In: Histopathology, Vol. 60, No. 5, 04.2012, p. 838-842.

Research output: Contribution to journalArticle

Harvard

Oparka, R, Cassidy, A, Reilly, S, Stenhouse, A, McCluggage, WG & Herrington, CS 2012, 'The C134W (402 C > G) FOXL2 mutation is absent in ovarian gynandroblastoma: insights into the genesis of an unusual tumour' Histopathology, vol 60, no. 5, pp. 838-842., 10.1111/j.1365-2559.2011.04148.x

APA

Oparka, R., Cassidy, A., Reilly, S., Stenhouse, A., McCluggage, W. G., & Herrington, C. S. (2012). The C134W (402 C > G) FOXL2 mutation is absent in ovarian gynandroblastoma: insights into the genesis of an unusual tumour. Histopathology, 60(5), 838-842. 10.1111/j.1365-2559.2011.04148.x

Vancouver

Oparka R, Cassidy A, Reilly S, Stenhouse A, McCluggage WG, Herrington CS. The C134W (402 C > G) FOXL2 mutation is absent in ovarian gynandroblastoma: insights into the genesis of an unusual tumour. Histopathology. 2012 Apr;60(5):838-842. Available from: 10.1111/j.1365-2559.2011.04148.x

Author

Oparka, Richard; Cassidy, Andrew; Reilly, Stephanie; Stenhouse, Alasdair; McCluggage, W. Glenn; Herrington, C. Simon / The C134W (402 C > G) FOXL2 mutation is absent in ovarian gynandroblastoma : insights into the genesis of an unusual tumour.

In: Histopathology, Vol. 60, No. 5, 04.2012, p. 838-842.

Research output: Contribution to journalArticle

Bibtex - Download

@article{70e09d83522f464da9c1ba4478e3850b,
title = "The C134W (402 C > G) FOXL2 mutation is absent in ovarian gynandroblastoma: insights into the genesis of an unusual tumour",
author = "Richard Oparka and Andrew Cassidy and Stephanie Reilly and Alasdair Stenhouse and McCluggage, {W. Glenn} and Herrington, {C. Simon}",
year = "2012",
doi = "10.1111/j.1365-2559.2011.04148.x",
volume = "60",
number = "5",
pages = "838--842",
journal = "Histopathology",
issn = "0309-0167",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - The C134W (402 C > G) FOXL2 mutation is absent in ovarian gynandroblastoma

T2 - insights into the genesis of an unusual tumour

A1 - Oparka,Richard

A1 - Cassidy,Andrew

A1 - Reilly,Stephanie

A1 - Stenhouse,Alasdair

A1 - McCluggage,W. Glenn

A1 - Herrington,C. Simon

AU - Oparka,Richard

AU - Cassidy,Andrew

AU - Reilly,Stephanie

AU - Stenhouse,Alasdair

AU - McCluggage,W. Glenn

AU - Herrington,C. Simon

PY - 2012/4

Y1 - 2012/4

N2 - <p>Aims: Ovarian gynandroblastomas are rare tumours that, by definition, comprise a combinationof components resembling both female, typically granulosa cell tumour (GCT), and male, typically Sertoli or Sertoli/Leydig cell tumour (ST/SLT), sex cord/stromal differentiation. The histogenesis of these tumours is unknown and, in view of the very strong association between the C134W (402 C&gt; G) FOXL2 mutation and adult- type GCT, we analysed a series of gynandroblastomas for this mutation.</p><p>Methods and results: Both components of each lesion were isolated by laser capture microdissection and the C134W (402 C&gt; G) FOXL2 mutation was analysed by polymerase chain reaction sequencing. No mutation was identified in either the GCT or ST / SLT component of six cases, three of which contained adult- type GCT.</p><p>Conclusions: This suggests that, despite their similar morphological appearances, the GCT- like component of gynandroblastoma has a different molecular basis from conventional adult- type GCT. This finding underscores a more general principle that morphological similarity does not necessarily indicate molecular identity.</p>

AB - <p>Aims: Ovarian gynandroblastomas are rare tumours that, by definition, comprise a combinationof components resembling both female, typically granulosa cell tumour (GCT), and male, typically Sertoli or Sertoli/Leydig cell tumour (ST/SLT), sex cord/stromal differentiation. The histogenesis of these tumours is unknown and, in view of the very strong association between the C134W (402 C&gt; G) FOXL2 mutation and adult- type GCT, we analysed a series of gynandroblastomas for this mutation.</p><p>Methods and results: Both components of each lesion were isolated by laser capture microdissection and the C134W (402 C&gt; G) FOXL2 mutation was analysed by polymerase chain reaction sequencing. No mutation was identified in either the GCT or ST / SLT component of six cases, three of which contained adult- type GCT.</p><p>Conclusions: This suggests that, despite their similar morphological appearances, the GCT- like component of gynandroblastoma has a different molecular basis from conventional adult- type GCT. This finding underscores a more general principle that morphological similarity does not necessarily indicate molecular identity.</p>

UR - http://www.scopus.com/inward/record.url?scp=84858999473&partnerID=8YFLogxK

U2 - 10.1111/j.1365-2559.2011.04148.x

DO - 10.1111/j.1365-2559.2011.04148.x

M1 - Article

JO - Histopathology

JF - Histopathology

SN - 0309-0167

IS - 5

VL - 60

SP - 838

EP - 842

ER -

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