Serum testosterone and dihydrotestosterone in carcinoma of the prostate

Ghanadian, R.; Puah, Chum Mok; O'donoghue, E. P. N.

doi:10.1038/bjc.1979.122

Cited by 75 publications

(21 citation statements)

References 13 publications

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“…We speculate that our model might fit and correlate with androgen hormonal dynamics reported after RP [4,5]. As known, TT is metabolized within the prostate to dihydrotestosterone (DHT) by the enzyme 5α-reductase; moreover, DHT is the major intracellular androgen that promotes growth within the prostate [37]. There are two studies demonstrating that preoperative DHT serum levels significantly decreased after RP [4,5]; as a result, we speculate that DHT dynamics after RP relates to our predicting model because of the biological dependence of DHT on TT.…”

Section: Discussionmentioning

confidence: 88%

Associations of Pretreatment Serum Total Testosterone Measurements with Pathology-Detected Gleason Score Cancer

Porcaro

Petrozziello²,

Ghimenton³

et al. 2013

Urol Int

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Background and Objective: Prostate cancer is an endocrine-dependent tumor which is still under-investigated for physiopathology factors related to its natural history. The association of pretreatment total testosterone (TT) serum levels with prostate cancer is still a controversial topic. The objective of this study was to investigate potential associations and functional relationships of preoperative TT serum level and pathology-detected Gleason score (pGS). Materials and Methods: Pretreatment and pathological variables of 220 patients operated with radical prostatectomy were retrospectively reviewed. Age, prostate-specific antigen (PSA), percentage of positive biopsy cores (P+), biopsy Gleason score (bGS), pGS, TT and free testosterone were the continuous variables, while clinical stage (cT: cT1c, cT2/3), biopsy Gleason pattern (bGP: ≤3+3, 3+4, >3+4), pathology Gleason pattern (pGP: ≤3+3, 3+4, >3+4), pathology stage (pT: pT2, pT3a, pT3b), pathology nodal staging (pN: pN0, pN1, pNx) and surgical margin invasion by cancer (R-, R+) were the categorical variables. Statistical methods were computed for assessing associations of TT and pGS; moreover, simple and multiple linear regression analysis (SLRA and MLRA) were used for assessing functional relationships of TT and pGS. Results: High-grade tumors (pGS ≥8.0) were associated with bGS >6.0 (p < 0.0001), pGP ≥3+4 (p < 0.0001), P+ >0.31% (p = 0.006), cT2/3 (p = 0.01), TT >15.5 nmol/l (p = 0.0004) and, to a lesser extent, PSA >6.27 μg/l (p = 0.06). The odds ratio (OR) ranked as follows: 2.01 (PSA >6.27 μg/l), 2.88 (cT2/3), 3.23 (P+ >0.31%), 5.53 (TT >15.5 nmol/l) and 12.09 (pGP ≥3+4 and pGS ≥8.0). On SLRA, pGS variation was significantly predicted by bGS (p < 0.0001), P+ (p < 0.0001), PSA (p = 0.0005) and TT (p = 0.02); on MLRA, pGS variation was still significantly predicted by bGS (p < 0.0001), P+ (p = 0.04), PSA (p = 0.03) and TT (p = 0.002). When bGS, P+, PSA and TT were dichotomized to their median value, only bGS (p < 0.0001) and TT (p = 0.001) showed independence in predicting pGS variation. The best model for predicting pGS variations was by dichotomizing TT above its median (>15.5 nmol/l) because the predictive coefficient increased to 0.32, which means that patients with TT >15.5 have a significantly higher estimated risk for high-grade pGS than patients with TT ≤15.5 nmol/l (OR = 1.31). Conclusion: In a patient population undergoing radical prostatectomy, increased pretreatment serum measurements of TT are associated with and functionally related to high-grade pGS; moreover, baseline TT together with bGS and PSA are important factors for predicting pGS and assessing high-grade tumors. Baseline TT serum levels might have prognostic potential for assessing treatment response for continuous as well as intermittent androgen deprivation therapy.

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Section: Discussionmentioning

confidence: 88%

Associations of Pretreatment Serum Total Testosterone Measurements with Pathology-Detected Gleason Score Cancer

Porcaro

Petrozziello²,

Ghimenton³

et al. 2013

Urol Int

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“…In general such comparisons have given conflicting results. Plasma testosterone levels in patients with prostatic cancer have been reported to be both higher than (Ghanadian et al, 1979;Jackson et al, 1980;Ahluwalia et al, 1981;Drafta et al, 1982), similar to (Young & Kent, 1968;Harper et al, 1976;Bartsch et al, 1977a;Bartsch et al, 1977b;Hammond et al, 1978;Habib, 1980;H0isaeter et al, 1982;Ranikko & Adlercreutz, 1983;Levell et al, 1985;Nomura et al, 1988;Hsing & Comstock, 1989;Barrett-Connor et al, 1990) and lower than (Jackson et al, 1980;Ahluwalia et al, 1981;Hill et al, 1982;Meikle & Stanish, 1982;Zumoff et al, 1982;Levell et al, 1985;Meikle et al, 1985) those in healthy controls. Similarly, conflicting results have been reported for estradiol (Harper et al, 1976;Bartsch et al, 1977a;Bartsch et al, 1977b;Hammond et al, 1978;Jackson et al, 1980;Jacobi et al, 1980;Ahluwalia et al, 1981;Drafta et al, 1982;Hill et al, 1982;H0isaeter et al, 1982;Meikle & Stanish, 1982;Ranikko & Adlercreutz, 1983;Hulka et al, 1987;Nomura et al, 1988;Hsing & Comstock, 1989;…”

mentioning

confidence: 88%

“…In two instances, steroid hormone levels were analysed in serum samples stored for a number of years before the disease was manifested, using a nested case-control design (Nomura et al, 1988;Barrett-Connor et al, 1990). In general, however, serum samples were drawn at the time of diagnosis of the cases (Harper et al, 1976;Bartsch et al, 1977a;Bartsch et al, 1977b;Hammond et al, 1978;Ghanadian et al, 1979;Habib, 1980;Jackson et al, 1980;Saroff et al, 1980;Ahluwalia et al, 1981;Drafta et al, 1982;Hill et al, 1982;H0isaeter et al, 1982;Meikle & Stanish, 1982;Zumoff et al, 1982;Ranikko & Adlercreutz, 1983;Meikle et al, 1985;Hulka et al, 1987;Hsing & Comstock, 1989). In general such comparisons have given conflicting results.…”

mentioning

confidence: 99%

Serum pituitary and sex steroid hormone levels in the etiology of prostatic cancer – a population-based case-control study

Andersson

Adami²,

Bergstrom³

et al. 1993

Br J Cancer

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“…Given the central role of androgens such as testosterone and dihydrotestosterone (DHT) in fostering prostate cancer growth (Henderson et al, 1982;Isaacs, 1996), these differences are especially noteworthy. The relationship between lifetime testosterone exposure and prostate cancer risk, however, remains undetermined (Carter et al, 1995;Ghanadian et al, 1979).…”

Section: Clinical Implications Of Population Variation Prostate Cancementioning

confidence: 99%

Reproductive ecology and life history of the human male

Bribiescas

2001

Am. J. Phys. Anthropol.

211

117

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Until recently, the reproductive ecology of human males has not been extensively investigated, primarily as a result of the need for a theoretical framework based on the reproductive constraints and energetics of mammalian males. More specifically, male reproductive ecology has necessitated an integrative interpretation of clinical and anthropological data based on the premise that the evolution of human male life histories has involved selection for physiological mechanisms aimed at optimizing trade-offs between survivorship and reproductive effort. This paper attempts to address this gap in our understanding by presenting the current state of male reproductive ecology, including physiologic data from clinical and anthropological investigations as well as recent theoretical developments. Recent investigations outlining population variation in reproductive endocrine function are discussed within the context of potential sources of variation, including energetic expediture, caloric intake, and developmental canalization during adolescence. Additional summaries of male senescence and behavior are presented to provide a complete overview of male life history. Implications of recent anthropological data on contemporary health issues such as prostate cancer and the development of a male contraceptive are also discussed. Finally, several theories are presented that may contribute to our understanding of the evolution of male life histories and reproductive ecology, including theoretical suggestions involving the role of competition, mate choosiness, and potential constraints on male insemination ability, as well as a theory suggesting that male reproductive ecology may be best understood by analyzing energetic allocation decisions between differing somatic tissues that may be indicative of the competing needs for optimizing survivorship and reproductive effort. Directions for future research are finally considered.

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Serum testosterone and dihydrotestosterone in carcinoma of the prostate

Cited by 75 publications

References 13 publications

Associations of Pretreatment Serum Total Testosterone Measurements with Pathology-Detected Gleason Score Cancer

Associations of Pretreatment Serum Total Testosterone Measurements with Pathology-Detected Gleason Score Cancer

Serum pituitary and sex steroid hormone levels in the etiology of prostatic cancer – a population-based case-control study

Reproductive ecology and life history of the human male

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