Overcoming chemotherapy resistance by targeting the insulin-like growth factor 1 (IGF-1) axis in a patient with metastatic castration-resistant prostate cancer and pituitary adenoma: Killing two birds with one stone
Tingrui Wang , Sydney Marsh , Zonghui Ding , Sai-Sridhar Boddupalli , Debra Wong
Affiliation
- 1Department of Internal Medicine, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, US
- 2Creighton University School of Medicine, Omaha, NE, US
- 3Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, Scottsdale, AZ, US
- 4University of Arizona Cancer Center at Dignity Health St. Joseph’s, Phoenix, AZ, US
Corresponding Author
Jue Wang, MD, FACP, University of Arizona Cancer Center at Dignity Health St. Joseph’s, 625 N 6th Street, Phoenix, AZ 85004, US, Tel: +1 602-406-8222, E-mail: jue.wang@dignityhealth.org
Citation
Wang, J, et al. Overcoming Chemotherapy Resistance by Targeting the Insulin-like Growth Factor 1 (IGF-1) Axis in a Patient with Metastatic Castration- Resistant Prostate Cancer and Pituitary Adenoma: Killing Two Birds with One Stone. (2017) J Clin Trials Pathol Case Stud 2(2): 70- 74.
Copy rights
© 2017 Wang, J. This is an Open access article distributed under the terms of Creative Commons Attribution 4.0 International License.
Abstract
Background: Prostate cancer is the most commonly diagnosed cancer in men. Currently, no durable cure exists for advanced metastatic castration-resistant prostate cancer, and only limited therapeutic success has been achieved in terms of improved overall survival. We report a case of prostate cancer with underlying acromegaly tremendously respond to the somatostatin analogs.
Case presentation: In a 63-year-old male with metastatic prostate cancer who had progressed through multiple lines of therapies, a previous unrecognized growth hormone producing pituitary adenoma was diagnosed after a clinical observation of acromegaly at the time of consultation. We hypothesized that up-regulation of the insulin-like growth factor-I (IGF-1) axis was involved in the progression and drug resistance of our patient’s prostate cancer. Given the anti-apoptotic properties of IGF-1, we reasoned that the efficacy of cytotoxic chemotherapeutic agents may be enhanced by co-administration of agents that inhibit IGF-1 bio-activity. Clinical partial response was achieved following the addition of Sandostatin® LAR to the hormone treatment and cabazitaxel, in addition, laboratory studies showed normalization of persistently elevated serum GH and IGF-1 concentrations and significant decrease in level of Prostate-specific antigen.
Conclusion: Our results suggest that upregulation of IGF signaling, may confer androgen independence and chemoresistance. Concomitant administration of octreotide may overcome the clinical resistance to these therapies and improve the clinical outcome in patient with metastatic prostate cancer. We reviewed the published evidences of IGF-1 in promoting disease aggressiveness and chemotherapy resistance in refractory prostate cancer and the clinical benefit of targeting the IGF-1 axis with a somatostatin analogue.