Photo of David Crowe

David Crowe, DDS, PhD





Periodontics Department 801 S. Paulina St., IL 60612

Office Phone:

(312) 996-9488

Selected Publications

Kramer K, Wu J, Crowe. 2016. Tumor suppressor control of the cancer stem cell niche. Oncogene 35:4165-4178

Bojovic B, Booth RE, Jin Y, Zhou X, Crowe DL. 2015. Alternative lengthening of telomeres in cancer stem cells in vivo. Oncogene 34:611-620

Bojovic B, Ho HY, Wu J, Crowe DL. 2013. Stem cell expansion during carcinogenesis in stem cell depleted conditional telomeric repeat factor 2 null mutant mice. Oncogene 32:5156-5166

Bojovic B, Crowe DL. 2011. Telomere dysfunction promotes metastasis in a TERC null mutant mouse model of head and neck cancer. Mol Cancer Res 9:901-913

Research Currently in Progress

The incidence of head and neck cancer is increasing in the United States.  Most oral cavity cancers are caused by use of tobacco products, and oropharyngeal cancers have been associated with human papillomavirus.  Oral cancers contain dividing cells which have different abilities to form new tumors.  Our laboratory is interested in the genetics, molecular, and cellular biology of oral cancer stem cells.  Our published work in high impact cancer research journals has shown that small populations of oral cancer stem cells are primarily responsible for initiating new tumors.  Genetic deletion of these cells causes dramatic regression and differentiation of primary and metastatic oral cancers.  Oral cancer stem cells derive from multiple distinct cellular lineages and drive tumor progression through paracrine signaling to other cancer stem cell populations.  We have identified cancer stem cell biomarkers which predict clinically aggressive tumors.  Our latest research demonstrated that metastatic stem cells arise in the earliest stages of oral cancer progression.  We have also demonstrated that regulating the DNA damage response of oral cancer stem cells using targeted therapies can result in dramatic regression of primary and metastatic tumors.  By targeting these oral cancer stem cell signaling pathways, we will improve clinical outcomes for our patients with this deadly disease.