Highlighted Publications

Loss of CDK4/6 activity in S/G2 phase leads to cell cycle reversal.
Cornwell JA, Crncec A, Afifi MM, Tang K, Amin R, Cappell SD.
Nature. 2023 Jul;619(7969):363-370. doi: 10.1038/s41586-023-06274-3

Schematic of the cell cycle feed-forward loop — A feed-forward loop underlies CDK2 reversibility.

Irreversible cell cycle exit associated with senescence is mediated by constitutive MYC degradation.
Afifi MM, Crncec A, Cornwell JA, Cataisson C, Paul D, Ghorab LM, Hernandez MO, Wong M, Kedei N, Cappell SD.
Cell Reports. 2023 Aug 31;42(9):113079. doi: 10.1016/j.celrep.2023.113079

Schematic diagram of model of cellular senescence entry and maintenance. — In response to various stresses, cells enter senescence via MYC transcriptional repression but maintain their
senescence state by constitutively degrading MYC.

A non-conserved histidine residue on KRAS drives paralog selectivity of the KRASG12D inhibitor MRTX1133.
Keats M, Han JJW, Lee Y-H, Lee C-S, Luo J.
Cancer Research. 2023 Sep 1;83(17):2816-2823. doi: 10.1158/0008-5472.CAN-23-0592

Schematic of KRAS G12D protein interaction with MRTX1133 — Structure of the MRTX1133 binding pocket in GDP-bound KRAS G12D.

SOX9 is a key component of RUNX2-regulated transcriptional circuitry in osteosarcoma.
Kim Y-I, Tseng Y-C, Ayaz G, Wang S, Yan H, du Bois W, Yang H, Zhen T, Lee MP, Liu P, Kaplan RN, Huang J.
Cell & Bioscience. 2023 Jul 25;13(1):136. doi: 10.1186/s13578-023-01088-2

Model of RUNX2-SOX9-JMJD1C network in osteosarcoma. — Model of the RUNX2-SOX9-JMJD1C network in osteosarcoma.

Apoptosis-induced nuclear expulsion in tumor cells drives S100a4-mediated metastatic outgrowth through the RAGE pathway.
Park W-Y, Gray JM, Holewinski RJ, Andresson T, So JY, Carmona-Rivera C, Hollander MC, Yang HH, Lee M, Kaplan MJ, Cappell SD, Yang L.
Nature Cancer. 2023 Mar;4(3):419-435. doi: 10.1038/s43018-023-00524-z

Diagram comparing conventional apoptosis and apoptosis-induced nuclear expulsion — Diagram comparing conventional apoptosis and apoptosis-induced nuclear expulsion.

Dysregulation of Mitochondrial Translation Caused by CBFB Deficiency Cooperates with Mutant PIK3CA and Is a Vulnerability in Breast Cancer.
Malik N, Kim Y-I, Yan H, Tseng Y-C, du Bois W, Ayaz G, Tran AD, Vera-Ramirez L, Yang H, Michalowski AM, Kruhlak M, Lee M, Hunter KW, Huang J.
Cancer Research. 2023 Apr 14;83(8):1280-1298. doi: 10.1158/0008-5472

Illustration showing dysregulation of mitochondrial translation caused by CBFB deficiency — Illustration showing how dysregulation of mitochondrial translation caused by CBFB deficiency cooperates with mutant PIK3CA and is a vulnerability in breast cancer