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CURRENT PUBLICATIONS
LABORATORY RESEARCH
Genomic Antagonism between Retinoic Acid and Estrogen Signaling in Breast Cancer
RAR binding throughout the genome is highly coincident with estrogen receptor-alpha (ER-alpha) binding, resulting in a widespread crosstalk of RA and estrogen signaling to antagonistically regulate breast cancer-associated genes. [Cell]
The mir-34 MicroRNA is Required for the DNA Damage Response
In Vivo in C. elegans and In Vitro in Human Breast Cancer Cells Observations confirm that mir-34 is required for a normal cellular response to DNA damage and point to a potential therapeutic use for anti-miR-34 as a radiosensitizing agent in p53-mutant breast cancer. [Oncogene]
Breast Cancer Stem Cells: Tools and Models One Can Rely On Authors review tools, markers, and in vitro and in vivo models used to study breast cancer stem cells. [BMC Cancer]
WW Domain Containing E3 Ubiquitin Protein Ligase 1 Targets the Full-Length ErbB4 for Ubiquitin-mediated Degradation in Breast Cancer WWP1 and its family members suppress ErbB4 expression and function in breast cancer. [Oncogene]
Targeting Inhibitor of Apoptosis Proteins in Combination with ErbB Antagonists in Breast Cancer Multiple Inhibitor of Apoptosis (IAPs) are concomitantly expressed in breast cancers. In combination with clinically relevant Her2 treatments, IAP antagonists promote apoptosis and reduce the cell turnover index of breast cancers. [Breast Cancer Res]
Trim24 Targets Endogenous p53 for Degradation Trim24 ubiquitylates and negatively regulates p53 levels, suggesting Trim24 as a therapeutic target to restore tumor suppression by p53. [PNAS]
Tissue-Specific Regulation of Porcine Prolactin Receptor Expression by Estrogen, Progesterone, and Prolactin Data reveal that specific combinations of estrogen, progestin, and prolactin (PRL) differentially regulate pPRLR-LF expression in the endometrium and mammary glands, and that the action of PRL on its target tissues is dependent upon pPRLR-LF abundance more so than the local PRL expression. [J Endocrinol]
Accelerated Mammary Maturation and Differentiation, and Delayed MMTVNeu-Induced Tumorigenesis of K303R Mutant ER-Alpha Transgenic Mice Aberrant estrogenic signaling through the K303R ER-alpha mutation may lead to precocious alveolar budding in virgin mice, and to an expedited maturation and differentiation phenotype in the mammary glands of hormonally stimulated animals. [Oncogene]
Gene Expression Profiling Identifies Activated Growth Factor Signaling in Poor Prognosis (Luminal-B) Estrogen Receptor Positive Breast Cancer Data demonstrate that activation of GF signaling pathways, independent of HER2 over-expression, could be contributing to the poor prognosis of the luminal-B ER+ BC subtype. [BMC Cancer]
The Role of YY1 in Reduced HP1 Alpha Gene Expression in Invasive Human Breast Cancer Cells A reduction of YY1 expression in breast cancer cells could contribute to the acquisition of an invasive phenotype through increased cell migration as well as by reduced expression of HP1alpha. [Breast Cancer Res]
CLINICAL RESEARCH
Endocrine Effects of Adjuvant Letrozole Compared with Tamoxifen in Hormone-Responsive Postmenopausal Patients with Early Breast Cancer: The HOBOE (Phase III) Trial
Adjuvant letrozole and tamoxifen result in significantly distinct endocrine effects. Such differences can explain the higher efficacy of letrozole as compared with tamoxifen. [J Clin Oncol]
American Society of Clinical Oncology Clinical Practice Guideline Update on the Use of Pharmacologic Interventions Including Tamoxifen, Raloxifene, and Aromatase Inhibition for Breast Cancer Risk Reduction
Update of the 2002 American Society of Clinical Oncology guideline on pharmacologic interventions for breast cancer (BC) risk reduction. [J Clin Oncol]
Phase I Study of Prolonged-Infusion Gemcitabine Combined with Cyclophosphamide in Patients with Metastatic Carcinoma of the Breast: Tolerability of an Optimal Dose Schedule
A phase I study was initiated to determine the maximum tolerated dose (MTD) of prolonged-infusion gemcitabine combined with cyclophosphamide in patients with metastatic breast carcinoma (MBC). [Oncology]

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