Gabriel N. Hortobagyi, MD, Oral History Interview, January 23, 2013

Major Topics Covered: The World Summit Against Cancer The Breast Cancer Research Group Breast cancer treatments and service: evolution at MD Andersonhttps://openworks.mdanderson.org/mchv_interviewsessions/1215/thumbnail.jp

OncoLog, Volume 52, Number 09, September 2007

Sparing Life and Limb Can a Common Spice Be Use to Treat Cancer? House Call: Your First Colonoscopy: Here\u27s What You Can Expect DiaLog: Targeted Therapies Are Here to Stay, by Gabriel N. Hortobagyi, MDhttps://openworks.mdanderson.org/oncolog/1165/thumbnail.jp

Gabriel N. Hortobagyi, MD, Oral History Interview, January 28, 2013

Major Topics Covered: Patient centered service, evolution of at MD Anderson Leadership and mentoring experiences and principles Educating breast medical oncologistshttps://openworks.mdanderson.org/mchv_interviewsessions/1216/thumbnail.jp

Gabriel N. Hortobagyi, MD, Oral History Interview, March 15, 2013

Major Topics Covered: Overview of breast medical oncology: as a field; history of at MD Anderson Service to organizations and projects in the United States and abroad Views on MD Anderson presidentshttps://openworks.mdanderson.org/mchv_interviewsessions/1217/thumbnail.jp

Gabriel N. Hortobagyi, MD, Oral History Interview, November 30, 2012

Major Topics Covered: Personal and educational background The Department of Developmental Therapeutics; Emil J Freireich, MDhttps://openworks.mdanderson.org/mchv_interviewsessions/1213/thumbnail.jp

First-cycle absolute neutrophil count can be used to improve chemotherapy-dose delivery and reduce the risk of febrile neutropenia in patients receiving adjuvant therapy: a validation study

BACKGROUND: The nadir value of the absolute neutrophil count (ANC) in the first cycle of chemotherapy is an effective predictor of subsequent neutropenic events. This study was designed to validate an earlier published study based on a retrospective data analysis from a prospective randomized clinical trial. METHODS: The original published model was applied to a trial of 143 patients to cross-validate the model. We also tested the specification of the model on our data by using a logistic regression model with several variables, including first-cycle nadir ANC, age, menopausal status, hormone-receptor status, previous radiotherapy, and first-cycle decrease in hemoglobin concentration. Patients received fluorouracil, doxorubicin, and cyclophosphamide every 21 or 28 days for six cycles without hematopoietic support from colony-stimulating factor. RESULTS: In the cross-validation analysis, the original model successfully classified patients by risk of neutropenic events (C = 0.78). When the model specification was tested, first-cycle nadir ANC was the sole significant (P < 0.0001) predictor of neutropenic events and the model had a good predictive power (C = 0.78). The estimated relative risk of 4.8 did not differ from the risk cited in the original model (P = 0.91). A significantly higher percentage of our patients with a low first-cycle nadir ANC of 0.25 × 10(9)/liter or less experienced febrile neutropenia (30% versus 10%, P = 0.04) and received at least 85% of the planned dose intensity (55% versus 32%, P = 0.05). CONCLUSIONS: The original risk model used to predict neutropenic events was validated by our study. This information can be used to target high-risk patients for prophylactic treatment with filgrastim (recombinant methionyl human granulocyte colony-stimulating factor) in chemotherapy cycles 2 to 6

Ribonuclease 1 Enhances Antitumor Immunity Against Breast Cancer by Boosting T Cell Activation

The secretory enzyme human ribonuclease 1 (RNase1) is involved in innate immunity and anti-inflammation, achieving host defense and anti-cancer effects; however, whether RNase1 contributes to adaptive immune response in the tumor microenvironment (TME) remains unclear. Here, we established a syngeneic immunocompetent mouse model in breast cancer and demonstrated that ectopic RNase1 expression significantly inhibited tumor progression. Overall changes in immunological profiles in the mouse tumors were analyzed by mass cytometry and showed that the RNase1-expressing tumor cells significantly induced CD4+ Th1 and Th17 cells and natural killer cells and reduced granulocytic myeloid-derived suppressor cells, supporting that RNase1 favors an antitumor TME. Specifically, RNase1 increased expression of T cell activation marker CD69 in a CD4+ T cell subset. Notably, analysis of cancer-killing potential revealed that T cell-mediated antitumor immunity was enhanced by RNase1, which further collaborated with an EGFR-CD3 bispecific antibody to protect against breast cancer cells across molecular subtypes. Our results uncover a tumor-suppressive role of RNase1 through adaptive immune response in breast cancer in vivo and in vitro, providing a potential treatment strategy of combining RNase1 with cancer immunotherapies for immunocompetent patients