Oncology Times

Featured Books

The Bethesda Handbook of Clinical Oncology

Jame Abraham,
James L. Gully,
Carman J. Allegra
Cancer management information is presented in a reader-friendly format that offers a comprehensive review of each disease along with the most commonly used treatment regimens, including chemotherapy dosing and schedules
Read sample content on Breast Cancer
Monthly Question:

A 65-year-old patient with invasive ductal cancer had a left modified radical mastectomy and 2 lymph nodes were positive for invasive cancer. Her tumor size was 2.7 cm and she was staged as T2 N1 M0 (IIB). ER/PR was 90% to 100% positive and K1 67 was 5%. HER-2/neu- was negative by immunohistochemistry. She is in your office to discuss about adjuvant therapy options. She is otherwise very healthy.
A. Since she has a IIB tumor, strongly recommend chemotherapy with TC for four cycles.
B. Chemotherapy may not add much value to her treatment; her maximum benefit will be from endocrine therapy.
C. She should receive radiation therapy since she had a 2.7 cm tumor and one lymph node positive.
D. It is up to the patient to decide about her therapy since she is older than 65
Check Back in November for the Answer!

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Dendritic Cells, Inflammation, and Breast Cancer
The Cancer Journal
FIGURE 1. Pathogenic type 2 cytokine loop in breast cancer. Dendritic cells in breast cancer are exposed to cancer-derived factors—for example, TSLP—that skew their maturation toward expression of OX40L and capacity to activate CD4+ T cells to secrete IL-13 and IL-4, type 2 cytokines. In this environment, responding lymphocytes secreting IL-4 and IL-13 promote tumor development either directly or indirectly via myeloid cells including macrophages. Direct effects include triggering antiapoptotic pathways and steroid metabolism in epithelial cancer cells, as well as promoting stromal fibroblast proliferation and differentiation. Indirect effects include triggering secretion of growth (epidermal growth factor) and proangiogenic (vascular endothelial growth factor) factors by tumor-infiltrating macrophages as well as PDL-1 expression and IL-10 secretion that blunt CD8+ T cell effector function. Cancer cells are likely to also directly activate innate lymphocytes secreting IL-13. The molecular and cellular factors contributing to the global IL-13 production in epithelial cancers likely extend beyond TSLP and are topics of intense study. Another active area is the question of TSLP regulation, whether all breast cancer express it, and at which stages, as well as its role in metastatic niche formation.