Search Results
You are looking at 1 - 2 of 2 items for
- Author: Christopher J Logothetis x
- Refine by access: All content x
Search for other papers by Estefania Labanca in
Google Scholar
PubMed
CONICET – Universidad de Buenos Aires, Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales (IQUIBICEN), Buenos Aires, Argentina
Search for other papers by Elba S Vazquez in
Google Scholar
PubMed
Search for other papers by Paul G Corn in
Google Scholar
PubMed
Search for other papers by Justin M Roberts in
Google Scholar
PubMed
Search for other papers by Fen Wang in
Google Scholar
PubMed
Search for other papers by Christopher J Logothetis in
Google Scholar
PubMed
Search for other papers by Nora M Navone in
Google Scholar
PubMed
Many solid tumors metastasize to bone, but only prostate cancer has bone as a single, dominant metastatic site. Recently, the FGF axis has been implicated in cancer progression in some tumors and mounting evidence indicate that it mediates prostate cancer bone metastases. The FGF axis has an important role in bone biology and mediates cell-to-cell communication. Therefore, we discuss here basic concepts of bone biology, FGF signaling axis, and FGF axis function in adult bone, to integrate these concepts in our current understanding of the role of FGF axis in bone metastases.
Search for other papers by Neha Venkatesh in
Google Scholar
PubMed
Search for other papers by Rebecca S Tidwell in
Google Scholar
PubMed
Search for other papers by Yao Yu in
Google Scholar
PubMed
Search for other papers by Ana Aparicio in
Google Scholar
PubMed
Search for other papers by Amado J Zurita in
Google Scholar
PubMed
Search for other papers by Sumit K Subudhi in
Google Scholar
PubMed
Search for other papers by Bilal A Siddiqui in
Google Scholar
PubMed
Search for other papers by Sagar S Mukhida in
Google Scholar
PubMed
Search for other papers by Justin R Gregg in
Google Scholar
PubMed
Search for other papers by Paul G Corn in
Google Scholar
PubMed
Search for other papers by Efstratios Koutroumpakis in
Google Scholar
PubMed
Search for other papers by Jennifer L McQuade in
Google Scholar
PubMed
Department of Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Search for other papers by Daniel E Frigo in
Google Scholar
PubMed
Search for other papers by Patrick G Pilie in
Google Scholar
PubMed
Search for other papers by Chad Huff in
Google Scholar
PubMed
Search for other papers by Christopher J Logothetis in
Google Scholar
PubMed
Search for other papers by Andrew W Hahn in
Google Scholar
PubMed
Hormone therapy (HT) to treat prostate cancer is reported to cause adverse changes in body composition. Clinically, interpatient body composition changes are heterogeneous, but the biological and clinical determinants of body composition toxicity are unknown. Herein, we test the hypothesis that inherited polymorphisms in steroidogenic genes are associated with differential changes in body composition after HT. Men with biochemically recurrent prostate cancer (BCR) who received 8 months of LHRH analog (LHRHa) +/− abiraterone acetate (AAP) were eligible if they had: i) CT imaging of L3 prior to and after treatment; and ii) nucleated cells collected. Cardiometabolic co-morbidities were retrospectively extracted. Body composition was measured using an AI-based segmentation tool. Germline DNA whole exome or genome sequencing was performed. In 162 men treated with 8 months of HT, median skeletal muscle mass (SMMi) loss was 6.6% and subcutaneous adipose gain was 12.3%. Men with type 2 diabetes had higher losses of SMMi after treatment (−11.1% vs −6.3%, P = 0.003). For the 150 men with germline NGS, SRD5A2 rs523349 genotype was associated with differential loss in skeletal muscle density after HT, (−1.3% vs −7.1%, P = 0.04). In addition, the HSD3B1 rs104703 genotype was associated with decreased baseline visceral adipose tissue (63.0 cm2/m2 vs 77.9, P = 0.05). In men with BCR, HT induced notable loss of skeletal muscle and increased subcutaneous adipose tissue. An inherited polymorphism in SRD5A2 and T2DM was associated with differential skeletal muscle toxicity. These findings suggest that inherited polymorphisms may contribute to the body composition toxicity observed with HT.