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Alea A. Mills

Alea A. Mills

Professor
Cancer Center Member

Ph.D., University of California, Irvine, 1997

mills@cshl.edu | 516-367-6910

Faculty Profile

Cells employ stringent controls to ensure that genes are turned on and off at the correct time and place. Accurate gene expression relies on several levels of regulation, including how DNA and its associated molecules are packed together. I study the diseases arising from defects in these control systems, such as aging and cancer.

Alea Mills is studying genetic pathways important in cancer, aging, and autism, identifying the genetic players and determining how aberrations in their functions culminate in human disease. Through innovative use of a technique called “chromosome engineering,” the Mills group discovered that one of the most common genetic alterations in autism—deletion of a 27-gene cluster on chromosome 16—causes autism-like features in mice. These autism-like movement impairments can be identified just days after birth, suggesting that these features could be used to diagnose autism. Mills has also used chromosome engineering to identify a tumor suppressor gene that had eluded investigators for three decades. The gene, called Chd5, was shown by Mills to regulate an extensive cancer-preventing network. This year, the Mills lab uncovered how Chd5 acts as a tumor suppressor: It binds to a protein found within chromatin to turn specific genes on or off, halting cancer progression. The epigenetic role of Chd5 in development, cancer, and stem-cell maintenance is currently being investigated. The Mills lab is also studying p63 proteins, which regulate development, tumorigenesis, cellular senescence, and aging in vivo. They succeeded in halting the growth of malignant tumors by turning on production of one of the proteins encoded by the p63 gene, called TAp63. TAp63 also exerts other protective effects. This year, the Mills lab generated a mouse model which allowed them to find that TAp63 is required to prevent a genetic disorder, known as EEC (ectrodactyly-ectodermal dysplasia cleft lip/palate syndrome), which is characterized by a cleft palate and major deformities of the skin and limbs in infants. In addition, they recently discovered that a different version of p63, called ΔNp63, reprograms stem cells of the skin to cause carcinoma development—the most prevalent form of human cancer. Modulation of these proteins may offer new ways to treat human malignancies in the future.

Woman of the Year in Health/Medicine – 2012

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All Publications

P63 targeted deletion under the FOXN1 promoter disrupts pre-and post-natal thymus development, function and maintenance as well as induces severe hair loss

25 Jan 2022 | PLoS One | 17(1)
Stefanski, Heather, Xing, Yan, Nicholls, Jemma, Jonart, Leslie, Goren, Emily, Taylor, Patricia, Mills, Alea, Riddle, Megan, McGrath, John, Tolar, Jakub, Hollander, Georg, Blazar, Bruce

BRD4 REGULATES TRANSCRIPTION FACTOR ∆Np63αTO DRIVE A CANCER STEM CELL PHENOTYPE IN SQUAMOUS CELL CARCINOMAS

25 Oct 2021 | Cancer Research | :canres.0707.2021
Fisher, Matthew, Balinth, Seamus, Hwangbo, Yon, Wu, Caizhi, Ballon, Carlos, Wilkinson, John, Goldberg, Gary, Mills, Alea

p63-related signaling at a glance

11 Sep 2020 | Journal of Cell Science | 133(17)
Fisher, M, Balinth, S, Mills, A

Reversal of Synaptic and Behavioral Deficits in a 16p11.2 Duplication Mouse Model via Restoration of the GABA Synapse Regulator Npas4

25 Feb 2020 | Molecular Psychiatry
Rein, B, Tan, T, Yang, F, Wang, W, Williams, J, Zhang, F, Mills, A, Yan, Z

The potential impact of tumor suppressor genes on human gametogenesis: a case-control study

2 Dec 2019 | Journal of Assisted Reproduction and Genetics
Hershlag, A, Peyser, A, Bristow, S, Puig, O, Pollock, A, Niknazar, M, Mills, A

Altered sleep architecture, rapid eye movement (REM) sleep, and neural oscillation in a mouse model of human chromosome 16p11.2 microdeletion

12 Dec 2018 | Sleep | 42(3)
Lu, H, Pollack, H, Lefante, J, Mills, A, Tian, D

Chromatin-mediated translational control is essential for neural cell fate specification

23 Aug 2018 | Life Science Alliance | 1(4):e201700016
Hwang, D, Jaganathan, A, Shrestha, P, Jin, Y, El-Amine, N, Wang, S, Hammell, M, Mills, A

Altered synaptic transmission and maturation of hippocampal CA1 neurons in a mouse model of human chr16p11.2 microdeletion

1 Mar 2018 | Journal of Neurophysiology | 119(3):1005-1018
Lu, H, Mills, A, Tian, D

Different regulation of limb development by p63 transcript variants

2017 | PLoS One | 12(3):e0174122
Kawata, M, Taniguchi, Y, Mori, D, Yano, F, Ohba, S, Chung, U, Shimogori, T, Mills, A, Tanaka, S, Saito, T

Regulation of Chondrocyte Survival in Mouse Articular Cartilage by p63

1 Mar 2017 | Arthritis and Rheumatology | 69(3):598-609
Taniguchi, Y, Kawata, M, Ho Chang, S, Mori, D, Okada, K, Kobayashi, H, Sugita, S, Hosaka, Y, Inui, H, Taketomi, S, Yano, F, Ikeda, T, Akiyama, H, Mills, A, Chung, U, Tanaka, S, Kawaguchi, H, Saito, T

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