ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ
Background. Neoadjuvant androgen deprivation therapy (NADT) before radical prostatectomy (RP) remains controversial in the management of localized and locally advanced prostate cancer. A major limitation of this strategy is the lack of biomarkers capable of identifying tumors biologically sensitive...
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2026
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Experimental Oncology| _version_ | 1874183256683839488 |
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| author | Afanasiev, Ye. Vozianov, S. Danylets, R. Grygorenko, V. Shulyak, O. Sosnin, M. Kholokharenko, I. |
| author_facet | Afanasiev, Ye. Vozianov, S. Danylets, R. Grygorenko, V. Shulyak, O. Sosnin, M. Kholokharenko, I. |
| author_institution_txt_mv | [
{
"author": "Ye. Afanasiev",
"institution": "O.F. Vozianov Institute of Urology, National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine",
"orcid": ""
},
{
"author": "S. Vozianov",
"institution": "O.F. Vozianov Institute of Urology, National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine",
"orcid": ""
},
{
"author": "R. Danylets",
"institution": "O.F. Vozianov Institute of Urology, National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine",
"orcid": ""
},
{
"author": "V. Grygorenko",
"institution": "O.F. Vozianov Institute of Urology, National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine",
"orcid": ""
},
{
"author": "O. Shulyak",
"institution": "O.F. Vozianov Institute of Urology, National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine",
"orcid": ""
},
{
"author": "M. Sosnin",
"institution": "O.F. Vozianov Institute of Urology, National Academy of Medical Sciences of Ukraine, Kyiv, Ukraine",
"orcid": ""
},
{
"author": "I. Kholokharenko",
"institution": "Department of Urology, Shupyk National Healthcare University of Ukraine, Kyiv, Ukraine",
"orcid": ""
}
] |
| author_sort | Afanasiev, Ye. |
| baseUrl_str | https://exp-oncology.com.ua/index.php/Exp/oai |
| collection | OJS |
| container_end_page | 171 |
| container_issue | 2 |
| container_start_page | 161 |
| container_title | Експериментальна онкологія |
| container_volume | 48 |
| datestamp_date | 2026-08-21T12:36:14Z |
| description | Background. Neoadjuvant androgen deprivation therapy (NADT) before radical prostatectomy (RP) remains controversial in the management of localized and locally advanced prostate cancer. A major limitation of this strategy is the lack of biomarkers capable of identifying tumors biologically sensitive to androgen deprivation. This study aimed to evaluate the prognostic value of a dynamic androgen response index (IAR) and develop a predictive model for biochemical recurrence (BCR) after RP. Materials and Methods. The retrospective single-center study included 84 patients with prostate cancer treated with NADT followed by RP. The IAR was defined as the ratio between logarithmic slopes of PSA and testosterone decline during neoadjuvant therapy. Cox regression analysis was performed to identify predictors of BCR. A predictive model and nomogram were constructed based on independent predictors. Model performance was evaluated using ROC analysis, calibration plots, and decision curve analysis. Results. During a median follow-up of 56 months, BCR occurred in 62 patients. Clinical stage ≥ cT3a (HR 2.34; p = 0.003) and IAR (HR 1.48; p = 0.024) were independent predictors of BCR. The model demonstrated moderate discrimination (AUC 0.68) and satisfactory calibration. Conclusions. The IAR may reflect the biological responsiveness of prostate cancer to androgen deprivation. These findings should be considered hypothesis-generating and require further validation in the context of risk stratification for BCR following RP after NADT. |
| doi_str_mv | 10.15407/exp-oncology.2026.02.161 |
| first_indexed | 2026-08-22T01:00:36Z |
| format | Article |
| fulltext |
ISSN 1812-9269. Experimental Oncology 48 (2). 2026 161
ORIGINAL CONTRIBUTION
C i t a t i o n: Afanasiev Ye, Vozianov S, Danylets R, Grygorenko V, Shulyak O, Sosnin M, Kholokharenko I. Dynamic andro-
gen response index and its association with biochemical recurrence after radical prostatectomy following neoadjuvant an-
drogen deprivation therapy. Exp Oncol. 2026; 48(2): 161-171. https://doi.org/10.15407/exp-oncology.2026.02.161
© PH “Akademperiodyka” of the NAS of Ukraine, 2026. This is an open access article under the CC BY-NC-ND license
(https://creativecommons.org/licenses/by-nc-nd/4.0/)
https://doi.org/10.15407/exp-oncology.2026.02.161
Ye. Afanasiev 1, 2, *, S. Vozianov 1, 2, R. Danylets 1, 2,
V. Grygorenko 1, O. Shulyak 1, M. Sosnin 1, 2, I. Kholokharenko 2
1 O.F. Vozianov Institute of Urology, National Academy
of Medical Sciences of Ukraine, Kyiv, Ukraine
2 Department of Urology, Shupyk National Healthcare University
of Ukraine, Kyiv, Ukraine
* Correspondence: E-mail: evhenii.afanasev@gmail.com
DYNAMIC ANDROGEN RESPONSE
INDEX AND ITS ASSOCIATION
WITH BIOCHEMICAL RECURRENCE
AFTER RADICAL PROSTATECTOMY
FOLLOWING NEOADJUVANT
ANDROGEN DEPRIVATION THERAPY
Background. Neoadjuvant androgen deprivation therapy (NADT) before radical prostatectomy (RP) remains controver-
sial in the management of localized and locally advanced prostate cancer. A major limitation of this strategy is the lack of
biomarkers capable of identifying tumors biologically sensitive to androgen deprivation. This study aimed to evaluate the
prognostic value of a dynamic androgen response index (IAR) and develop a predictive model for biochemical recurrence
(BCR) after RP. Materials and Methods. The retrospective single-center study included 84 patients with prostate cancer
treated with NADT followed by RP. The IAR was defined as the ratio between logarithmic slopes of PSA and testosterone
decline during neoadjuvant therapy. Cox regression analysis was performed to identify predictors of BCR. A predictive
model and nomogram were constructed based on independent predictors. Model performance was evaluated using ROC
analysis, calibration plots, and decision curve analysis. Results. During a median follow-up of 56 months, BCR occurred
in 62 patients. Clinical stage ≥ cT3a (HR 2.34; p = 0.003) and IAR (HR 1.48; p = 0.024) were independent predictors of
BCR. The model demonstrated moderate discrimination (AUC 0.68) and satisfactory calibration. Conclusions. The IAR
may reflect the biological responsiveness of prostate cancer to androgen deprivation. These findings should be considered
hypothesis-generating and require further validation in the context of risk stratification for BCR following RP after NADT.
Keywords: prostate cancer, neoadjuvant androgen deprivation therapy, biochemical recurrence, predictive model, no-
mogram, androgen response.
Prostate cancer (PCa) remains one of the most
commonly diagnosed malignancies among men
worldwide [1]. While radical prostatectomy (RP)
represents an established treatment option for pa-
tients with low and intermediate risk [2], oncolog-
ical outcomes remain suboptimal in men with high
https://doi.org/10.15407/exp-oncology.2026.02.161
https://creativecommons.org/licenses/by-nc-nd/4.0/
https://doi.org/10.15407/exp-oncology.2026.02
mailto:evhenii.afanasev@gmail.com
162 ISSN 1812-9269. Experimental Oncology 48 (2). 2026
Ye. Afanasiev, S. Vozianov, R. Danylets, V. Grygorenko, O. Shulyak, M. Sosnin, I. Kholokharenko
and very high risk features, frequently necessitating
multimodal treatment strategies [3, 4].
Neoadjuvant androgen deprivation therapy
(NADT) before RP has been investigated for se
veral decades as a strategy to improve oncological
outcomes in patients with localized and locally ad-
vanced PCa. Randomized studies have demonstrat-
ed that NADT may reduce tumor volume and the
rate of positive surgical margins; however, its effect
on long-term oncological outcomes such as bio-
chemical recurrence (BCR) and overall survival
(OS) remains uncertain [5—7]. One of the major
limitations of this therapeutic approach is the lack
of reliable biomarkers capable of identifying pa-
tients who are biologically sensitive to androgen
deprivation and therefore most likely to benefit
from NADT.
Traditionally, the response to androgen depri-
vation therapy (ADT) has been evaluated using
absolute prostate-specific antigen (PSA) values,
including baseline PSA, post-treatment PSA, and
PSA nadir [8, 9]. While these parameters are
widely used in clinical practice, they represent
static measurements that may be strongly influ-
enced by initial tumor burden and inter-indivi
dual variability. Consequently, absolute PSA val-
ues alone may provide limited insight into the bio
logical dynamics of tumor response to ADT and
may not accurately reflect intrinsic sensitivity of
PCa to androgen deprivation.
To overcome this limitation, increasing atten-
tion has been directed toward the evaluation of
PSA kinetics during hormonal therapy. Parame-
ters such as the rate of PSA decline, PSA half-life,
or logarithmic slopes of PSA change have been
proposed as more informative indicators of treat-
ment response [10—12]. These dynamic measures
reflect the rate of biomarker changes compared to
static PSA measurements. Nevertheless, PSA ki-
netics alone cannot fully distinguish whether PSA
decline results from effective androgen suppres-
sion or from intrinsic tumor sensitivity to andro-
gen deprivation.
Since the principal mechanism of NADT is the
suppression of testosterone production, the rela-
tionship between PSA dynamics and testosterone
decline may more accurately reflect the biological
responsiveness of PCa to androgen deprivation. In-
tegrating the dynamics of these two biomarkers
may therefore provide a more comprehensive as-
sessment of treatment response. Based on this con-
cept, we hypothesized that integrating the dynam-
ics of PSA and testosterone decline may provide a
more accurate representation of tumor sensitivity
to androgen deprivation. Therefore, we set forward
a dynamic androgen response index (IAR), defined
as the ratio between the slopes of PSA and testos-
terone decline during NADT.
The aim of the present study was to evaluate the
prognostic significance of IAR and to develop a
predictive model for biochemical recurrence in pa-
tients undergoing NADT before RP.
Materials and Methods
Study population. This retrospective single-center
study was conducted in the O.F. Vozianov Institute
of Urology, the National Academy of Medical Sci-
ences of Ukraine (IU NAMS) and included patients
with clinically localized and locally advanced PCa
who underwent NADT followed by RP at a tertiary
referral center. Clinical and pathological data were
obtained from institutional medical records bet
ween January 2015 and December 2021.
Patients were eligible for inclusion if they had
histologically confirmed PCa with a clinical stage
≤ cT4 and no evidence of pelvic wall or urethral
sphincter invasion on pretreatment magnetic reso-
nance imaging performed before the initiation of
any systemic or local therapy. Availability of base-
line clinical data, including measurements of PSA
and serum testosterone levels both before initiation
of NADT and completion of neoadjuvant treat-
ment, biopsy ISUP, as well as long-term oncological
outcomes (date of BCR), was required.
Patients with oligometastatic disease at diagno-
sis, prior intermittent ADT, previous radiation
therapy, and/or systemic chemotherapy before RP,
treatment with antiandrogens (AA) monotherapy,
or insufficient clinical data precluding reliable on-
cological assessment were excluded. A total of
84 patients met the inclusion criteria and were in-
cluded in the final study cohort. The decision to
administer NADT before surgery was made on an
individual basis, primarily in patients with high- or
very high-risk disease features.
All patients subsequently underwent RP with
standard pathological evaluation. Postoperative fol-
low-up included serial PSA measurements per-
formed according to the institutional protocols.
ISSN 1812-9269. Experimental Oncology 48 (2). 2026 163
Dynamic Androgen Response Index and its Association with Biochemical Recurrence after Radical Prostatectomy
The study protocol was approved by the ethics
committee of the IU NAMS. The study was con-
ducted in accordance with the principles of the
Declaration of Helsinki. The median follow-up du-
ration was 56 months (IQR 38—82).
Neoadjuvant androgen-deprivation therapy.
NADT consisted of luteinizing hormone-releasing
hormone (LHRH) agonists administered as
monotherapy or in combination with nonsteroidal
AA. A combined androgen blockade was prefer-
entially used in patients with high-risk disease
characteristics. The duration of NADT ranged
from 1 to 12 months and was determined by clin-
ical considerations, tumor burden, and treatment
planning factors.
Calculations of biomarker dynamics. To quan-
tify the rate of biomarker change during NADT,
logarithmic slopes of PSA and testosterone decline
were calculated. For each patient, the slope of PSA
decline (kPSA) was estimated using the following
equation:
� � � ��
�
ln lnbaseline NADTPSA PSA
kPSA
t
where PSAbaseline represents the PSA level before ini-
tiation of NADT, PSANADT is the PSA level mea-
sured after therapy, and t is the duration of NADT
in months.
Similarly, the slope of testosterone decline (kT)
was calculated as:
� � � �ln lnbaseline NADTT T
kT
t
�
�
where Tbaseline and TNADT correspond to the serum
testosterone levels before and after NADT.
Based on these parameters, a dynamic IAR was
defined as the ratio between the slopes of PSA and
testosterone decline:
kPSAIAR
kT
�
This index reflects the relationship between tu-
mor PSA response and the degree of androgen sup-
pression.
Study endpoint. The primary endpoint of the
study was BCR after RP. BCR was defined as a post-
operative PSA level ≥ 0.2 ng/mL confirmed by a
second measurement. Biochemical recurrence-free
survival (BCRFS) was calculated from the date of
RP to the date of BCR or the last follow-up.
Statistical analysis. Descriptive statistics were
used to summarize baseline clinical and patho-
logical characteristics of the study cohort. The
continuous variables were reported as medians
with interquartile ranges (IQRs), whereas the cat-
egorical variables were reported as frequencies
and percentages.
Comparisons between patients with and without
biochemical recurrence (BCR) were performed us-
ing the Mann—Whitney U-test for continuous
variables and the Chi-square test or Fisher’s exact
test for categorical variables, as appropriate.
The BCRFS was estimated using the Kaplan—
Meier method, and differences between groups
were assessed using the log-rank test.
To identify factors associated with BCR, an ini-
tial univariable Cox proportional hazards regres-
sion analysis was performed. Variables demonstrat-
ing potential prognostic significance in the univari-
able Cox regression were included in an initial
multivariable Cox regression model. Variables that
retained statistical significance in the initial multi-
variable analysis were subsequently included in the
final reduced prognostic model used for nomo-
gram construction. Therefore, the initial multivari-
able Cox regression model and the final reduced
predictive model were presented separately.
Based on the independent predictors identified
in the multivariable analysis, a predictive model for
BCR was constructed and presented as a nomo-
gram. The discriminatory performance of the
model was evaluated using the receiver operating
characteristic (ROC) curve analysis, with the area
under the curve (AUC) and corresponding 95%
confidence intervals reported.
The model calibration was assessed using cali-
bration plots comparing the predicted probabilities
with the observed outcomes. An internal validation
of the model was performed using bootstrap resa-
mpling (1,000 iterations) to estimate model opti-
mism and stability.
The potential clinical utility of the predictive
model was further evaluated using a decision curve
analysis, which quantified the net benefit of the
model across a range of threshold probabilities.
All statistical analyses were performed using
IBM SPSS Statistics version 22 (IBM Corp., Ar-
monk, NY, USA), GraphPad Prism version 10.4.1
164 ISSN 1812-9269. Experimental Oncology 48 (2). 2026
Ye. Afanasiev, S. Vozianov, R. Danylets, V. Grygorenko, O. Shulyak, M. Sosnin, I. Kholokharenko
(GraphPad Software, Boston, MA, USA), and R
statistical software version 4.5.2. A two-sided p-va
lue < 0.05 was considered statistically significant.
Results
Patient characteristics. A total of 84 patients were
included in the study. Detailed baseline character-
istics are summarized in Table 1.
The baseline characteristics in patients with and
without BCR are compared in Table 2. Patients who
developed BCR had significantly higher baseline
PSA levels compared to patients without recur-
rence (26.1 vs 12.2 ng/mL, p = 0.007). Baseline tes-
tosterone levels were significantly lower in patients
who experienced BCR (11.1 vs 15.1 nmol/L,
p < 0.001), while testosterone levels after neoadju-
vant therapy were significantly higher (1.4 vs
0.6 nmol/L, p < 0.001). Clinical stage ≥ cT3a was
significantly more frequent among patients with re-
currence (p = 0.002). Similarly, patients classified
as high-risk according to NCCN criteria demon-
strated a higher likelihood of BCR (p = 0.01). The
other clinical parameters, including body mass in-
dex, prostate volume, neutrophil-to-lymphocyte
ratio, platelet-to-lymphocyte ratio, and Charlson
comorbidity index, were not significantly associ-
ated with recurrence.
Cox regression analysis. Univariable Cox regres-
sion analysis identified several predictors associ-
ated with BCR, including clinical stage ≥ cT3a (HR
2.52, 95% CI: 1.49—4.28, p = 0.001), testosterone
level after neoadjuvant therapy (HR 2.48, 95% CI:
1.42—4.35, p = 0.001), log-transformed PSA (HR
1.52, 95% CI: 1.13—2.06, p = 0.006), and the IAR
(HR 1.60, 95% CI: 1.18—2.17, p = 0.003).
In the multivariable model, clinical stage ≥ cT3a
(HR 2.34, 95% CI: 1.34—4.07, p = 0.003) and IAR
(HR 1.48, 95% CI: 1.05—2.09, p = 0.024) remained
independent predictors of BCR. Although log-trans-
formed PSA was significant in the univariable anal-
ysis, its significance was lost in the multivariable
model. The results of the Cox regression analysis are
summarized in Table 3. In the initial multivariable
model including the clinical stage ≥ cT3a, IAR, and
log-transformed PSA, clinical stage ≥ cT3a and IAR
remained independently associated with BCR,
whereas log-transformed PSA was not statistically
significant. Therefore, log-transformed PSA was not
retained in the final reduced predictive model.
Table 1. Baseline clinical and laboratory
characteristics of the study population
Parameter Overall (n = 84)
Clinical parameters
Age, years, median (IQR) 64.5 (60.0—68.7)
BMI, kg/m2, median (IQR) 27.8 (25.3—30.0)
Baseline PSA (PSA0), ng/mL,
median (IQR) 20.9 (11.5—38.3)
Post-NADT PSA (PSA1), ng/mL,
median (IQR) 1.1 (0.4—3.9)
Baseline testosterone (T0),
nmol/L, median (IQR) 14.3 (11.5—16.7)
Post-NADT testosterone (T1),
nmol/L, median (IQR) 0.7 (0.5—1.1)
Initial prostate volume, cm³,
median (IQR) 55.0 (42.7—75.8)
NADT prostate volume, cm³,
median (IQR) 36.1 (24.7—53.1)
NLR, median (IQR) 3.0 (2.3—4.2)
PLR, median (IQR) 156.8 (121.7—216.3)
CCI, median (IQR) 2.0 (2—3)
Biopsy ISUP grade
ISUP <4
ISUP ≥4
64 (76.2%)
20 (23.8%)
Clinical stage
≤ T2c
≥ T3a
54 (64.3%)
30 (35.7%)
NCCN Risk Group
≤ Intermediate risk
≥ High risk
27 (32.1%)
57 (67.9%)
Duration of NADT
1—2 months
3 months
>3 months
28 (33.3%)
29 (34.5%)
27 (32.1%)
Type of NADT
LHRH agonists
LHRH agonists + AA
54 (64.3%)
30 (35.7%)
Notes: IQR — interquartile range; NADT — neoadjuvant
androgen deprivation therapy; BMI — body mass index;
PSA0 — initial PSA level; PSA1 — post-NADT PSA
level; T0 — initial testosterone level; T1 — post-NADT
testosterone level; NLR — neutrophil-to-lymphocyte ratio;
PLR — platelet-to-lymphocyte ratio; CCI — Charlson’s
comorbidity index; ISUP — International Society of
Urological Pathology; NCCN — National Comprehensive
Cancer Network; LHRH — luteinizing hormone-releasing
hormone; AA — antiandrogens.
ISSN 1812-9269. Experimental Oncology 48 (2). 2026 165
Dynamic Androgen Response Index and its Association with Biochemical Recurrence after Radical Prostatectomy
Development of the predictive model. Based on
the independent predictors identified in the mul-
tivariable analysis, a predictive model incorporat-
ing clinical stage ≥ cT3a and the IAR was devel-
oped (Table 4). A nomogram was plotted to esti-
mate the probability of BCR within 36 months
following RP (Fig. 1).
The discriminative ability of the model was eva
luated using Harrell’s concordance index. The
model demonstrated moderate discrimination with
a C-index of 0.64. Time-dependent ROC analysis
at 36 months yielded an AUC of 0.68 (95% CI
0.56—0.80) (Fig. 2). The Brier score was 0.221
(95% CI: 0.181—0.260), indicating acceptable pre-
dictive accuracy. An internal validation using boot-
strap resampling (1000 iterations) yielded a Somer’s
Dxy of 0.27, corresponding to a C-index of 0.64,
indicating stable predictive performance.
Table 2. Comparison of baseline characteristics between
patients with and without BCR
Parameter BCR (n = 62) No BCR (n = 22) p
Clinical parameters
Age, years, median (IQR) 64.0 (60.0—68.0) 66.5 (60.7—69.2) 0.384*
BMI, kg/m2, median (IQR) 27.6 (24.8—29.9) 28.1 (26.0—30.6) 0.368*
Baseline PSA (PSA0), ng/mL, median (IQR) 26.1 (13.9—46.5) 12.2 (8.8—27.1) 0.007*
Post-NADT PSA (PSA1), ng/mL, median (IQR) 1.25 (0.4—5.0) 0.65 (0.2—3.1) 0.136*
Baseline testosterone (T0), nmol/L, median (IQR) 11.1 (9.3—13.9) 15.1 (13.5—16.9) <0.001*
Post-NADT testosterone (T1), nmol/L, median (IQR) 1.4 (0.7—1.6) 0.6 (0.4—0.9) <0.001*
Initial prostate volume, cm³, median (IQR) 54.5 (42.5—73.6) 56.7 (43.6—81.9) 0.522*
NADT prostate volume, cm³, median (IQR) 36.1 (23.4—47.7) 35.4 (29.2—70.1) 0.242*
NLR, median (IQR) 2.9 (2.3—4.0) 3.0 (2.0—4.5) 0.737*
PLR, median (IQR) 155.9 (123.4—220.7) 165.1 (109.9—201.2) 0.919*
CCI, median, (IQR) 2 (2—3) 2 (2—3) 0.776χ²
Biopsy ISUP grade
ISUP <4
ISUP ≥4
45 (72.6%)
17 (27.4%)
19 (86.4%)
3 (13.6%)
0.156χ²
Clinical stage
≤ T2c
≥ T3a
34 (54.8%)
28 (45.2%)
20 (90.9%)
2 (9.1%)
0.002χ²
NCCN Risk Group
≤ Intermediate-risk
≥ High-risk
15 (24.2%)
47 (75.8%)
12 (54.5%)
10 (45.5%)
0.01χ²
Duration of NADT
Duration 1—2 months
Duration 3 months
Duration > 3 months
21 (33.9%)
19 (30.6%)
22 (35.5%)
7 (31.8%)
10 (45.5%)
5 (22.7%)
0.392χ²
Type of NADT
LHRH agonists
LHRH agonists + AA
39 (62.9%)
23 (37.1%)
15 (68.2%)
7 (31.8%)
0.431χ²
Notes: * Comparison of groups by Mann-Whitney test; χ² Comparison of categorical variables by chi-square test; BCR —
biochemical recurrence; IQR — interquartile range; NADT — neoadjuvant androgen deprivation therapy; BMI — body
mass index; PSA0 — initial PSA level; PSA1 — post-NADT PSA level; T0 — initial testosterone level; T1 — post-NADT
testosterone level; NLR — neutrophil-to-lymphocyte ratio; PLR — platelet-to-lymphocyte ratio; CCI — Charlson’s
comorbidity index; ISUP — International Society of Urological Pathology; NCCN — National Comprehensive Cancer
Network; LHRH — luteinizing hormone-releasing hormone; AA — antiandrogens.
166 ISSN 1812-9269. Experimental Oncology 48 (2). 2026
Ye. Afanasiev, S. Vozianov, R. Danylets, V. Grygorenko, O. Shulyak, M. Sosnin, I. Kholokharenko
Calibration analysis demonstrated good agreement
between predicted and observed probabilities of BCR
at 36 months (Fig. 3). The calibration curve indicated
satisfactory agreement between predicted and ob-
served event rate across the range of predicted risks.
Decision curve analysis demonstrated that the
predictive model provided a higher net benefit
compared to both the “treat-all” and “treat-none”
strategies across a wide range of threshold proba-
bilities (Fig. 4). These findings suggest that the
model may provide clinically useful risk stratifica-
tion for patients undergoing RP after NADT.
Risk stratification analysis. To evaluate the cli
nical applicability of the proposed predictive mo
del, the patients were stratified into three risk
groups (low, intermediate, and high) according to
the calculated risk score derived from the multi-
variable Cox regression model.
Kaplan—Meier analysis demonstrated a clear sep-
aration of BCRFS among the three groups (Fig. 5).
The median BCRFS was 69 months in the low-risk
group, 57 months in the intermediate-risk group,
and 26 months in the high-risk group. Similarly,
the estimated mean BCRFS was 62.4 months in the
low-risk group, 53.9 months in the intermediate-
risk group, and 29.6 months in the high-risk group,
indicating a progressive reduction in survival with
increasing risk. The differences in survival distri-
butions between the groups were significant ac-
cording to the log-rank test (χ2 = 18.95, p < 0.001).
These findings support the proposed model’s abili
ty to effectively stratify patients by risk of BCR fol-
lowing RP.
Discussion
The present study evaluated the prognostic sig-
nificance of a novel IAR and developed a predic-
tive model for BCR in patients undergoing NADT
before RP. The main findings of this study are
threefold. First, the IAR integrating PSA and tes-
tosterone kinetics during NADT was indepen-
dently associated with BCR. Second, the integra-
tion of IAR with the clinical stage enabled the de-
velopment of a simple predictive model capable of
stratifying patients into distinct recurrence-risk
groups. Third, the proposed model demonstrated
acceptable discrimination, satisfactory calibra-
tion, and potential clinical benefit in decision
curve analysis.
Neoadjuvant systemic therapy before RP has
been investigated for several decades. Early ran-
domized trials demonstrated that NADT could
reduce prostate volume, tumor burden, and the
rate of positive surgical margins. However, these
studies failed to consistently demonstrate im-
provements in long-term oncologic outcomes
such as BCR or OS [6, 7]. For instance, Soloway
et al. [6] reported improved pathological findings
Table 3. Cox proportional hazard regression
analysis for predictors of biochemical recurrence
Parameter HR 95% CI p
Univariable analysis
cT
≥ T3a 2.52 1.49—4.28 0.001
ISUP Grade after biopsy
≥ ISUP 4 1.29 0.74—2.25 0.378
Baseline testosterone (T0) 0.84 0.77—0.91 < 0.001
Post-NADT testosterone (T1) 2.48 1.42—4.35 0.001
kPSA 0.94 0.69—1.29 0.716
kT 0.69 0.49—0.96 0.027
Log (PSA) 1.52 1.13—2.06 0.006
IAR 1.60 1.18—2.17 0.003
Multivariable analysis
cT
≥ T3a 2.34 1.34—4.07 0.003
IAR 1.48 1.05—2.09 0.024
Log (PSA) 1.17 0.84—1.62 0.367
Notes: HR — hazard ratio; CI — confidence interval; cT —
clinical stage; ISUP — International Society of Urological
Pathology; T0 — initial testosterone level; T1 — post-
NADT testosterone level; kPSA — logarithmic slope of
PSA level decline; kT — logarithmic slope of testosterone
level decline; IAR — dynamic androgen response index.
Fig. 1. Nomogram for prediction of biochemical recur-
rence at 36 months: IAR — androgen response index;
BCR — biochemical recurrence
ISSN 1812-9269. Experimental Oncology 48 (2). 2026 167
Dynamic Androgen Response Index and its Association with Biochemical Recurrence after Radical Prostatectomy
the degree of achieved androgen suppression may
provide an incomplete representation of biological
treatment response.
The present study addresses this limitation by
integrating PSA and testosterone kinetics into a
composite biomarker — the IAR. Since the prima-
ry mechanism of ADT action involves suppression
of circulating testosterone levels, evaluating PSA
decline relative to testosterone suppression may
following neoadjuvant androgen ablation but no
significant reduction in BCR after surgery. Simi-
larly, Schulman et al. [7] observed favorable path-
ological outcomes without a clear survival advan-
tage in patients receiving neoadjuvant hormonal
therapy before RP.
In recent years, interest in neoadjuvant therapy
has re-emerged due to the development of intensi-
fied androgen receptor signaling inhibitors (ARSI)
and combination systemic approaches. Current
studies suggest that neoadjuvant treatment with
AR-targeted agents such as abiraterone, enzalu-
tamide, or apalutamide can induce significant
pathological responses in patients with high-risk
localized PCa, including the rates of minimal re-
sidual disease and complete pathological response
[13—16]. Despite these promising results, patient
selection remains a major challenge, as tumors ex-
hibit heterogeneous biological sensitivity to andro-
gen deprivation.
Several recent reviews emphasize that reliable
predictive biomarkers capable of selecting patients
most likely to benefit from neoadjuvant therapy
represent a major unmet clinical need in localized
high-risk and locally advanced PCa [17]. In this
context, dynamic biomarkers reflecting biological
response during treatment may provide clinically
valuable information about tumor endocrine sen-
sitivity and treatment responsiveness.
PSA kinetics have long been investigated as a
marker of treatment response in PCa. Several stu
dies have demonstrated that dynamic PSA chan
ges during hormonal therapy may provide prog-
nostic information beyond baseline PSA measure-
ments. Foo et al. [10] reported that PSA kinetics
during neoadjuvant hormonal treatment was as-
sociated with BCR and PCa-mortality. Similarly,
Kang et al. [11] demonstrated that PSA half-life
during neoadjuvant hormone therapy predicted
the risk of developing castration-resistant PCa fol-
lowing RP. McDonald et al. [12] further con-
firmed that PSA response to NADT may serve as
an independent prognostic indicator of oncologic
outcomes. Despite these findings, PSA dynamics
alone may not fully reflect tumor sensitivity to an-
drogen deprivation. PSA reduction during ADT
may reflect both suppression of androgen-de-
pendent PSA production and intrinsic tumor
susceptibility to endocrine therapy. Therefore,
PSA kinetics evaluated without consideration of
Fig. 3. Calibration plot demonstrating agreement between
predicted and observed probabilities of biochemical re-
currence at 36 months. AUC and Brier score values shown
in the figure are expressed as percentages
Se
ns
iti
vi
ty
, %
Fig. 2. ROC curve for prediction of biochemical recur-
rence at 36 months based on the final Cox regression
model: AUC — area under the curve
168 ISSN 1812-9269. Experimental Oncology 48 (2). 2026
Ye. Afanasiev, S. Vozianov, R. Danylets, V. Grygorenko, O. Shulyak, M. Sosnin, I. Kholokharenko
better reflect the biological responsiveness of PCa
to endocrine treatment. However, this interpreta-
tion should be considered hypothesis-generating.
The present study did not directly evaluate mole
cular, genetic, or pathological markers of androgen
sensitivity. Therefore, IAR should be interpreted as
a potential surrogate dynamic marker of response
to androgen deprivation rather than as a definitive
marker of biological sensitivity. In our analysis, IAR
remained independently associated with BCR in
multivariable Cox regression analysis, while PSA-
related parameters lost statistical significance after
adjustment. These findings suggest that composite
biomarker dynamics may capture clinically rele-
vant biological information beyond conventional
PSA measures alone.
Based on the results, a predictive model incor-
porating clinical stage and IAR was developed and
presented as a nomogram. The model demonstra
ted moderate discrimination with a concordance
index of approximately 0.64 and a time-dependent
AUC of approximately 0.67 for prediction of BCR
in 36 months. Although these values indicate mo
derate predictive accuracy, similar levels of dis-
crimination have been reported in several widely
used clinical prediction models for PCa. Classic
predictive tools such as the Partin tables, CAPRA
score, and Kattan nomograms rely primarily on
baseline clinicopathological parameters, including
PSA level, biopsy Gleason grade, and clinical stage
[18—20]. While these models remain useful in
clinical practice, they primarily reflect tumor bur-
den and disease extent rather than biological re-
sponse to therapy. In contrast, the model pro-
posed in the present study incorporates dynamic
treatment-response biomarkers obtained during
neoadjuvant therapy. By combining tumor bio-
marker kinetics with endocrine suppression pa-
rameters, the IAR may represent a more biologi-
cally informative measure of treatment sensitivity.
Another important feature of the present model is
its simplicity. The final model includes only two
variables — clinical stage ≥cT3a and the IAR,
which facilitates straightforward clinical imple-
mentation in routine practice. Compared with
more complex models, requiring multiple clinico-
pathological variables of postoperative pathologi-
cal data, such parsimony may enhance reprodu
cibility and applicability in routine clinical prac-
tice. The integration of biomarker kinetics and
endocrine suppression parameters may therefore
represent a promising strategy for identifying pa-
tients with biologically sensitive tumors, who are
more likely to benefit from NADT.
Importantly, the proposed model demonstrated
the ability to stratify patients into low-, interme
diate-, and high-risk groups with significantly dif-
ferent BCRFS. This risk stratification may have po-
Fig. 4. Decision curve analysis evaluating the clinical util-
ity of the predictive model
Fig. 5. Kaplan–Meier curves for biochemical recurrence-
free survival according to the risk groups derived from
the predictive model. BCR — biochemical recurrence;
BCRFS — biochemical recurrence-free survival
ISSN 1812-9269. Experimental Oncology 48 (2). 2026 169
Dynamic Androgen Response Index and its Association with Biochemical Recurrence after Radical Prostatectomy
tential clinical implications, particularly in the con-
text of neoadjuvant therapy. Patients demonstrating
poor biological response to NADT may represent
a subgroup at increased risk of early recurrence de-
spite surgery and may therefore benefit from closer
postoperative monitoring or consideration of mul-
timodal treatment strategies. From a clinical per-
spective, early identification of patients demon-
strating poor biological response to NADT may be
particularly relevant. Such patients could potential-
ly benefit from intensified postoperative surveil-
lance, earlier initiation of adjuvant therapies, or en-
rollment in clinical trials evaluating multimodal
treatment strategies.
The findings of this study should be interpret-
ed in light of several limitations. First, the retro-
spective and single-center design may introduce
potential selection bias. Second, the relatively
modest sample size may limit statistical power
and the generalizability of the results. Third, al-
though internal validation was performed, exter-
nal validation in independent cohorts is required
before the proposed model can be implemented
in routine clinical practice. In addition, the in-
cremental prognostic value of IAR compared
with models based solely on conventional static
biomarkers or individual components of the in-
dex was not directly assessed. Future studies
should evaluate whether the addition of IAR im-
proves the model discrimination, calibration, and
clinical utility beyond established clinical and
laboratory predictors. Another limitation relates
to the treatment regimens used in this cohort.
The study population primarily received conven-
tional ADT with LHRH agonists and AA rather
than modern intensified androgen receptor sig-
naling inhibitors. Therefore, the predictive per-
formance of the proposed model in patients
treated with contemporary intensified neoadju-
vant regimens remains to be determined. Future
studies, including larger multicenter cohorts and
patients treated with modern intensified ARSI,
will be necessary to validate and further refine
the proposed model.
Despite these limitations, the study has several
strengths. It proposes a biologically plausible com-
posite biomarker reflecting endocrine treatment re-
sponse, applies a comprehensive predictive mode
ling workflow including Cox regression, nomogram
development, calibration analysis, and decision
curve analysis, and demonstrates clinically meaning-
ful survival-based risk stratification. In a field where
the main challenge is identifying patients who may
truly benefit from neoadjuvant therapy, biomarker-
oriented approaches such as the one proposed in this
study may contribute to more individualized treat-
ment strategies. Importantly, the present findings
should be interpreted in an exploratory context. The
proposed index may reflect biological tumor respon-
siveness to androgen deprivation; however, it should
not be considered a definitive predictive tool without
external validation.
In sum, the present study introduces a novel dy-
namic androgen response index integrating PSA
and testosterone kinetics during NADT. The pro-
posed index was independently associated with
BCR and enabled the development of a simple pre-
dictive model capable of stratifying patients ac-
cording to their risk of recurrence following RP.
IAR may serve as a surrogate dynamic marker of
response to androgen deprivation. However, this
interpretation remains hypothesis-generating and
requires further validation. Further prospective
studies with external validation are warranted to
confirm the clinical applicability of this approach
and to explore its potential role in guiding perso
nalized neoadjuvant treatment strategies in PCa.
Conflict of interests
The authors declare no conflict of interest.
Funding
This research received no external funding.
Ethics approval
and informed consent
The study was conducted in accordance with the
Declaration of Helsinki and approved by the Ethics
Committee of the IU NAMS (Protocol #6, 14 De-
cember 2023). Given the retrospective design of the
study, the requirement for informed consent was
waived by the ethics committee.
170 ISSN 1812-9269. Experimental Oncology 48 (2). 2026
Ye. Afanasiev, S. Vozianov, R. Danylets, V. Grygorenko, O. Shulyak, M. Sosnin, I. Kholokharenko
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ISSN 1812-9269. Experimental Oncology 48 (2). 2026 171
Dynamic Androgen Response Index and its Association with Biochemical Recurrence after Radical Prostatectomy
Є. Афанас’єв 1, 2, С. Возіанов 1, 2, Р. Данилець 1, 2,
В. Григоренко 1, О. Шуляк 2, М. Соснін 1, 2, І. Холохаренко 2
1 ДУ «Інститут урології ім. акад. О.Ф.Возіанова
НАМН України», Київ, Україна
2 Кафедра урології, Національного університету охорони
здоров’я України імені П.Л. Шупика, Київ, Україна
ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ
ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ
ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ
НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ
Стан питання. Неоад’ювантна андроген-деприваційна терапія (НАДТ) перед радикальною простатектомі-
єю (РПЕ) залишається дискусійним підходом у лікуванні локалізованого та місцево розповсюдженого раку
передміхурової залози (РПЗ). Одним з основних обмежень цієї стратегії є відсутність біомаркерів, які могли
б ідентифікувати пухлини, біологічно чутливі до андрогенної депривації. Метою цього дослідження було
оцінити прогностичне значення динамічного індексу андрогенної відповіді (ІАВ) та розробити прогностич-
ну модель біохімічного рецидиву (БР) після РПЕ. Матеріали та методи. У ретроспективне одноцентрове
дослідження було включено 84 пацієнти з РПЗ, які отримували НАДТ із подальшим виконанням РПЕ. ІАВ
визначали як співвідношення логарифмічних нахилів зниження концентрацій простат-специфічного анти-
гену (ПСА) та тестостерону під час неоад’ювантної терапії. Для визначення предикторів БР проведено ре-
гресійний аналіз Кокса. На основі незалежних предикторів побудовано прогностичну модель та номограму.
Ефективність цієї моделі оцінювали за допомогою ROC-аналізу, калібрувальних графіків та аналізу кривих
клінічної доцільності. Результати. Протягом спостереження (медіана 56 місяців) БР виник у 62 пацієнтів.
Клінічна стадія ≥ cT3a (ВР 2,34; p = 0,003) та ІАВ (ВР 1,48; p = 0,024) були незалежними предикторами БР. Мо-
дель продемонструвала помірну дискримінаційну здатність (AUC 0,68) та задовільне калібрування. Висно-
вки. ІАВ може відображати біологічну відповідь РПЗ на андрогенну депривацію. Отримані результати слід
розглядати як такі, що генерують гіпотезу, і вони потребують подальшої валідації в контексті стратифікації
ризику БР після РПЕ на тлі НАДТ.
Ключові слова: рак передміхурової залози, неоад’ювантна андроген-деприваційна терапія, біохімічний реци-
див, прогностична модель, номограма, андрогенна відповідь.
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| id | oai:ojs2.ex.aqua-time.com.ua:article-651 |
| institution | Experimental Oncology |
| issn | 2312-8852 |
| keywords_txt_mv | |
| language | English |
| last_indexed | 2026-08-22T01:00:36Z |
| publishDate | 2026 |
| publisher | PH Akademperiodyka |
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| resource_txt_mv | exp-oncologycomua/c0/260a29c08551429e58accfdb407d99c0.pdf |
| spelling | oai:ojs2.ex.aqua-time.com.ua:article-6512026-08-21T12:36:14Z DYNAMIC ANDROGEN RESPONSE INDEX AND ITS ASSOCIATION WITH BIOCHEMICAL RECURRENCE AFTER RADICAL PROSTATECTOMY FOLLOWING NEOADJUVANT ANDROGEN DEPRIVATION THERAPY ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ Afanasiev, Ye. Vozianov, S. Danylets, R. Grygorenko, V. Shulyak, O. Sosnin, M. Kholokharenko, I. рак передміхурової залози, неоад’ювантна андроген-деприваційна терапія, біохімічний рецидив, прогностична модель, номограма, андрогенна відповідь prostate cancer, neoadjuvant androgen deprivation therapy, biochemical recurrence, predictive model, nomogram, androgen response Background. Neoadjuvant androgen deprivation therapy (NADT) before radical prostatectomy (RP) remains controversial in the management of localized and locally advanced prostate cancer. A major limitation of this strategy is the lack of biomarkers capable of identifying tumors biologically sensitive to androgen deprivation. This study aimed to evaluate the prognostic value of a dynamic androgen response index (IAR) and develop a predictive model for biochemical recurrence (BCR) after RP. Materials and Methods. The retrospective single-center study included 84 patients with prostate cancer treated with NADT followed by RP. The IAR was defined as the ratio between logarithmic slopes of PSA and testosterone decline during neoadjuvant therapy. Cox regression analysis was performed to identify predictors of BCR. A predictive model and nomogram were constructed based on independent predictors. Model performance was evaluated using ROC analysis, calibration plots, and decision curve analysis. Results. During a median follow-up of 56 months, BCR occurred in 62 patients. Clinical stage ≥ cT3a (HR 2.34; p = 0.003) and IAR (HR 1.48; p = 0.024) were independent predictors of BCR. The model demonstrated moderate discrimination (AUC 0.68) and satisfactory calibration. Conclusions. The IAR may reflect the biological responsiveness of prostate cancer to androgen deprivation. These findings should be considered hypothesis-generating and require further validation in the context of risk stratification for BCR following RP after NADT. Стан питання. Неоад’ювантна андроген-деприваційна терапія (НАДТ) перед радикальною простатектомією (РПЕ) залишається дискусійним підходом у лікуванні локалізованого та місцево розповсюдженого раку передміхурової залози (РПЗ). Одним з основних обмежень цієї стратегії є відсутність біомаркерів, які могли б ідентифікувати пухлини, біологічно чутливі до андрогенної депривації. Метою цього дослідження було оцінити прогностичне значення динамічного індексу андрогенної відповіді (ІАВ) та розробити прогностичну модель біохімічного рецидиву (БР) після РПЕ. Матеріали та методи. У ретроспективне одноцентрове дослідження було включено 84 пацієнти з РПЗ, які отримували НАДТ із подальшим виконанням РПЕ. ІАВ визначали як співвідношення логарифмічних нахилів зниження концентрацій простат-специфічного антигену (ПСА) та тестостерону під час неоад’ювантної терапії. Для визначення предикторів БР проведено регресійний аналіз Кокса. На основі незалежних предикторів побудовано прогностичну модель та номограму. Ефективність цієї моделі оцінювали за допомогою ROC-аналізу, калібрувальних графіків та аналізу кривих клінічної доцільності. Результати. Протягом спостереження (медіана 56 місяців) БР виник у 62 пацієнтів. Клінічна стадія ≥ cT3a (ВР 2,34; p = 0,003) та ІАВ (ВР 1,48; p = 0,024) були незалежними предикторами БР. Модель продемонструвала помірну дискримінаційну здатність (AUC 0,68) та задовільне калібрування. Висновки. ІАВ може відображати біологічну відповідь РПЗ на андрогенну депривацію. Отримані результати слід розглядати як такі, що генерують гіпотезу, і вони потребують подальшої валідації в контексті стратифікації ризику БР після РПЕ на тлі НАДТ. PH Akademperiodyka 2026-08-21 Article Article application/pdf https://exp-oncology.com.ua/index.php/Exp/article/view/651 10.15407/exp-oncology.2026.02.161 Experimental Oncology; Vol. 48 No. 2 (2026): Experimental Oncology; 161-171 Експериментальна онкологія; Том 48 № 2 (2026): Експериментальна онкологія; 161-171 2312-8852 1812-9269 10.15407/exp-oncology.2026.02 en https://exp-oncology.com.ua/index.php/Exp/article/view/651/477 Copyright (c) 2026 Experimental Oncology https://creativecommons.org/licenses/by-nc-nd/4.0/ |
| spellingShingle | рак передміхурової залози неоад’ювантна андроген-деприваційна терапія біохімічний рецидив прогностична модель номограма андрогенна відповідь Afanasiev, Ye. Vozianov, S. Danylets, R. Grygorenko, V. Shulyak, O. Sosnin, M. Kholokharenko, I. ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ |
| title | ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ |
| title_alt | DYNAMIC ANDROGEN RESPONSE INDEX AND ITS ASSOCIATION WITH BIOCHEMICAL RECURRENCE AFTER RADICAL PROSTATECTOMY FOLLOWING NEOADJUVANT ANDROGEN DEPRIVATION THERAPY |
| title_full | ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ |
| title_fullStr | ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ |
| title_full_unstemmed | ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ |
| title_short | ДИНАМІЧНИЙ ІНДЕКС АНДРОГЕННОЇ ВІДПОВІДІ ТА ЙОГО АСОЦІАЦІЯ З БІОХІМІЧНИМ РЕЦИДИВОМ ПІСЛЯ РАДИКАЛЬНОЇ ПРОСТАТЕКТОМІЇ НА ТЛІ НЕОАД‘ЮВАНТНОЇ АНДРОГЕН-ДЕПРИВАЦІЙНОЇ ТЕРАПІЇ |
| title_sort | динамічний індекс андрогенної відповіді та його асоціація з біохімічним рецидивом після радикальної простатектомії на тлі неоад‘ювантної андроген-деприваційної терапії |
| topic | рак передміхурової залози неоад’ювантна андроген-деприваційна терапія біохімічний рецидив прогностична модель номограма андрогенна відповідь |
| topic_facet | рак передміхурової залози неоад’ювантна андроген-деприваційна терапія біохімічний рецидив прогностична модель номограма андрогенна відповідь prostate cancer neoadjuvant androgen deprivation therapy biochemical recurrence predictive model nomogram androgen response |
| url | https://exp-oncology.com.ua/index.php/Exp/article/view/651 |
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