Katie Hobbing

Katie Richardson Hobbing

Assistant Professor Educator

Medical Sciences Building

4203

COM PSP Pharmacology - 0576

Department of Pharmacology & Systems Physiology
University of Cincinnati College of Medicine
Cincinnati, Ohio 45267-0576

Professional Summary

My research interests center around the tumor suppressor RASSF1A (and its related family members).  Rassf1a is epigenetically silenced in over 37 different tumor types and is the most frequently methylated gene in human cancers.  It is estimated that a staggering 95% of breast cancers, 88% of small-cell lung cancers (SCLCs), and approximately 39% of non-small-cell lung cancers have enhanced promoter methylation of Rassf1a.  Moreover, in young ER/PR negative breast cancer patients, 78% of African American women compared with 20% of Caucasian women had Rassf1a promoter methylation.  This differential loss of RASSF1A function may be a key contributor to the racial disparity in breast cancer morbidity rates.  Loss of Rassf1a expression is associated with a poorer prognosis, decreased overall survival, and altered responsiveness to common chemotherapeutic agents. While RASSF1A is frequently inactivated in human cancer, it also exhibits several single nucleotide polymorphisms (SNPs) associated with an increased cancer risk.  A specific SNP occurs in approximately 26% of the Caucasian population and is more prevalent in BRCA1 associated breast cancers.   What is astounding is that women with BRCA1 mutations plus RASSF1A SNP expression present with breast cancer 6 years earlier than those with BRCA1 mutations alone. This compelling evidence not only implicates BRCA1 but RASSF1A in the early formation of breast cancer.

While RASSF1A has no enzymatic activity, it is best known to bind and modulate Ras signaling while serving as a cellular protein scaffold, coordinating various protein-protein interactions.  These protein interactions regulate numerous cellular processes including pro-apoptotic signaling, inflammatory signaling, microtubule dynamics, cell cycle control, genomic stability, and motility/invasion. However, the exact and far-reaching cellular mechanisms regulated by RASSF1A are not fully understood.  My research attempts to identify the dysregulated cellular mechanisms altered by loss/SNP expression by utilizing both in vivo and in vitro models.

Education

Doctor of Philosopy, University of Louisville Louisville, KY, 2008 (Pharmacology and Toxicology)

Master of Science, University of Louisville Louisville, KY, 2006 (Pharmacology and Toxicology)

Bachelor of Engineering, Vanderbilt University Nashville, TN, 2001 (Chemical Engineering)

Research and Practice Interests

My research interests center around the tumor suppressor RASSF1A (and its related family members).  Rassf1a is epigenetically silenced in over 37 different tumor types and is the most frequently methylated gene in human cancers.  It is estimated that a staggering 95% of breast cancers, 88% of small-cell lung cancers (SCLCs), and approximately 39% of non-small-cell lung cancers have enhanced promoter methylation of Rassf1a.  Moreover, in young ER/PR negative breast cancer patients, 78% of African American women compared with 20% of Caucasian women had Rassf1a promoter methylation.  This differential loss of RASSF1A function may be a key contributor to the racial disparity in breast cancer morbidity rates.  Loss of Rassf1a expression is associated with a poorer prognosis, decreased overall survival, and altered responsiveness to common chemotherapeutic agents. While RASSF1A is frequently inactivated in human cancer, it also exhibits several single nucleotide polymorphisms (SNPs) associated with an increased cancer risk.  One example is RASSF1A SNP A(133)S.  This SNP occurs in approximately 26% of the Caucasian population and is more prevalent in BRCA1 associated breast cancers.   What is astounding is that women with BRCA1 mutations plus RASSF1A A(133)S SNP expression present with breast cancer 6 years earlier than those with BRCA1 mutations alone. This compelling evidence not only implicates BRCA1 but RASSF1A in the early formation of breast cancer.

Research Support

Grant: #URS Hobbing New Faculty Development Award – 2017/18 Investigators:Hobbing, Katharine 06-01-2018 -06-30-2019 UC's Research Support URS Hobbing New Faculty Development Award – 2017/18 Role:PI $2,500.00 Active Level:Internal UC

Publications

Peer Reviewed Publications

Schmidt ML, Hobbing KR, Clark GJ (2017. ) RASSF1A deficiency enhances Ras driven lung tumorigenesis .

Donninger, Howard; Hobbing, Katharine; Schmidt, M L; Walters, Eric; Rund, Laurie; Schook, Larry; Clark, Geoffrey J (2015. ) A porcine model system of BRCA1 driven breast cancer.Frontiers in genetics, , 6 ,269

Donninger, Howard; Clark, Jennifer; Rinaldo, Francesca; Nelson, Nicholas; Barnoud, Thibaut; Schmidt, M Lee; Hobbing, Katharine R; Vos, Michele D; Sils, Brian; Clark, Geoffrey J (2015. ) The RASSF1A tumor suppressor regulates XPA-mediated DNA repair.Molecular and cellular biology, , 35 (1 ) ,277-87

Watkins, Stephanie K; Li, Bing; Richardson, Katharine S; Head, Kimberly; Egilmez, Nejat K; Zeng, Qun; Suttles, Jill; Stout, Robert D (2009. ) Rapid release of cytoplasmic IL-15 from tumor-associated macrophages is an initial and critical event in IL-12-initiated tumor regression.European journal of immunology, , 39 (8 ) ,2126-35

Richardson, Katharine S; Zundel, Wayne (2005. ) The emerging role of the COP9 signalosome in cancer.Molecular cancer research : MCR, , 3 (12 ) ,645-53

Guo, Luping; Richardson, Katharine S; Tucker, Lindsay M; Doll, Mark A; Hein, David W; Arteel, Gavin E (2004. ) Role of the renin-angiotensin system in hepatic ischemia reperfusion injury in rats.Hepatology (Baltimore, Md.), , 40 (3 ) ,583-9

Harrell Stewart, Desmond; Hobbing, Katherine; Schmidt, M Lee; Donninger, Howard; Clark, Geoffrey J (2019. ) The role of RASSF proteins in modulating RAS driven lung tumors in vivo.Journal of thoracic disease, , 11 (Suppl 9 ) ,S1436-S1437

Schmidt, M Lee; Hobbing, Katharine R; Donninger, Howard; Clark, Geoffrey J (2018. ) RASSF1A Deficiency Enhances RAS-Driven Lung Tumorigenesis.Cancer research, , 78 (10 ) ,2614-2623

Jones, Dominique Z; Schmidt, M Lee; Suman, Suman; Hobbing, Katharine R; Barve, Shirish S; Gobejishvili, Leila; Brock, Guy; Klinge, Carolyn M; Rai, Shesh N; Park, Jong; Clark, Geoffrey J; Agarwal, Rajesh; Kidd, LaCreis R (2018. ) Micro-RNA-186-5p inhibition attenuates proliferation, anchorage independent growth and invasion in metastatic prostate cancer cells.BMC cancer, , 18 (1 ) ,421

Contact Information

Academic - Department of Pharmacology & Systems Physiology
University of Cincinnati College of Medicine
Cincinnati  Ohio, 45267-0576
Phone: 513-558-4159
Fax: 513-558-5738
katie.hobbing@uc.edu