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Updated: Aug 15, 2026

Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays
07:42

Assessment of Resistance to Tyrosine Kinase Inhibitors by an Interrogation of Signal Transduction Pathways by Antibody Arrays

Published on: September 19, 2018

Tyrosine kinase receptor--nuclear protooncogene interactions in breast cancer

R B Dickson, D S Salomon, M E Lippman

    Cancer Treatment and Research
    |January 1, 1992
    PubMed

    Insights

    Tyrosine kinase receptors and steroid hormones are crucial for mammary gland development. Their interaction with protooncogenes like c-myc can drive breast cancer progression, especially when amplified.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Developmental Biology

    Background:

    • Tyrosine kinase receptors (TKRs) and steroid hormones play key roles in mammary gland development and differentiation.
    • Protooncogenes, such as c-myc, are implicated in growth control mechanisms.
    • Aberrant signaling through TKRs and protooncogenes is linked to breast cancer development.

    Purpose of the Study:

    • To explore the roles of TKRs, growth factors, steroid hormones, and protooncogenes in mammary gland development and carcinogenesis.
    • To investigate the intersection of these pathways in controlling cell growth and transformation.
    • To understand the distinct mechanisms by which these factors contribute to breast cancer.

    Main Methods:

    • Review of accumulating evidence on growth factor and hormone signaling in mammary development.
    • Analysis of protooncogene induction and amplification in relation to TKR activity.
    • Examination of findings from transgenic mouse studies investigating specific genes in mammary carcinogenesis.

    Main Results:

    • TKRs and steroid hormones are vital for normal mammary gland development.
    • Amplification of c-myc, alongside activated TKRs (EGF, FGF), can lead to transformation, not just proliferation, in breast cancer.
    • Overexpression/amplification of c-erbB-2 and EGF receptor correlates with increased malignancy and poor prognosis.
    • Transgenic models confirm roles for TGF-alpha, EGF receptor, and c-myc in mammary carcinogenesis, with distinct initiating vs. promoting mechanisms.

    Conclusions:

    • TKRs and steroid hormones are essential for mammary gland development.
    • Aberrant signaling, particularly TKR activation and protooncogene amplification (e.g., c-myc), contributes significantly to breast cancer initiation and progression.
    • Specific genetic alterations, like c-erbB-2 amplification, worsen prognosis, highlighting distinct roles in tumorigenesis.

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