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In bringing new technologies to the field, the Director's Challenge grant will fund institutions to use novel technologies in devising molecular classifications for human cancers including breast.
Previous ground-breaking studies have reported molecular classifications for key cancer types based on their global patterns of gene expression [ 13- 16].
In this review we will focus on proteomic analysis of the leukemic cells in CML, juvenile chronic myelomonocytic leukemia (JCMML), adult chronic myelomonocytic leukemia (CMML), and AML, and illustrate how proteomics may create new diagnostics and molecular classifications for the disease.
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The focus of this review is on implications of molecular classification for prognosis and therapeutic decision making in HCC patients.
Our findings suggest that the gene expression signature of DCs can provide a molecular classification for use in the selection of anti-inflammatory or adjuvant molecules with specific effects on DC activity.
These kinds of studies indicate the complexity in finding a consistent molecular classification for such a problem.
The existence of this MA subgroup suggests a new molecular classification for breast cancers, including luminal, MA and BL breast cancer subgroups [ 5].
Based on the gene expression profile (GEP) of a tumor, a molecular classification for breast cancer was proposed [ 1] and several molecular signatures were reported to predict the risk of recurrence and treatment response [ 2- 5].
As there are over a hundred types of cancers, and potentially even more subtypes, it is essential to develop multi-category methodologies for molecular classification for any meaningful practical application.
As there are over a hundred types of cancers, and potentially even more subtypes [ 8], it is essential to develop multi-category methodologies for molecular classification for any practical application [ 9].
Genomic information has been increasingly used for molecular classifications of tumors because it provides a more objective view than histopathological approach and it sheds light on the molecular mechanisms of tumor heterogeneity.
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