Expression of kinase genes in primary hyperparathyroidism;
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Pinhas P. Schachter1 M.D., Suhail Ayesh2 PhD, Tamar Schneider2, PowerPoint PPT Presentation


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Expression of kinase genes in primary hyperparathyroidism; Adenoma versus hyperplastic parathyroid tissue. Pinhas P. Schachter1 M.D., Suhail Ayesh2 PhD, Tamar Schneider2, Morris Laster M.D., Abraham Czerniak1 M.D. and Abraham Hochberg2. Background.

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Pinhas P. Schachter1 M.D., Suhail Ayesh2 PhD, Tamar Schneider2,

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Pinhas p schachter1 m d suhail ayesh2 phd tamar schneider2

Expression of kinase genes in primary hyperparathyroidism;Adenoma versus hyperplastic parathyroid tissue

Pinhas P. Schachter1 M.D., Suhail Ayesh2 PhD, Tamar Schneider2,

Morris Laster M.D., Abraham Czerniak1 M.D. and Abraham Hochberg2


Background

Background

Differentiation between parathyroid hyperplasia and adenoma is difficult and based on the surgeon’s skill. Microarrays and other sophisticated research tools generate information about differential gene expression in various tissues.

Exploration of genes that express differentially in one tissue will enable identification and perhaps development of new methods of preoperative or intraoperative diagnosis.


Methods

Methods

  • RNA was extracted from parathyroid hyperplasia and adenoma tissue and hybridized to a microarray containing 359 human cDNAs of known kinase genes.

  • Signals of exposure were scanned and quantified with Atlas – Image, version 2, software for digital image analysis. The program generates a color schematic comparison view and numerical data in a tabular format for further analysis.


Expression of kinase genes in adenoma parathyroid tissue

Expression of kinase genes In Adenoma Parathyroid Tissue


Expression of kinase genes in hyperplasia parathyroid tissue

Expression of kinase genes In hyperplasia Parathyroid Tissue


The first row data format in text mode

The first row data format in text mode


The second excel format of data

The second excel format of data


The third access format after classefication

The third access format after classefication


Table 1 genes expressed in parathyroid hyperplasia only

Table 1 Genes expressed in Parathyroid hyperplasia only


Table 2 genes expressed in parathyroid adenoma only

Table 2 Genes expressed in Parathyroid adenoma only


Table 3 genes up regulated in parathyroid adenoma

Table 3 Genes up regulated in Parathyroid adenoma


Table 4 genes down regulated in parathyroid adenoma

Table 4 Genes down regulated in Parathyroid adenoma


Table 5 genes categories by function

Table 5 Genes categories by function


Conclusion

Conclusion

The ratio values that are considered significant (<0.5 or >1.5) suggest that genes up-regulated in parathyroid adenoma are those responsible for angiogenesis and production of blood vessels. Genes down-regulated in parathyroid adenoma and expressed in hyperplasia are related to a decrease in apoptosis. Moreover, an interesting gene expressed only in the hyperplasia sample is increased in relation to in vivo proliferation activities


Http research dfci harvard edu korsmeyer mll htm

http://research.dfci.harvard.edu/korsmeyer/MLL.htm

  • MLL translocations specify a distinct gene

    expression profile that distinguishes a

    unique leukemia

    Scott A. Armstrong1–4, Jane E. Staunton5, Lewis B. Silverman1,3,4, Rob Pieters6, Monique L. den Boer6, Mark

    D. Minden7, Stephen E. Sallan1,3,4, Eric S. Lander5, Todd R. Golub1,3,4,5* & Stanley J. Korsmeyer2,4,8*

    *These authors contributed equally to this work.


Abstract

Abstract

  • Acute lymphoblastic leukemias carrying a chromosomal translocation involving the mixed-lineage leukemia gene (MLL, ALL1, HRX) have a particularly poor prognosis. Here we show that they have a characteristic, highly distinct gene expression profile that is consistent with an early hematopoietic progenitor expressing select multilineage markers and individual HOX genes.

    Clustering algorithms reveal that lymphoblastic leukemias with MLL translocations can clearly be separated from conventional acute lymphoblastic and acute myelogenous leukemias.

    We propose that they constitute a distinct disease, denoted here as MLL, and show that the differences in gene expression are robust enough to classify leukemias correctly as MLL, acute lymphoblastic leukemia or acute myelogenous leukemia.

    Establishing that MLL is a unique entity is critical, as it mandates the examination of

    selectively expressed genes for urgently needed molecular targets.


Pinhas p schachter1 m d suhail ayesh2 phd tamar schneider2

Genes that distinguish ALL from MLL. The 100 genes that are most highly correlated with the class distinction


Selected early lymphocyte gene expression in all and mll

Selected early lymphocyte gene expression in ALL and MLL


Selected hox gene expression in all and mll

Selected HOX gene expression in ALL and MLL


Comparison of gene expression between all mll and aml all red mll blue aml yellow

Comparison of gene expression between ALL, Mll and AML ALL (red), MLL (blue), AML (yellow)


Genes that are specifically expressed in mll all or mll

Genes that are specifically expressed in MLL, ALL or MLL


Pinhas p schachter1 m d suhail ayesh2 phd tamar schneider2

Classification of ALL, MLL and AML on the basis of their gene expression profile. The error rate in class prediction (y axis) is plotted against the number of genes used to build the model (x axis).


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