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Role of inflammatory infiltrates in triple negative breast cancer
  1. Hirofumi Matsumoto1,2,
  2. Si-lin Koo3,
  3. Rebecca Dent3,
  4. Puay Hoon Tan1,
  5. Jabed Iqbal1
  1. 1Department of Pathology, Singapore General Hospital, Singapore, Singapore
  2. 2Department of Pathology, Ryukyu University Hospital, Okinawa, Japan
  3. 3Department of Medical Oncology, National Cancer Centre, Singapore, Singapore
  1. Correspondence to Dr Jabed Iqbal, Department of Pathology, Singapore General Hospital, 20 College Road, Academia, Diagnostic Tower, Level 10, Singapore 169608, Singapore; jabed.iqbal{at}


Triple negative breast cancer (TNBC) is a heterogenous disease often characterised by aggressive biology and poor prognosis. Efforts to precisely treat TNBC have been compounded by the lack of specific therapeutic molecular targets. Recent transcriptomic studies have revealed, among others, an immunomodulatory subtype of TNBC, whereby activated immune response genes are associated with good prognosis. Since then, a great deal of effort has been made to understand the immune microenvironment of some TNBC subtype, which comprises several immune cell populations including lymphocytes and macrophages. There is increasing evidence that the basal subtype may be significantly regulated by tumour-infiltrating T-cells and that high levels of tumour-infiltrating CD8+ T-cells may be a reflection of improved prognosis with chemotherapy sensitivity in TNBC. On the other hand, tumour-associated macrophages have been associated with a relatively poor outcome in TNBC. Comparison of the immune signatures in TNBC with non-TNBC may furthermore help us to understand these immune mechanisms potentially leading to new therapeutic approaches. Within this short review, we discuss the current scientific evidence regarding (a) the role of tumour-infiltrating lymphocytes in the clinical outcome in TNBC and (b) the newly discovered immunomodulatory genotype that may provide for a therapeutic target in TNBC.

  • Breast cancer
  • lymphocytes
  • macrophages
  • inflammation
  • immunology

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