Vol 16, Issue 8, 2023 Online - 2455-3891 Print - 0974-2441 SERUM TESTOSTERONE AS A MARKER OF RESPONSE TO ANDROGEN DEPRIVATION THERAPY IN METASTATIC PROSTATE CANCER 1 Department of General Surgery, Post Graduate Institute of Medical Education and Research, Chandigarh, India. 2 Department of Urology, Post Graduate Institute of Medical Education and Research, Chandigarh, India. 3 Department of Endocrinology, Post Graduate Institute of Medical Education and Research, Chandigarh, India. *Corresponding author: ???; Email: ??? Received: 12 April 2023, Revised and Accepted: 14 July 2023 ABSTRACT Methods: This retrospective cohort was conducted from July 2017 to December 2019 in the Department of Urology, Post Graduate Institute of Medical Education and Research, Chandigarh on patients diagnosed with mPCa of age >40 years. Total serum testosterone was measured by Electro chemiluminescent immune assay before the treatment. PSA in serum specimens was evaluated. Results: The mean age was 67.74±8.12 (55–80) years. Serum PSA levels at baseline, 3 months were 530.98±617.28 (ng/dL), and 56.31±89.04 (ng/dL), respectively. The baseline S. testosterone was 288.89±246.53 (ng/mL). Weak negative correlation between the two (p=0.051) As the serum testosterone levels decrease the PSA levels increase and vice-versa. Positive correlation between baseline testosterone and PSA decline (p<0.05). On histopathology, 58.7% (n=71) of the patients had perineural involvement, while 41.3% (n=50) did not have perineural involvement. Conclusion: We conclude that the effect of testosterone might have a possible role in the assessment of treatment response as assessed by PSA. However, the exact implication and its role in disease assessment need to be examined in a larger prospective cohort. Keywords: Prostate-specific antigen, S. testosterone, Metastatic prostate cancer, Androgen. INTRODUCTION Prostate cancer (PCa) is the second most widespread cause of cancer and the sixth foremost cause of cancer death among men worldwide. The worldwide PCa burden is expected to grow to 1.7 million new cases and 4,99,000 new deaths by 2030, simply due to the growth and aging of the global population [1]. PCa has become a major health dilemma in the industrialized world during the last decades of the 20 th century contributing to three fourth of the registered cases across the globe [2]. Despite the high incidence and mortality rates associated with PCa, little is known about the biological processes that underlie the disease’s onset and progression. The sustained presence of particular hormones and growth factors stimulates the prostate, like other sex accessory tissues, in its growth, maintenance, and secretory function. Given that androgens regulate the prostate, there has long been concern about how androgens may contribute to PCa development. For a healthy prostate to develop, grow, and maintain its mature physiological functions, androgens and the transcriptional programs they activate via binding to the androgen receptor (AR) are essential. Although the precise mechanisms governing the initiation and development of PCa are still unknown, signaling through the AR axis is believed to be important in promoting prostate carcinogenesis [3]. Studies have shown little or no association between serum testosterone concentrations and PCa and also demonstrated there is a limit to the ability of testosterone to simulate PCa growth, PCa has often been associated with low testosterone levels [4,5]. A study stated that “Prostate-specific antigen (PSA) is an androgen- regulated serine protease and member of the tissue kallikrein family of proteases.” It is produced primarily by the prostate ductal and acinar epithelium and is secreted into the lumen, where its function is to cleave semenogelin I and II in the seminal coagulum. However, its main significance in oncology is as a biomarker to detect PCa and to assess responses to treatment. A decline in PSA levels in response to androgen deprivation therapy (ADT) is specifically caused in part by tumor cell death, it is also the result of decreased AR-stimulated PSA production by surviving tumor cells. As a result, ADT may in some cases have better effects on PSA production than on tumor survival [4]. However, PSA is limited by its comparative lack of specificity when serum concentration moderately increases (4.0–10.0 ng/mL) [5]. Androgen relation with prostate Androgens which regulate proliferation, apoptosis, angiogenesis, metastasis, and differentiation. The prostate is stimulated in its growth, maintenance, and secretary function presence of androgens and growth factors. Testosterone and dihydrotestosterone are the two most important androgens in adult men. Testosterone is the major male androgen in circulation, while DTH is the principal androgen in tissues. In healthy adult men, 90% of circulating levels of T is secreted by Leydig cells of the testes. It has been indicated that 5.6% of men aged 30–79 years have a prevalence of symptomatic hypogonadism. It is estimated that by the year 2025, there will be approximately 6.5 million American men 30–80 years of age diagnosed with androgen deficiency [6,7]. © 2023 The Authors. Published by Innovare Academic Sciences Pvt Ltd. This is an open access article under the CC BY license (http://creativecommons.org/ licenses/by/4.0/) DOI: http://dx.doi.org/10.22159/ajpcr.2023v16i8.48075. Journal homepage: https://innovareacademics.in/journals/index.php/ajpcr Research Article Objective: Prostate cancer (PCa) is the second most widespread cause of cancer and the sixth foremost cause of cancer death among men worldwide. The sustained presence of particular hormones and growth factors stimulates the prostate, such as other sex accessory tissues, in its growth, maintenance, and secretory function. In the current study, we investigated the association of serum testosterone level and prostate-specific antigen (PSA) level before androgen deprivation therapy in metastatic PCa (mPCa) treated with hormone therapy. BHARAT BHUSHAN BAMANIYA 1 , RAVI MOHAN S MAVUDURU 2 , GIRDHAR S BORA 2 , ADITYA PRAKASH SHARMA 2 , SINGH SK 2 , ASHU RASTOGI 3