Alea A. Mills
Cancer Center Member
Ph.D., University of California, Irvine, 1997
firstname.lastname@example.org | 516-367-6910
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
The evolution of autism research
May 25, 2023
The conversation around autism has evolved over the past two decades. So has CSHL research. This retrospective shows how we’ve helped move the needle.
Cracking the mystery behind a deadly brain cancer
December 21, 2022
Scientists solve the mystery of how glioblastoma turns off cancer defenses without the usual cancer-inducing mutations.
Cold Spring Harbor Laboratory 2022 Ph.D.’s
May 1, 2022
The School of Biological Sciences awarded Ph.D. degrees to ten students this year. Here are some stories and memories from their time at CSHL.
The Darlene Carbone Brain Tumor Foundation donates $25,000 to CSHL
January 24, 2022
The Darlene Carbone Brain Tumor Foundation donates $25,000 to Dr. Alea Mills lab for glioblastoma research.
Breaking the chain that culminates in cancer
December 1, 2021
CSHL scientists have discovered a way to shut down a cancer-causing protein by inhibiting a cascade of proteins that activate it.
CSHL graduate student wins HHMI fellowship
August 15, 2019
WSBS student David Johnson won a 2019 Gilliam Fellowships for Advanced Study for leadership and diversity in science.
What does sight mean to a cancer researcher?
February 26, 2019
Postdoc Leah Banks discusses vision’s role in cancer research, and how nearly losing her sight gave her a new perspective on her work.
Path to cancer in the brain set by protein CHD5
September 14, 2018
Researchers find that protein keeps neural stem cells from activating too soon and hindering brain development
Portrait of a Neuroscience Powerhouse
April 27, 2018
A relatively small neuroscience group at CSHL is having an outsized impact on a dynamic and highly competitive field
Realizing a dream: How a program for undergraduates placed me at the center of CRISPR research
August 16, 2017
Hands-on experience using CRISPR and access to top scientists from around the world who are pioneering its use made this a memorable summer for.
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
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