Alea A. Mills

Alea A. Mills

Cancer Center Member

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

mills@cshl.edu | 516-367-6910

Mills Lab Website   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

Cancer-associated fibroblasts promote cancer stemness by inducing expression of the chromatin-modifying protein CBX4 in squamous cell carcinoma

18 Aug 2023 | Carcinogenesis | 44(6):485-496
Fisher, Matthew, Balinth, Seamus, Hwangbo, Yon, Wu, Caizhi, Ballon, Carlos, Goldberg, Gary, Mills, Alea

Chd5 regulates the transcription factor Six3 to promote neuronal differentiation

13 Jan 2023 | Stem Cells | :sxad002
Shrestha, Padmina, Jaganathan, Anbalagan, Huilgol, Dhananjay, Ballon, Carlos, Hwangbo, Yon, Mills, Alea

BRD8 maintains glioblastoma by epigenetic reprogramming of the p53 network

21 Dec 2022 | Nature
Sun, Xueqin, Klingbeil, Olaf, Lu, Bin, Wu, Caizhi, Ballon, Carlos, Ouyang, Meng, Wu, Xiaoli, Jin, Ying, Hwangbo, Yon, Huang, Yu-Han, Somerville, Tim, Chang, Kenneth, Park, Jung, Chung, Taemoon, Lyons, Scott, Shi, Junwei, Vogel, Hannes, Schulder, Michael, Vakoc, Christopher, Mills, Alea

ΔNp63α in cancer: importance and therapeutic opportunities

14 Sep 2022 | Trends in Cell Biology | :S0962-8924(22)00194
Fisher, Matthew, Balinth, Seamus, Mills, Alea

EZH2 regulates a SETDB1/ΔNp63α axis via RUNX3 to drive a cancer stem cell phenotype in squamous cell carcinoma

21 Jul 2022 | Oncogene
Balinth, Seamus, Fisher, Matthew, Hwangbo, Yon, Wu, Caizhi, Ballon, Carlos, Sun, Xueqin, Mills, Alea

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


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

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