The Experts below are selected from a list of 417 Experts worldwide ranked by ideXlab platform

Andrew P Jackson - One of the best experts on this subject based on the ideXlab platform.

  • microcephalic osteodysplastic primordial dwarfism type ii a clinical review
    Current Osteoporosis Reports, 2017
    Co-Authors: Andrew P Jackson
    Abstract:

    This review will provide an overview of the microcephalic primordial dwarfism (MPD) class of disorders and provide the reader comprehensive clinical review with suggested care guidelines for patients with microcephalic osteodysplastic primordial dwarfism, type II (MOPDII). Over the last 15 years, significant strides have been made in the diagnosis, natural history, and management of MOPDII. MOPDII is the most common and well described form of MPD. The classic features of the MPD group are severe pre- and postnatal growth retardation, with marked microcephaly. In addition to these features, individuals with MOPDII have characteristic facies, skeletal dysplasia, abnormal dentition, and an increased risk for cerebrovascular disease and insulin resistance. Biallelic loss-of-function mutations in the pericentrin gene cause MOPDII, which is inherited in an autosomal recessive manner.

  • mechanisms and pathways of growth failure in primordial dwarfism
    Genes & Development, 2011
    Co-Authors: Anna Klingseisen, Andrew P Jackson
    Abstract:

    The greatest difference between species is size; however, the developmental mechanisms determining organism growth remain poorly understood. Primordial dwarfism is a group of human single-gene disorders with extreme global growth failure (which includes Seckel syndrome, microcephalic osteodysplastic primordial dwarfism I [MOPD] types I and II, and Meier-Gorlin syndrome). Ten genes have now been identified for microcephalic primordial dwarfism, encoding proteins involved in fundamental cellular processes including genome replication (ORC1 [origin recognition complex 1], ORC4, ORC6, CDT1, and CDC6), DNA damage response (ATR [ataxia-telangiectasia and Rad3-related]), mRNA splicing (U4atac), and centrosome function (CEP152, PCNT, and CPAP). Here, we review the cellular and developmental mechanisms underlying the pathogenesis of these conditions and address whether further study of these genes could provide novel insight into the physiological regulation of organism growth.

  • set nuclear oncogene associates with Microcephalin mcph1 and regulates chromosome condensation
    Journal of Biological Chemistry, 2011
    Co-Authors: Justin W C Leung, Louise S. Bicknell, Andrea Leitch, Andrew P Jackson, Jamie L Wood, Charles Shawsmith, Kay Metcalfe, Junjie Chen
    Abstract:

    Primary microcephaly is an autosomal recessive disorder characterized by marked reduction in human brain size. Microcephalin (MCPH1), one of the genes mutated in primary microcephaly, plays an important role in DNA damage checkpoint control and mitotic entry. Additionally, MCPH1 ensures the proper temporal activation of chromosome condensation during mitosis, by acting as a negative regulator of the condensin II complex. We previously found that deletion of the of the MCPH1 N terminus leads to the premature chromosome condensation (PCC) phenotype. In the present study, we unexpectedly observed that a truncated form of MCPH1 appears to be expressed in MCPH1S25X/S25X patient cells. This likely results from utilization of an alternative translational start codon, which would produce a mutant MCPH1 protein with a small deletion of its N-terminal BRCT domain. Furthermore, missense mutations in the MCPH1 cluster at its N terminus, suggesting that intact function of this BRCT protein-interaction domain is required both for coordinating chromosome condensation and human brain development. Subsequently, we identified the SET nuclear oncogene as a direct binding partner of the MCPH1 N-terminal BRCT domain. Cells with SET knockdown exhibited abnormal condensed chromosomes similar to those observed in MCPH1-deficient mouse embryonic fibroblasts. Condensin II knockdown rescued the abnormal chromosome condensation phenotype in SET-depleted cells. In addition, MCPH1 V50G/I51V missense mutations, impair binding to SET and fail to fully rescue the abnormal chromosome condensation phenotype in Mcph1−/− mouse embryonic fibroblasts. Collectively, our findings suggest that SET is an important regulator of chromosome condensation/decondensation and that disruption of the MCPH1-SET interaction might be important for the pathogenesis of primary microcephaly.

  • Microcephalin coordinates mitosis in the syncytial drosophilaembryo
    Development, 2007
    Co-Authors: Kathrin Brunk, Bertrand Vernay, Elen Griffith, Natalie L Reynolds, David Strutt, Philip W Ingham, Andrew P Jackson
    Abstract:

    1. 1. Brunk K., 2. et al. 2007. J. Cell Sci. doi:10.1242/jcs.014290 [OpenUrl][1][Abstract/FREE Full Text][2] [1]: {openurl}?query=rft.jtitle%253DJ.%2BCell%2BSci.%26rft_id%253Dinfo%253Adoi%252F10.1242%252Fjcs.014290%26rft_id%253Dinfo%253Apmid%252F17895363%26rft.genre%

  • Microcephalin a causal link between impaired damage response signalling and microcephaly
    Cell Cycle, 2006
    Co-Authors: Mark Odriscoll, Andrew P Jackson, Penny A Jeggo
    Abstract:

    Seckel Syndrome (SS) and Primary Microcephaly (MCPH) are disorders exhibiting marked microcephaly with a head circumference less than three standard deviations below the mean. ATR-Seckel Syndrome is conferred by mutations in ataxia and telangiectasia and Rad3 related (ATR), a kinase that activates a DNA damage signalling response. Cell lines from additional SS patients, who are normal for ATR, show defective ATR signalling, suggesting that they carry mutations in other components of the ATR pathway. Primary Microcephaly is distinct from SS since patients display solely microcephaly without accompanying marked growth delay. MCPH1, the first Primary Microcephaly causative gene identified, encodes three BRCT domains, similar to other damage response proteins. Recent studies employing MCPH1 siRNA or exploiting cell lines from MCPH1 patients have shown that MCPH1 functions in the ATR-dependent DNA damage response pathway. Additionally, MCPH1 has a function in the regulation of mitotic entry that is ATR-independent and confers a characteristic phenotype of premature chromosome condensation. Recent studies will be reviewed and their relationship to the aetiology of microcephaly discussed.

Sandra M. Bell - One of the best experts on this subject based on the ideXlab platform.

  • deregulation of Microcephalin and aspm expression are correlated with epithelial ovarian cancer progression
    PLOS ONE, 2014
    Co-Authors: Rawiah A Alsiary, Jacquelyn Bond, Ewan E. Morrison, Nafisa Wilkinson, Anke Bruningrichardson, Sandra M. Bell
    Abstract:

    Mutations in the MCPH1 (Microcephalin) and ASPM (abnormal spindle-like microcephaly associated) genes cause primary microcephaly. Both are centrosomal associated proteins involved in mitosis. Microcephalin plays an important role in DNA damage response and ASPM is required for correct division of proliferative neuro-epithelial cells of the developing brain. Reduced MCPH1 mRNA expression and ASPM mRNA over-expression have been implicated in the development of human carcinomas. Epithelial ovarian cancer (EOC) is characterised by highly aneuploid tumours. Previously we have reported low Microcephalin and high ASPM protein levels and associations with clinico-pathological parameters in malignant cells from ascitic fluids. To confirm these previous findings on a larger scale Microcephalin and ASPM expression levels and localisations were evaluated by immunohistochemistry in two cohorts; a training set of 25 samples and a validation set of 322 EOC tissue samples. Results were correlated to the associated histopathological data. In normal ovarian tissues the Microcephalin nuclear staining pattern was consistently strong. In the cancer tissues, we identified low nuclear Microcephalin expression in high grade and advanced stage tumours (p<0.0001 and p = 0.0438 respectively). ASPM had moderate to high nuclear and low to moderate cytoplasmic expression in normal tissue. Cytoplasmic ASPM expression decreased with tumour grade and stage in the serous subtype of EOC (p = 0.023 and p = 0.011 respectively). Cytoplasmic ASPM increased with tumour stage in the endometrioid subtype (p = 0.023). Increasing tumour invasiveness (T3) and lymph node involvement (N1) also correlated with a decrease in cytoplasmic ASPM in EOC (p = 0.02 and p = 0.04 respectively). We have validated previous findings of deregulated expression of Microcephalin and ASPM in EOC by confirming associations for low nuclear Microcephalin levels and high cytoplasmic ASPM levels in a larger scale tumour tissue study. Microcephalin and ASPM may prove useful biomarkers in EOC.

  • Microcephalin expression in EOC validation set samples correlates with tumour grade.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Ai. Normal ovarian epithelial tissue with high Microcephalin expression. Aii-iv. Adenocarcinoma TMA cores showing strong Microcephalin expression in a low grade tumour (Aii), moderate Microcephalin in grade 2 (Aiii) and low levels of nuclear Microcephalin expression in a high grade tumour (Aiv). All images are 40x magnification. B. The correlation between nuclear Microcephalin expression decreases with increasing tumor grade (p

  • Microcephalin expression in EOC validation set samples inversely correlates with tumour stage.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Ai. Normal ovarian epithelial tissue demonstrating high Microcephalin expression levels. Aii-4iv Adenocarcinoma TMA cores showing strong Microcephalin (Aii), moderate Microcephalin (Aiii) and low levels of nuclear Microcephalin expression (Aiv) in stage 1, 2 and 3 tumours respectively. All images are 40x magnification. B. Weak Microcephalin levels in the nucleus are associated with advanced tumour stage (p = 0.0438 using an ANOVA test).

  • Deregulation of Microcephalin and ASPM Expression Are Correlated with Epithelial Ovarian Cancer Progression
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Mutations in the MCPH1 (Microcephalin) and ASPM (abnormal spindle-like microcephaly associated) genes cause primary microcephaly. Both are centrosomal associated proteins involved in mitosis. Microcephalin plays an important role in DNA damage response and ASPM is required for correct division of proliferative neuro-epithelial cells of the developing brain. Reduced MCPH1 mRNA expression and ASPM mRNA over-expression have been implicated in the development of human carcinomas. Epithelial ovarian cancer (EOC) is characterised by highly aneuploid tumours. Previously we have reported low Microcephalin and high ASPM protein levels and associations with clinico-pathological parameters in malignant cells from ascitic fluids. To confirm these previous findings on a larger scale Microcephalin and ASPM expression levels and localisations were evaluated by immunohistochemistry in two cohorts; a training set of 25 samples and a validation set of 322 EOC tissue samples. Results were correlated to the associated histopathological data. In normal ovarian tissues the Microcephalin nuclear staining pattern was consistently strong. In the cancer tissues, we identified low nuclear Microcephalin expression in high grade and advanced stage tumours (p

  • Microcephalin expression in different EOC subtypes.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    A. Clear cell carcinoma and B. Endometrioid adenocarcinoma both showing strong Microcephalin expression. C. Mucinous adenocarcinoma and D. Serous adenocarcinoma both presenting weak Microcephalin expression. All images are x40 magnification.

Jacquelyn Bond - One of the best experts on this subject based on the ideXlab platform.

  • deregulation of Microcephalin and aspm expression are correlated with epithelial ovarian cancer progression
    PLOS ONE, 2014
    Co-Authors: Rawiah A Alsiary, Jacquelyn Bond, Ewan E. Morrison, Nafisa Wilkinson, Anke Bruningrichardson, Sandra M. Bell
    Abstract:

    Mutations in the MCPH1 (Microcephalin) and ASPM (abnormal spindle-like microcephaly associated) genes cause primary microcephaly. Both are centrosomal associated proteins involved in mitosis. Microcephalin plays an important role in DNA damage response and ASPM is required for correct division of proliferative neuro-epithelial cells of the developing brain. Reduced MCPH1 mRNA expression and ASPM mRNA over-expression have been implicated in the development of human carcinomas. Epithelial ovarian cancer (EOC) is characterised by highly aneuploid tumours. Previously we have reported low Microcephalin and high ASPM protein levels and associations with clinico-pathological parameters in malignant cells from ascitic fluids. To confirm these previous findings on a larger scale Microcephalin and ASPM expression levels and localisations were evaluated by immunohistochemistry in two cohorts; a training set of 25 samples and a validation set of 322 EOC tissue samples. Results were correlated to the associated histopathological data. In normal ovarian tissues the Microcephalin nuclear staining pattern was consistently strong. In the cancer tissues, we identified low nuclear Microcephalin expression in high grade and advanced stage tumours (p<0.0001 and p = 0.0438 respectively). ASPM had moderate to high nuclear and low to moderate cytoplasmic expression in normal tissue. Cytoplasmic ASPM expression decreased with tumour grade and stage in the serous subtype of EOC (p = 0.023 and p = 0.011 respectively). Cytoplasmic ASPM increased with tumour stage in the endometrioid subtype (p = 0.023). Increasing tumour invasiveness (T3) and lymph node involvement (N1) also correlated with a decrease in cytoplasmic ASPM in EOC (p = 0.02 and p = 0.04 respectively). We have validated previous findings of deregulated expression of Microcephalin and ASPM in EOC by confirming associations for low nuclear Microcephalin levels and high cytoplasmic ASPM levels in a larger scale tumour tissue study. Microcephalin and ASPM may prove useful biomarkers in EOC.

  • Microcephalin expression in EOC validation set samples correlates with tumour grade.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Ai. Normal ovarian epithelial tissue with high Microcephalin expression. Aii-iv. Adenocarcinoma TMA cores showing strong Microcephalin expression in a low grade tumour (Aii), moderate Microcephalin in grade 2 (Aiii) and low levels of nuclear Microcephalin expression in a high grade tumour (Aiv). All images are 40x magnification. B. The correlation between nuclear Microcephalin expression decreases with increasing tumor grade (p

  • Microcephalin expression in EOC validation set samples inversely correlates with tumour stage.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Ai. Normal ovarian epithelial tissue demonstrating high Microcephalin expression levels. Aii-4iv Adenocarcinoma TMA cores showing strong Microcephalin (Aii), moderate Microcephalin (Aiii) and low levels of nuclear Microcephalin expression (Aiv) in stage 1, 2 and 3 tumours respectively. All images are 40x magnification. B. Weak Microcephalin levels in the nucleus are associated with advanced tumour stage (p = 0.0438 using an ANOVA test).

  • Deregulation of Microcephalin and ASPM Expression Are Correlated with Epithelial Ovarian Cancer Progression
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Mutations in the MCPH1 (Microcephalin) and ASPM (abnormal spindle-like microcephaly associated) genes cause primary microcephaly. Both are centrosomal associated proteins involved in mitosis. Microcephalin plays an important role in DNA damage response and ASPM is required for correct division of proliferative neuro-epithelial cells of the developing brain. Reduced MCPH1 mRNA expression and ASPM mRNA over-expression have been implicated in the development of human carcinomas. Epithelial ovarian cancer (EOC) is characterised by highly aneuploid tumours. Previously we have reported low Microcephalin and high ASPM protein levels and associations with clinico-pathological parameters in malignant cells from ascitic fluids. To confirm these previous findings on a larger scale Microcephalin and ASPM expression levels and localisations were evaluated by immunohistochemistry in two cohorts; a training set of 25 samples and a validation set of 322 EOC tissue samples. Results were correlated to the associated histopathological data. In normal ovarian tissues the Microcephalin nuclear staining pattern was consistently strong. In the cancer tissues, we identified low nuclear Microcephalin expression in high grade and advanced stage tumours (p

  • Microcephalin expression in different EOC subtypes.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    A. Clear cell carcinoma and B. Endometrioid adenocarcinoma both showing strong Microcephalin expression. C. Mucinous adenocarcinoma and D. Serous adenocarcinoma both presenting weak Microcephalin expression. All images are x40 magnification.

Nafisa Wilkinson - One of the best experts on this subject based on the ideXlab platform.

  • deregulation of Microcephalin and aspm expression are correlated with epithelial ovarian cancer progression
    PLOS ONE, 2014
    Co-Authors: Rawiah A Alsiary, Jacquelyn Bond, Ewan E. Morrison, Nafisa Wilkinson, Anke Bruningrichardson, Sandra M. Bell
    Abstract:

    Mutations in the MCPH1 (Microcephalin) and ASPM (abnormal spindle-like microcephaly associated) genes cause primary microcephaly. Both are centrosomal associated proteins involved in mitosis. Microcephalin plays an important role in DNA damage response and ASPM is required for correct division of proliferative neuro-epithelial cells of the developing brain. Reduced MCPH1 mRNA expression and ASPM mRNA over-expression have been implicated in the development of human carcinomas. Epithelial ovarian cancer (EOC) is characterised by highly aneuploid tumours. Previously we have reported low Microcephalin and high ASPM protein levels and associations with clinico-pathological parameters in malignant cells from ascitic fluids. To confirm these previous findings on a larger scale Microcephalin and ASPM expression levels and localisations were evaluated by immunohistochemistry in two cohorts; a training set of 25 samples and a validation set of 322 EOC tissue samples. Results were correlated to the associated histopathological data. In normal ovarian tissues the Microcephalin nuclear staining pattern was consistently strong. In the cancer tissues, we identified low nuclear Microcephalin expression in high grade and advanced stage tumours (p<0.0001 and p = 0.0438 respectively). ASPM had moderate to high nuclear and low to moderate cytoplasmic expression in normal tissue. Cytoplasmic ASPM expression decreased with tumour grade and stage in the serous subtype of EOC (p = 0.023 and p = 0.011 respectively). Cytoplasmic ASPM increased with tumour stage in the endometrioid subtype (p = 0.023). Increasing tumour invasiveness (T3) and lymph node involvement (N1) also correlated with a decrease in cytoplasmic ASPM in EOC (p = 0.02 and p = 0.04 respectively). We have validated previous findings of deregulated expression of Microcephalin and ASPM in EOC by confirming associations for low nuclear Microcephalin levels and high cytoplasmic ASPM levels in a larger scale tumour tissue study. Microcephalin and ASPM may prove useful biomarkers in EOC.

  • Microcephalin expression in EOC validation set samples correlates with tumour grade.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Ai. Normal ovarian epithelial tissue with high Microcephalin expression. Aii-iv. Adenocarcinoma TMA cores showing strong Microcephalin expression in a low grade tumour (Aii), moderate Microcephalin in grade 2 (Aiii) and low levels of nuclear Microcephalin expression in a high grade tumour (Aiv). All images are 40x magnification. B. The correlation between nuclear Microcephalin expression decreases with increasing tumor grade (p

  • Microcephalin expression in EOC validation set samples inversely correlates with tumour stage.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Ai. Normal ovarian epithelial tissue demonstrating high Microcephalin expression levels. Aii-4iv Adenocarcinoma TMA cores showing strong Microcephalin (Aii), moderate Microcephalin (Aiii) and low levels of nuclear Microcephalin expression (Aiv) in stage 1, 2 and 3 tumours respectively. All images are 40x magnification. B. Weak Microcephalin levels in the nucleus are associated with advanced tumour stage (p = 0.0438 using an ANOVA test).

  • Deregulation of Microcephalin and ASPM Expression Are Correlated with Epithelial Ovarian Cancer Progression
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    Mutations in the MCPH1 (Microcephalin) and ASPM (abnormal spindle-like microcephaly associated) genes cause primary microcephaly. Both are centrosomal associated proteins involved in mitosis. Microcephalin plays an important role in DNA damage response and ASPM is required for correct division of proliferative neuro-epithelial cells of the developing brain. Reduced MCPH1 mRNA expression and ASPM mRNA over-expression have been implicated in the development of human carcinomas. Epithelial ovarian cancer (EOC) is characterised by highly aneuploid tumours. Previously we have reported low Microcephalin and high ASPM protein levels and associations with clinico-pathological parameters in malignant cells from ascitic fluids. To confirm these previous findings on a larger scale Microcephalin and ASPM expression levels and localisations were evaluated by immunohistochemistry in two cohorts; a training set of 25 samples and a validation set of 322 EOC tissue samples. Results were correlated to the associated histopathological data. In normal ovarian tissues the Microcephalin nuclear staining pattern was consistently strong. In the cancer tissues, we identified low nuclear Microcephalin expression in high grade and advanced stage tumours (p

  • Microcephalin expression in different EOC subtypes.
    2014
    Co-Authors: Rawiah Alsiary, Jacquelyn Bond, Anke Brüning-richardson, Ewan E. Morrison, Nafisa Wilkinson, Sandra M. Bell
    Abstract:

    A. Clear cell carcinoma and B. Endometrioid adenocarcinoma both showing strong Microcephalin expression. C. Mucinous adenocarcinoma and D. Serous adenocarcinoma both presenting weak Microcephalin expression. All images are x40 magnification.

Anke Bruningrichardson - One of the best experts on this subject based on the ideXlab platform.

  • deregulation of Microcephalin and aspm expression are correlated with epithelial ovarian cancer progression
    PLOS ONE, 2014
    Co-Authors: Rawiah A Alsiary, Jacquelyn Bond, Ewan E. Morrison, Nafisa Wilkinson, Anke Bruningrichardson, Sandra M. Bell
    Abstract:

    Mutations in the MCPH1 (Microcephalin) and ASPM (abnormal spindle-like microcephaly associated) genes cause primary microcephaly. Both are centrosomal associated proteins involved in mitosis. Microcephalin plays an important role in DNA damage response and ASPM is required for correct division of proliferative neuro-epithelial cells of the developing brain. Reduced MCPH1 mRNA expression and ASPM mRNA over-expression have been implicated in the development of human carcinomas. Epithelial ovarian cancer (EOC) is characterised by highly aneuploid tumours. Previously we have reported low Microcephalin and high ASPM protein levels and associations with clinico-pathological parameters in malignant cells from ascitic fluids. To confirm these previous findings on a larger scale Microcephalin and ASPM expression levels and localisations were evaluated by immunohistochemistry in two cohorts; a training set of 25 samples and a validation set of 322 EOC tissue samples. Results were correlated to the associated histopathological data. In normal ovarian tissues the Microcephalin nuclear staining pattern was consistently strong. In the cancer tissues, we identified low nuclear Microcephalin expression in high grade and advanced stage tumours (p<0.0001 and p = 0.0438 respectively). ASPM had moderate to high nuclear and low to moderate cytoplasmic expression in normal tissue. Cytoplasmic ASPM expression decreased with tumour grade and stage in the serous subtype of EOC (p = 0.023 and p = 0.011 respectively). Cytoplasmic ASPM increased with tumour stage in the endometrioid subtype (p = 0.023). Increasing tumour invasiveness (T3) and lymph node involvement (N1) also correlated with a decrease in cytoplasmic ASPM in EOC (p = 0.02 and p = 0.04 respectively). We have validated previous findings of deregulated expression of Microcephalin and ASPM in EOC by confirming associations for low nuclear Microcephalin levels and high cytoplasmic ASPM levels in a larger scale tumour tissue study. Microcephalin and ASPM may prove useful biomarkers in EOC.

  • aspm and Microcephalin expression in epithelial ovarian cancer correlates with tumour grade and survival
    British Journal of Cancer, 2011
    Co-Authors: Anke Bruningrichardson, Jacquelyn Bond, Nafisa Wilkinson, Julie Richardson, Rawiah A Alsiary, L Mccormack, R Hutson, David A Cairns, Philip A Burns, Geoffrey Hall
    Abstract:

    ASPM and Microcephalin expression in epithelial ovarian cancer correlates with tumour grade and survival