Mechanisms / Pathophysiology of Breast Cancer

Rodrigo Arrangoiz MS, MD, FACS, FSSO
  • The exact mechanism by which breast cancer is initiated is unknown:
    • However, much effort has been made to molecularly characterize breast cancer and delineate its formation and progression
  • At the cell of origin level:
    • The clonal evolution model:
      • In which mutations accumulate
      • Epigenetic changes in tumor cells occur
      • The ‘fittest’ cells survive
    • The cancer stem cell model:
      • In which only the precursor cancer cells:
        • Initiate and sustain progression
    • The clonal evolution model and the cancer stem cell model:
      • Are both implicated, and further complicated by the fact that cancer stem cells may also evolve in a clonal fashion
  • At the morphological level:
    • There is a continuum of lesions and genetic modifications from normal glands to cancer
  • At the molecular level:
    • There is evidence showing that breast cancer evolves along two divergent molecular pathways of progression:
      • Mainly related to ER expression, and tumor grade and proliferation:
        • Described in the intrinsic classification
      • Furthermore, the identification of breast cancer susceptibility genes:
        • Has shed the light on some aspects of the pathogenesis of both sporadic and inherited breast cancer
      • The first pathway:
        • The low-grade-like pathway — is characterized by gain of 1q, loss 16q, infrequent amplification of 17q12 and a gene expression signature (GES) with a majority of genes associated with the ER phenotype, diploid or near diploid karyotypes and low tumour grade. The luminal A group and to some extent the luminal B group fall into this pathway. The second pathway — the high-grade-like pathway — is charac- terized by loss of 13q, gain of chromosomal region 11q13, amplification of 17q12 (containing ERBB2, encoding HER2) and an expression signature of genes involved in the cell cycle and cellular proliferation61. Tumours composed of intermediate to high grade, including HER2-positive tumours and TNBC, fall into this pathway

Published by Rodrigo Arrangoiz MS, MD, FACS, FSSO

My name is Rodrigo Arrangoiz I am a breast surgeon/ thyroid surgeon / parathyroid surgeon / head and neck surgeon / surgical oncologist that works at Center for Advanced Surgical Oncology in Miami, Florida. I was trained as a surgeon at Michigan State University from (2005 to 2010) where I was a chief resident in 2010. My surgical oncology and head and neck training was performed at the Fox Chase Cancer Center in Philadelphia from 2010 to 2012. At the same time I underwent a masters in science (Clinical research for health professionals) at the University of Drexel. Through the International Federation of Head and Neck Societies / Memorial Sloan Kettering Cancer Center I performed a two year head and neck surgery and oncology / endocrine fellowship that ended in 2016. Mi nombre es Rodrigo Arrangoiz, soy cirujano oncólogo / cirujano de tumores de cabeza y cuello / cirujano endocrino que trabaja Center for Advanced Surgical Oncology en Miami, Florida. Fui entrenado como cirujano en Michigan State University (2005 a 2010 ) donde fui jefe de residentes en 2010. Mi formación en oncología quirúrgica y e n tumores de cabeza y cuello se realizó en el Fox Chase Cancer Center en Filadelfia de 2010 a 2012. Al mismo tiempo, me sometí a una maestría en ciencias (investigación clínica para profesionales de la salud) en la Universidad de Drexel. A través de la Federación Internacional de Sociedades de Cabeza y Cuello / Memorial Sloan Kettering Cancer Center realicé una sub especialidad en cirugía de cabeza y cuello / cirugia endocrina de dos años que terminó en 2016.

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