Prostatic intraepithelial neoplasia and putative precursor lesions of prostate cancer: a clinical perspective.
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Independent origin of multiple foci of prostatic intraepithelial neoplasia: comparison with matched foci of prostate carcinoma.
BACKGROUND: Prostate carcinoma usually is heterogeneous and multifocal, with diverse clinical and morphologic manifestations. Understanding of the molecular basis for this heterogeneity is limited, particularly for the putative precursor, high grade prostatic intraepithelial neoplasia (PIN). In this study, the authors attempted to determine the genetic relation between multiple foci of PIN and matched foci of carcinoma, and whether they are independent in origin. METHODS: The distribution and prevalence of allelic imbalance at 6 microsatellite polymorphic markers on chromosomes 7q, 8p, 8q, and 18q were examined in 84 microscopically excised PIN foci (mean, 1.6 foci/case) and 95 foci of prostate carcinoma (mean, 1.8 foci/case) from 52 completely embedded, mapped whole mount prostates. RESULTS: PIN contained a lower overall proportion of allelic imbalance than matched prostate carcinoma foci for the 6 polymorphic microsatellite markers (65% vs. 82%), but this difference was not significant. The rate of allelic imbalance in PIN was similar to that in prostate carcinoma at 5 of 6 loci studied; the exception, D18S34 (18q12.2-12.3), had a significantly lower rate of allelic imbalance in PIN than in prostate carcinoma (19% vs. 52%), suggesting that genetic alterations in this chromosomal region may be important in carcinogenesis. Of 22 cases with allelic imbalance in at least 1 focus of PIN and 1 focus of prostate carcinoma, 21 informative cases (95%) showed a similar pattern of allelic imbalance at > or = 1 markers in the matched PIN and prostate carcinoma foci. Significant genetic heterogeneity was observed in both PIN and prostate carcinoma. Allelic imbalance was observed in at least 1 focus in 11 of 25 cases with multiple foci of PIN (44%) and 20 of 25 cases with multiple foci of prostate carcinoma (80%). There was no significant correlation between allelic imbalance and pathologic stage or tumor grade. CONCLUSIONS: Our findings indicate that multiple foci of PIN arise independently within the same prostate. This observation suggests that a field effect underlies prostatic neoplasia. Multiple foci of prostate carcinoma also often arise independently, lending additional support for this hypothesis. The strong genetic similarities between PIN and prostate carcinoma strongly suggest that evolution and clonal expansion of PIN may account for the multifocal etiology of carcinomas.
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Ratio of free to total prostate-specific antigen in patients with prostatic intraepithelial neoplasia.
OBJECTIVE: There are many reports about the effects of prostatic intraepithelial neoplasia (PIN) on serum prostate-specific antigen (PSA) level. The aim of this study was to determine the relationship between PIN and serum free PSA/total PSA (fPSA/tPSA) ratios. METHODS: We evaluated 46 patients with PIN, 15 patients with benign prostatic hyperplasia (BPH), and 16 patients with localized prostatic carcinoma (CaP) for the amount of fPSA and tPSA with the chemiluminescent enzyme assay. RESULTS: fPSA values from BPH to high-grade PIN (PIN2 and PIN3) was increased, and then a decrease was observed from high-grade PIN to CaP. fPSA was significantly different between BPH and low-grade PIN and high-grade PIN. There was no significant difference observed between BPH and CaP. tPSA values increased from BPH to CaP. tPSA was significantly different between BPH and high-grade PIN and CaP. fPSA/tPSA ratios decreased from BPH to CaP. This ratio was significantly different between CaP and BPH and low-grade PIN. There was no significant difference between CaP and high-grade PIN. CONCLUSIONS: Our results confirm that fPSA/tPSA ratio is better at discriminating between patients with CaP and those with BPH, but not between patients with CaP and those with high-grade PIN. Due to similarities between CaP and high-grade PIN, we think that decreased fPSA/tPSA ratio obtained at the time of intial diagnosis of PIN without concurrent carcinoma could be used as predictive factors to distinguish patients in whom carcinoma will be found on subsequent biopsies from those with PIN not associated with cancer on repeat biopsy.
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Prostatic intraepithelial neoplasia and putative precursor lesions of prostate cancer: a clinical perspective.
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Biopsy↗
Cell kinetic studies on prostatic intraepithelial neoplasia (PIN) and atypical adenomatous hyperplasia (AAH) of the prostate.
To investigate possible cell kinetic relations between benign prostatic hyperplasia (BPH), atypical adenomatous hyperplasia (AAH), prostatic intraepithelial neoplasia (PIN) and carcinoma, cell kinetic analyses were performed using radiolabelled DNA-precursors (3H-thymidine autoradiography), immunohistochemistry (proliferation marker Ki67/MIB1 and/or PCNA) and silver staining of nucleolar organizer regions (AgNOR). All methods yielded the lowest values for BPH and AAH, while maximal values were found in carcinoma of high malignancy. PIN was equal to GII-carcinomas, while AAH was between BPH and carcinoma of low malignancy. This investigation ranks BPH, AAH, low grade carcinoma, PIN and high grade carcinoma in order using different methods of cell kinetic analysis. The preneoplastic character of PIN is apparent whereas the character of AAH remains uncertain.
Carcinoma↗
Reversibility of prostatic intraepithelial neoplasia: implications for chemoprevention.
High-grade prostatic intraepithelial neoplasia is the most likely precursor of prostatic adenocarcinoma, according to virtually all available evidence. It has a high predictive value as a marker for adenocarcinoma, and its identification in biopsy specimens of the prostate warrants further search for concurrent invasive carcinoma. Androgen deprivation therapy and radiation therapy decrease its prevalence and extent, suggesting a role in chemoprevention.
Adenocarcinoma↗
Production of serum-free and total prostate-specific antigen due to prostatic intraepithelial neoplasia.
OBJECTIVE: High serum total prostate-specific antigen (PSA) levels have proven to be predictive of concurrent cancer but the role of prostatic intraepithelial neoplasia (PIN) in the production of total (t) and free (f) PSA is still the subject of research. In this study we wanted to discover whether variations in serum fPSA and tPSA levels are caused by PIN. MATERIAL AND METHODS: We reviewed the medical records of 87 patients: in 32 of them the diagnosis of isolated PIN was made from surgical samples (simple prostatectomy, n = 19; radical cystectomy, n = 13); in 30 patients a diagnosis of benign prostatic hyperplasia (BPH) without PIN or prostatic carcinoma was made after simple prostatectomy (n = 20) or radical cystectomy (n = 10); and in 25 patients a clinically significant prostatic cancer was diagnosed and these patients underwent radical prostatectomy. All patients underwent a standard preoperative evaluation, including serum fPSA and tPSA determinations and PSA density. RESULTS: The frequency of isolated PIN in simple prostatectomy specimens was 6.3%. The mean f/t PSA ratios were 17.66% in the 32 patients with PIN, 19.2% in the 8 patients with low-grade PIN, 17.6% in the 24 patients with high-grade PIN, 24.2% in patients with BPH and 13% in patients who underwent radical prostatectomy. CONCLUSIONS: We believe that to make a definitive diagnosis of isolated PIN without carcinoma, study of the whole prostate gland is necessary, in order to definitively exclude the presence of concurrent neoplastic foci. Our data show that PIN does not contribute to tPSA levels and density; however, it may be responsible for a slight reduction in the f/t PSA ratio, with a significant reduction in cases with high-grade PIN (17.6%) compared to those with BPH (24.2%).
Adenocarcinoma↗
The significance of the P504S expression pattern of high-grade prostatic intraepithelial neoplasia (HGPIN) with and without adenocarcinoma of the prostate in biopsy and radical prostatectomy specimens.
Diagnosis of prostatic adenocarcinoma is usually not difficult in biopsy specimens. Problems may occur in biopsy specimens, containing only a few suspicious lesions. Recently, P504S has been tested as a new marker for prostatic carcinoma. When over-expressed in atypical glands without basal cells, it establishes the diagnosis of prostatic carcinoma. We analysed the staining intensity of P504S in 208 biopsy specimens from prostates (1) with adenocarcinoma (n=132), (2) with high-grade prostatic intraepithelial neoplasia (HGPIN) with adenocarcinoma (n=36), (3) with HGPIN alone (n=40) and in radical prostatectomy specimens with HGPIN adjacent to (n=54) or distant from adenocarcinoma (n=64). P504S expression was negative to weakly positive in biopsy specimens showing HGPIN without carcinoma and weakly positive in radical prostatectomy specimens revealing HGPIN distant from adenocarcinoma. In biopsy specimens with a combination of HGPIN and adenocarcinoma and in radical prostatectomy specimens with HGPIN adjacent to adenocarcinoma, P504S was strongly expressed. The same findings were made in radical prostatectomy specimens containing adenocarcinoma and HGPIN adjacent to or distant from adenocarcinoma and in preoperative biopsies revealing adenocarcinoma and HGPIN. These results suggest that moderate to strong P504S expression in HGPIN of biopsy specimens is indicative of an associated adenocarcinoma and may be helpful in the choice of therapy.
Adenocarcinoma↗
The extent and zonal location of prostatic intraepithelial neoplasia and atypical adenomatous hyperplasia: relationship with carcinoma in radical prostatectomy specimens.
High grade prostatic intraepithelial neoplasia (PIN) and atypical adenomatous hyperplasia (AAH) are considered putative precursors of prostatic adenocarcinoma. We determined the extent and zonal distribution of PIN and AAH in totally-embedded radical prostatectomies with prostate cancer, including 195 cases with PIN and 217 with AAH. PIN was identified in 86% of the cases. The mean volume of PIN was 1.32 cc (range, 0-8.12 cc), and was greater for PIN within 2 mm of cancer (mean, 1.0 cc) than for PIN more than 2 mm from cancer (mean, 0.3 cc). PIN was usually multicentric (64.5% of cases) and located in the non-transition zone (63%) or all zones (36%). The volume of PIN was positively correlated with the volume of cancer, patient age, pathologic stage and Gleason score. AAH was identified in 23.0% of the cases, and was more frequent in the transition zone (19.8% of cases) than in the non-transition (peripheral and central) zone (6.0%). The number of foci of AAH in the transition zone was always greater than that in the non-transition zone. AAH was frequently multicentric (46% of cases), especially in the transition zone (47% of transition zone cases) compared with the non-transition zone (23% of non-transition zone cases). The mean volume of AAH was 0.029 cc (range, 0-1.29 cc), and was much higher in the transition zone than in the non-transition zone. AAH was more common in older patients and those with greater prostatic weight, higher prostatic volume, greater percent of nodular hyperplasia, greater volume of cancer, greater percent of Gleason patterns 4 and 5 cancer, higher volume of prostatic intraepithelial neoplasia and higher serum prostate specific antigen concentration. Our results indicate that the extent and zonal distribution of high grade PIN and carcinoma are strongly associated, and that PIN is frequently multicentric; this supports the hypothesis that PIN is a premalignant lesion. AAH and carcinoma show a weak but significant association; if AAH is a premalignant lesion, it probably is associated with a subset of cancers arising in the transition zone.
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Identification of numerical chromosomal changes detected by interphase fluorescence in situ hybridization in high-grade prostate intraepithelial neoplasia as a predictor of carcinoma.
CONTEXT: High-grade prostate intraepithelial neoplasia (HPIN) is the most likely precursor of prostate cancer. The condition of many patients with a diagnosis of HPIN in prostate needle core biopsy could, if left untreated, progress to invasive cancer. Currently there is no available clinical, immunohistochemical, or morphologic criteria that are predictive of this progression. OBJECTIVE: To determine whether chromosomal instability in these precursor lesions could increase their predictive value for cancer detection. DESIGN: Dual-color interphase fluorescence in situ hybridization analysis was performed on archived prostate needle core biopsies from 54 patients with initial diagnosis of isolated HPIN and follow-up of 3 years or more. We used commercially available centromere probes for chromosomes 4, 7, 8, and 10. We had interpretable results in 44 patients as follows: (1) group A: 24 HPIN patients with persistent HPIN and/or benign lesions in the follow-up biopsies, and (2) group B: 20 HPIN patients with progression to prostate carcinoma. RESULTS: Twenty-five percent of the patients in group B displayed numeric chromosomal aberrations. Only 8.3% of the patients from group A had chromosomal abnormalities (P =.1). The observed overall chromosomal changes in HPIN were higher than those in normal or hyperplastic epithelium, with a statistically significant difference (P <.05). All aberrations were detected in the form of chromosomal gain. Overall, the commonest aberration was gain of chromosome 8, followed by gains of chromosomes 7 and 10. CONCLUSION: These results indicated that although no single numeric chromosomal abnormality could be assigned as a predictor of HPIN progression to carcinoma, the overall level of numeric chromosomal abnormalities shows a trend of elevation in HPIN patients whose condition subsequently progressed to carcinoma.
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Evidence of multifocality of telomere erosion in high-grade prostatic intraepithelial neoplasia (HPIN) and concurrent carcinoma.
Mechanisms underlying prostate cancer (CaP) initiation and progression are poorly understood. A chromosomal instability mechanism leading to the generation of numerical and structural chromosomal changes has been implicated in the preneoplastic and neoplastic stages of CaP. Telomere dysfunction is one potential mechanism associated with the onset of such instability. To determine whether there was alteration in telomere length and chromosome number, 15 paraffin-embedded prostatectomy specimens were investigated using quantitative peptide nucleic acid (PNA) FISH analysis of representative foci of carcinoma, putative precancerous lesions (high-grade prostatic intraepithelial neoplasia, HPIN) and nondysplastic prostate epithelium. A significant decrease in telomere length was shown in both HPIN and CaP in comparison with normal epithelium. In addition, elevated rates of aneusomy suggested that increased levels of chromosomal aberrations were associated with decreased telomere length. Moreover, multiple foci of HPIN were shown to have a heterogeneous overall reduction of telomere length. This reduction was more evident in the histologic regions of the prostate containing CaP. Such observations lend support to the hypothesis that telomere erosion may be a consistent feature of CaP oncogenesis and may also be associated with the generation of chromosomal instability that characterizes this malignancy.
Adenocarcinoma↗
Is low-grade prostatic intraepithelial neoplasia a risk factor for cancer?
INTRODUCTION: High-grade prostatic intraepithelial neoplasia (HGPIN) is generally accepted to be a precursor lesion of prostate cancer. The likely outcome of isolated low-grade PIN (LGPIN) lesions in prostate biopsies remains unclear. A follow-up study of 106 patients with LGPIN- and HGPIN lesions was performed. MATERIALS AND METHODS: In a 2-y period, 207 men were diagnosed with isolated PIN on standard systematic sextant biopsy of the prostate. In total, 104 patients had LGPIN and 103 had HGPIN. No patients had ever received androgen deprivation therapy, chemotherapy or radiation therapy. In all, 106 patients who underwent repeat second or third sextant biopsies were analysed in the study; 30% of these patients received a selenium-vitamin E supplement for at least 6 months. RESULTS: In total, 43 had LGPIN and 63 HGPIN on the first biopsy. The mean age was 63.5 y (range 46-77) in the LGPIN group and 64.9 y in the HGPIN group. The mean total PSA was 6.96 ng/ml (range 0.59-34.13) in the LGPIN group and 8.44 ng/ml (range 0.59-35.3) in the HGPIN group. In the LGPIN group, 30% of the patients had cancer in at least one of the repeat biopsy cores. In the HGPIN group, 27% had cancer in at least one of the repeat biopsy cores. The mean total PSA of patients who had cancer in repeat biopsies with LGPIN was 7.84 ng/ml (range 2.92-34.13). The mean total PSA of the patients who had cancer in repeat biopsy in the HGPIN was 6.73 ng/ml (range 0.56-25). There was no significant difference in PSA and pathological stage between those patients who did and those who did not receive selenium-vitamin E supplements. CONCLUSIONS: These data are intriguing since the risk of finding prostate carcinoma on repeat sextant biopsy in the LGPIN group is 30%. This is higher than commonly reported. The importance of recognising and re-biopsying HGPIN was confirmed. If chemoprevention could be shown to be effective, it might be beneficial not only in HGPIN but also in LGPIN. The possible activity of chemopreventive agents and their combination with iso-flavonoids needs further investigation.
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Prostatic intraepithelial neoplasia: significance and management.
Prostatic intraepthelial neoplasia (PIN) is a putative premalignant change that bears a morphological similarity to prostatic cancer and shows increased frequency, severity, and extent in patients with prostate cancer. This article discusses the evidence for PIN as a premalignant lesion, reviews the morphology, terminology, appropriate grading system, and diagnostic significance of PIN, as well as describes management recommendations for further evaluation when PIN is diagnosed in prostate resection and biopsy specimens. Clinical management of high-grade PIN found in transurethral resection of the prostate (TURP) or prostate biopsy specimens should include repeat transrectal ultrasound (TRUS) and prostate biopsy for early detection of prevalent coexistent prostate cancer. In cases of high-grade PIN, increased surveillance methods have the potential to decrease morbidity and mortality by early cancer diagnosis.
Humans↗
Glycoprotein A-80 in the human prostate: immunolocalization in prostatic intraepithelial neoplasia, carcinoma, radiation failure, and after neoadjuvant hormonal therapy.
OBJECTIVES: To review the expression of A-80 in prostate cancer and prostatic intraepithelial neoplasia and compare it with that of normal and hyperplastic prostatic tissue. The ability to recognize cancer after androgen deprivation therapy and residual and/or recurrent cancer after radiotherapy using A-80 staining was also examined. A-80 is a glycoprotein linked to exocrine differentiation that shows little or no expression in normal exocrine cells, but is selectively overexpressed in dysplasias and adenocarcinomas. METHODS: We studied 277 prostate samples with a monoclonal antibody (MAb) to A-80. We applied this MAb to paraffin sections of specimens of fetal (n = 12), benign prostatic hyperplasia (n = 26, from transurethral prostate resection specimens), atypical adenomatous hyperplasia (n = 11), prostate cancer (n = 103, from radical prostatectomy specimens), and autopsy (n = 7) tissue. In addition, 54 prostatectomy specimens after androgen-deprivation therapy and 64 specimens after radiotherapy were similarly studied. RESULTS: MAb A-80 stained the epithelial component of all 12 prostate specimens from fetal tissue; no staining was seen in normal adult prostatic tissue (0 of 7). In benign prostatic hyperplasia, sporadic cells reacted in 13% of cases (4 of 30); the atypical adenomatous hyperplasia samples were all negative (0 of 11). In patients with prostate cancer, more than 99% (102 of 103) stained positive, regardless of the grade or stage of cancer. Low and high-grade prostatic intraepithelial neoplasia reacted in 73% (38 of 52) and 92% (77 of 84) of cases, respectively. All 64 (100%) salvage prostatectomy samples after external beam radiotherapy stained positive for A-80. Carcinoma subsequent to neoadjuvant hormonal therapy stained positive in 98% (53 of 54) of cases. CONCLUSIONS: A-80 is useful in differentiating benign prostatic hyperplasia and atypical adenomatous hyperplasia from prostate cancer. Also, the strong A-80 reactions in most high-grade prostatic intraepithelial neoplasia provide strong molecular support to the precancerous nature of the lesion. In particular, A-80 staining of biopsies may be useful in detecting residual and/or recurrent prostate carcinoma after radiation or hormonal therapy.
Adenocarcinoma↗
[Occurrence of prostatic intraepithelial neoplasia in needle biopsy of the prostate and its clinical significance].
From March 1994 to September 1996 485 patients of median age 67 years (range 49-82) underwent transrectal prostate needle biopsy at the Urological Clinic JLF UK in Martin. PIN was detected in 31 (6.4%) patients. Median age of patients with PIN was 67 years (range 58-75). There were 21 (68%) patients with low-grade PIN and 10 (32%) patients with high-grade PIN. In this group concomitant invasive cancer of the prostate was detected in 6 (19.4%) patients with PIN, of whom 5 (16.0%) had high-grade PIN and 1 (3.4%) nad low-grade PIN. Median concentration of PSA in patients with PIN was 9.1 ng/ml (range 1.3-85 ng/ml), significantly higher (p < 0.001) than PSA concentration in patients with BPH. We did not find significant differences between PSA concentrations in patients with PIN and in those with prostate cancer (p = 0.77). In conclusion we recommend clinical management of patients newly diagnosed with PIN.
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Chromosomal anomalies in prostatic intraepithelial neoplasia and carcinoma detected by fluorescence in situ hybridization.
The pathogenetic relationship between high-grade prostatic intraepithelial neoplasia (PIN), prostatic carcinoma, and metastases is poorly understood. We used fluorescence in situ hybridization (FISH) with centromere-specific probes for chromosomes 7, 8, 10, 12, and Y to evaluate numeric chromosomal anomalies in PIN (68 foci), localized prostatic carcinoma (78 foci), and lymph node metastases (8 foci) in 40 whole-mount radical prostatectomy and pelvic lymphadenectomy specimens. Chromosomal anomalies were found in 50, 51, and 100% of the foci of PIN, carcinoma, and metastases, respectively. The mean numbers of abnormal chromosomes per focus were 0.66 in PIN, 1.09 in carcinoma, and 3.75 in metastases. The most frequent anomaly in PIN was a gain of chromosome 8 (32% of foci), followed by gains of chromosomes 10 (13%), 7 (10%), 12 (4%), and Y (4%). The most frequent anomalies in foci of carcinoma were gains of chromosomes 7 and 8 (28% and 30% of foci, respectively), followed by gains of chromosomes 10 (23%), 12 (9%), and Y (9%). There was a positive correlation of the gain of chromosome 8 with the pathological stage and Gleason score (both P < 0.05). Usually, carcinoma foci contained more anomalies than paired PIN foci, but five prostates contained one or more foci of PIN with more anomalies than carcinoma. Among the cases with metastases, usually one or more foci of the primary tumor shared chromosomal anomalies with the matched metastases. Our results indicate that PIN and prostatic carcinoma foci have similar proportions of chromosomal anomalies, but foci of carcinoma usually have more alterations. This observation supports the hypothesis that PIN is often a precursor of carcinoma, although there are some carcinoma foci that have few or no apparent chromosomal alterations, whereas concurrent PIN foci have multiple alterations. A gain of chromosome 8 was the most common numerical alteration and was associated with increasing cancer stage and grade, suggesting that it may play a role in the initiation and progression of prostatic carcinoma. Usually, one or more foci of the primary tumor shared chromosomal anomalies with associated lymph node metastases, suggesting that, often, just a single focus of carcinoma gives rise to metastases.
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Prostatic intraepithelial neoplasia: a lesion that may be confused with cancer on prostatic ultrasound.
Most prostatic adenocarcinomas reveal a hypoechoic peripheral zone lesion on transrectal ultrasonography. Numerous benign processes can have similar transrectal ultrasound findings. We report 8 cases of transrectal ultrasound-guided prostatic biopsies of peripheral zone hypoechoic lesions that demonstrated prostatic intraepithelial neoplasia, a presumed premalignant lesion. Immunohistochemistry using an antibody directed against cytokeratins 5 and 14 was performed to exclude carcinoma. Of the men 2 had invasive carcinoma on repeat biopsy and 1 had carcinoma diagnosed on subsequent transurethral resection. Patients with prostatic intraepithelial neoplasia on biopsy of hypoechoic peripheral zone lesions merit careful monitoring.
Adenocarcinoma↗
Persistence of prostatic intraepithelial neoplasia after effective chemoprevention of microscopic prostate cancer with antiandrogen in a rat model.
PURPOSE: We determined the chemopreventive effect of the antiandrogen bicalutamide (Zeneca Co., Ltd., Osaka, Japan) on Fisher 344 rat prostate carcinogenesis induced by DMAB (3,2'-dimethyl-4-aminobiphenyl) (Nard Co., Ltd., Osaka, Japan). We have previously reported that rat prostate microscopic carcinogenesis in this model was paradoxically enhanced when continuous treatment with bicalutamide was begun 20 weeks after the initiation of DMAB. In the current study we determined whether antiandrogen would promote or suppress the prostate carcinogenesis when administration was begun at a later period of carcinogenesis. MATERIALS AND METHODS: DMAB at a dose of 50 mg/kg was injected subcutaneously into all animals 10 times at 2-week intervals. To clarify the target lesions of bicalutamide we used 2 control groups (groups 1 and 2). Animals in groups 1 and 2 were autopsied at 60 and 74 weeks, respectively, after the initiation of DMAB. Treatment with bicalutamide began in the 60th week in group 3 rats and continued for 14 weeks. They were sacrificed in the 74th week. RESULTS: Microscopic cancer was revealed in 27% of group 1 rats and the incidence was increased to 42% in group 2 (statistically not significant). Delayed bicalutamide treatment significantly suppressed the cancer lesion. No cancerous lesion was detected in the ventral or other lobes of the prostate of the rats in group 3. In contrast, bicalutamide did not affect the incidence of PIN. The difference in the incidence of PIN in groups 2 and 3 (84% and 78%, respectively) was not significant. CONCLUSIONS: The current investigation indicates that, if bicalutamide is started in the later period, it can efficiently eradicate existing microscopic cancer. Despite this suppressive effect on microscopic cancer bicalutamide permits the persistence of PIN. The latter finding suggests that the sensitivity of PIN to antiandrogen might be more complicated than previously recognized.
Aminobiphenyl Compounds↗