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Anna Arnal Estape, PhD, BS

Associate Research Scientist

Contact Information

Anna Arnal Estape, PhD, BS

Office Location

  • FMP 112
    Fitkin Memorial Pavilion
    789 Howard Avenue
    New Haven, CT 06519

Extensive Research Description

Cancer cells disobey signaling networks that control cell division and differentiation during tumor progression and metastasis. My early work during my PhD focused on the role of a breast cancer oncogenic signal, ERBB2, in the evasion of two tumor suppressor mechanisms in breast cancer cells, namely TGFb cytostasis and oncogene-induced senescence. We identified C/EBPb as the molecular link between ERBB2 oncogenic signal and the evasion of these two potent suppressive functions in tumor cells. Despite improvement in primary tumor targeted, metastasis accounts for 90% of solid tumors-related death. We performed an in vivo screen that identified mediators of bone metastasis in breast cancer cells. We validated Noggin and Maf as key effectors of bone metastasis. These publications report the need for stratification of breast cancer patients to determine those with increased risk of bone relapse that will benefit from the therapeutic targeting of these pathways.

In my postdoctoral training at Albert Einstein, I acquired expertise in genetically engineered mouse models (GEMMs) of prostate cancer and microenvironmental cues that promotes tumor progression and metastasis such as angiogenesis and the autonomous nervous system. We identified that adrenergic signaling is responsible for a metabolic switch on endothelial cells that allow prostate progression from PIN stage to adenocarcinoma.

In 2014 I joined the laboratory of Don Nguyen in the Pathology department to continue my studies of tumor biology and metastasis of non-small cell lung cancers (NSCLCs). We are interested in determining the function of a transcriptional network, which normally controls epithelial differentiation in the airways, in different NSCLC subtypes. We found that this transcriptional network correlates with poor outcome in patients with lung adenocarcinoma (LUAD), a distinct subtype of NSCLC. To this end, we have developed several GEMMs of LUAD to interrogate the requirements of the metastasis suppressors Hopx and Gata6 in tumor initiation.

I believe science requires a collaborative environment for success. During my PhD and postdoctoral training, I developed my research in tight collaboration with different coworkers within the laboratory as well as researchers from different institutions. From these fruitful collaborations, several projects were published in high impact journals within our field.

Coauthors

Research Interests

Adenocarcinoma; Cell Biology; Disease Models, Animal; Neoplasm Metastasis; Pathology; Tumor Microenvironment

Public Health Interests

Community Engagement

Selected Publications

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