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PubMed1994

Neuroendocrine differentiation in prostatic intraepithelial neoplasia and adenocarcinoma.

Neuroendocrine cells are thought to have a regulatory role in prostatic epithelial growth and may be prognostically useful in prostatic adenocarcinoma. To determine the extent of neuroendocrine differentiation in high-grade prostatic intraepithelial neoplasia (PIN), a putative precursor of cancer, we studied the immunohistochemical expression of 10 markers in 26 radical prostatectomy specimens with PIN and adenocarcinoma. Expression was measured as mean percent of positive cases and positive high-power (x40) fields. The highest percentage of cases showed immunoreactivity for serotonin (73%, PIN; 54%, carcinoma), neuron-specific enolase (NSE) (67%, PIN; 46%, carcinoma), chromogranin (62%, PIN; 65%, carcinoma), and human chorionic gonadotropin (hCG) (30%, PIN; 22%, carcinoma); the remaining markers showed immunoreactivity in fewer than 5% of cases (somatostatin, calcitonin, corticotropin) or in no cases (thyrotropin, prolactin, and glucagon). At least one of the markers was present in 88% of cases of PIN and 92% of carcinoma. Non-neoplastic epithelial cells expressed serotonin, NSE, chromogranin, and hCG in every case, and the expression was significantly greater than in PIN and cancer. Stepwise regression analysis revealed the following positive correlations: chromogranin expression in PIN and patient age, NSE expression in cancer and number of lymph node metastases, and hCG expression in cancer and percentage of Gleason pattern 5; serotonin expression in PIN and cancer did not correlate with any of the clinical and pathologic factors. Neuroendocrine differentiation is downregulated in prostatic carcinogenesis, with intermediate levels of expression in PIN compared with normal cells and carcinoma.

Adenocarcinoma↗
PubMed1996

Construction of a representative cDNA library from prostatic intraepithelial neoplasia.

We report the construction of a plasmid-based cDNA library made from microdissected cells derived from prostatic intraepithelial neoplasia. Total RNA was extracted and converted to blunt-ended, double-stranded cDNA by oligo(dT)-mediated reverse transcription followed by linker addition. A linker-specific primer with UDG-compatible ends was used to amplify the cDNA and the resulting PCR product was subcloned. A total of 154 clones were sequenced and results indicated that 81.5% of the clones derived from either known genes, anonymous expressed sequence tags, or novel transcripts with very little redundancy of screened clones. These results demonstrate the feasibility of constructing complex representative cDNA libraries from specific microdissected cell populations that represent microscopic precursor stages of cancer progression. This method should facilitate identification of transcripts specifically expressed in cells of a distinct histological origin and tumorigenic stage.

Adenocarcinoma↗
PubMed2006

Tyrosine kinase Etk/BMX is up-regulated in human prostate cancer and its overexpression induces prostate intraepithelial neoplasia in mouse.

The nonreceptor tyrosine kinase Etk/BMX was originally identified from the human prostate xenograft CWR22. Here, we report that Etk is up-regulated in human prostate tumor specimens surveyed. Knocking down Etk expression by a specific small interfering RNA (siRNA) in prostate cancer cells attenuates cell proliferation, suggesting an essential role of Etk for prostate cancer cell survival and growth. Targeted expression of Etk in mouse prostate epithelium results in pathologic changes resembling human prostatic intraepithelial neoplasia, indicating that up-regulation of Etk may contribute to prostate cancer development. A marked increase of luminal epithelial cell proliferation was observed in the Etk transgenic prostate, which may be attributed in part to the elevated activity of Akt and signal transducers and activators of transcription 3 (STAT3). More interestingly, the expression level of acetyltransferase cyclic AMP-responsive element binding protein-binding protein (CBP) is also increased in the Etk transgenic prostate as well as in a prostate cancer cell line overexpressing Etk, concomitant with elevated histone 3 acetylation at lysine 18 (H3K18Ac). Down-modulation of Etk expression by a specific siRNA leads to a decrease of H3 acetylation in prostate cancer cell lines. Our data suggest that Etk may also modulate chromatin remodeling by regulating the activity of acetyltransferases, such as CBP. Given that Etk may exert its effects in prostate through modulation of multiple signaling pathways altered in human prostate cancer, the Etk transgenic mouse model may be a useful tool for studying the functions of Etk and identification of new molecular markers and drug targets relevant to human diseases.

Animals↗
PubMed1996

Molecular biology of prostatic intraepithelial neoplasia.

High-grade PIN is the most likely precursor of prostatic adenocarcinoma, according to virtually all available evidence to date. The clinical importance of recognizing PIN is based on its strong association with prostatic carcinoma. PIN has a high predictive value as a marker for adenocarcinoma. Its identification in biopsy specimens of the prostate warrants further search for concurrent invasive carcinoma. PIN is associated with progressive abnormalities of phenotype and genotype intermediate between normal prostatic epithelium and cancer, indicating impairment of cell differentiation and regulatory control with advancing stages of prostatic carcinogenesis. There is progressive gain or loss of a wide variety of biomarkers, including morphometric markers, differentiation markers, stromal markers, growth factors and associated receptors, oncogenes, tumor suppressor genes, and chromosomes. Abnormalities in expression of most biomarkers are amplified in the progression from high-grade PIN to localized cancer, metastatic cancer, and hormone-refractory cancer. Oncogenesis of prostatic carcinoma probably occurs through the selection of several genetic changes, each modifying the expression or function of genes controlling cell growth and differentiation. Further studies are needed to evaluate the function and prognostic value of oncogene expression in the normal, preneoplastic, and neoplastic prostate.

Adenocarcinoma↗
PubMed2004

Amphiregulin expression in prostatic intraepithelial neoplasia and adenocarcinoma: a study of 93 cases.

BACKGROUND: Amphiregulin (AMP) is a heparin-binding glycoprotein that is structurally and functionally related to epidermal growth factor. Its effects are mediated by the tyrosine kinase activity of the epidermal growth factor receptor (EGF-R), and specific nuclear targeting sequences. AMP induces cell proliferation after androgen stimulation of human prostate cancer cell lines. An autocrine proliferative loop involving AMP, androgen, and EGF-R may, therefore, play a role in prostatic carcinogenesis. The purpose of this study was to compare the expression of AMP in benign prostatic epithelium, high-grade prostatic intraepithelial neoplasia (PIN), and adenocarcinoma. METHODS: We performed an immunohistochemical study of select sections from 93 radical prostatectomies performed at the Mayo Clinic between 1987 and 1991. All patients were previously untreated and found to have pathologic stage T2N0M0 adenocarcinoma after routine handling of surgical specimens. Affinity-purified polyclonal antibody directed against AMP was applied to tissue sections using the streptavidin-biotin method. For each case, the percentage of immunoreactive cells in benign epithelium, PIN, and adenocarcinoma was estimated in 10% increments. Intensity on a scale from 0 (negative) to 3 (strongly immunoreactive) and pattern of expression (nuclear versus cytoplasmic) also were recorded. RESULTS: AMP immunoreactivity was present in benign prostatic epithelium, PIN, and prostatic adenocarcinoma in all cases. The mean percentage of AMP-immunoreactive cells was 53.8% in benign epithelium, 65.9% in PIN, and 74.3% in cancer. Intensity was moderate in all cases. The pattern of expression was usually nuclear in benign epithelium (secretory and basal cells), and usually cytoplasmic or nuclear and cytoplasmic in PIN and adenocarcinoma. There were rare scattered immunoreactive cells in the stroma, ejaculatory duct epithelium, and urethral urothelium. Endothelial cells were invariably unstained. CONCLUSIONS: AMP expression in prostate increases progressively from benign epithelium to PIN and cancer. Increased expression of AMP may contribute to the development of prostatic adenocarcinoma. Predominantly nuclear staining was observed in benign epithelium, whereas cytoplasmic or nuclear and cytoplasmic staining was observed in PIN and adenocarcinoma. The differences in nuclear and cytoplasmic localization of immunoreactivity may reflect the presence of two pathways of activation, and hence varying biological functions of AMP.

Adenocarcinoma↗
PubMed1998

Genetic heterogeneity in a prostatic carcinoma and associated prostatic intraepithelial neoplasia as demonstrated by combined use of laser-microdissection, degenerate oligonucleotide primed PCR and comparative genomic hybridization.

We combined laser-assisted microdissection from H&E-stained paraffin sections, degenerated oligonucleotide-primed polymerase chain reaction (DOP-PCR), and comparative genomic hybridization (CGH) to analyse chromosomal imbalances in small tumour areas consisting of 50-100 cells. This approach was used to investigate intratumour genetic heterogeneity in a case of metastatic prostatic adenocarcinoma and chromosomal changes in areas of prostatic intraepithelial neoplasia (PIN) adjacent to the invasive tumour. In four microdissected invasive tumour areas with different histological patterns (acinar, cribriform, papillary and solid) marked intratumour heterogeneity was found by CGH. Recurrent chromosomal imbalances detected in at least two microdissected tumour areas were gains on 1p32-->p36, 2p22, 3q21, 7, 8q21-->q24, 11q12-->q13, 16p12-->p13, 17, 19 and loss on 16q23. Additional chromosomal changes were found in only one of the microdissected areas (gains on 16q21-->q23, 20q22 and losses on 8p21-->p23, 12p11-->q12, 12q21-->q26, 13q21-->q34, 16q12, and 18q22). In PIN, gains on chromosomes 8q21-->q24 and 17 were found in both samples investigated (low and high grade PIN), while gains on chromosomes 7, 11q, 12q, 16p, and 20q and losses on 2p, 8p21-->p23, 12q were found only in one PIN area. Controls to ensure reliable CGH results consisted in CGH analyses of (i) approximately 80 microdissected normal epithelial cells, which showed no aberrations after DOP-PCR and (ii) larger cell numbers (approximately 10(5) or 10(7) cells) of the primary tumour investigated without DOP-PCR and partially displaying the chromosomal imbalances (gain on 16p12-->p13, losses on 2p25, 8p21-->p23, 12p11-->p12, 12q21-->q26, 18q22) found in the small microdissected areas. Microsatellite and FISH analyses further confirmed our CGH results from microdissected cells. The combined approach of laser-assisted microdissection, DOP-PCR and CGH is suitable to identify early genetic changes in PIN and chromosomal imbalances associated with the particular histological patterns of invasive prostatic adenocarcinoma.

Adenocarcinoma↗
PubMed1999

Ep-Cam levels in prostatic adenocarcinoma and prostatic intraepithelial neoplasia.

PURPOSE: The monoclonal antibody (mAb) 323/A3, a second generation high affinity antibody of the 17-1A antibody family, recognizes a 40 kDa transmembrane glycoprotein that has been referred to as Ep-CAM, 17-1A recognized antigen, or EGP40. While Ep-CAM is expressed on the basolateral surface of a variety of epithelia, the strongest expression is frequently detected among several types of carcinoma. In this regard, Ep-CAM may be useful in therapy, in diagnosis, and/or in prognosis. We examined the distribution of Ep-CAM in normal, dysplastic, and malignant prostatic epithelium. MATERIALS AND METHODS: Paraffin sections of prostate tissue from 76 patients with clinically localized (pT2) prostatic adenocarcinoma were immunostained with mouse mAb 323/A3 using the avidin-biotin horseradish peroxidase method. RESULTS: Within benign prostatic epithelium, immunoreactivity typically was low and frequently was restricted to the luminal cells. In contrast, moderate to strong immunostaining was detected frequently in the luminal cells of high grade prostatic intraepithelial neoplasia (PIN). Furthermore, strong immunostaining usually was detected in the cells of adenocarcinomas. The immunostaining in PIN (p<0.0001) and in adenocarcinoma (p<0.0001) was significantly greater than that observed in the normal epithelium. Expression of Ep-CAM did not vary significantly with the Gleason score of tumors or the clinical outcome of patients. Expression of Ep-CAM was demonstrated also in the malignant prostatic cell lines LNCaP, DU145 and PC3 using immunohistochemistry and an immunoblot technique. CONCLUSIONS: These findings suggest that increased levels of Ep-CAM represent an early event in the development of prostatic adenocarcinoma.

Adenocarcinoma↗
PubMed1995

Neuroendocrine cells in peripheral prostatic zone: age, prostatic intraepithelial neoplasia and latent cancer-related changes.

The neuroendocrine cells (NCs) in the peripheral prostatic zone of 32 patients without prostatic symptoms and with an average age of 61.4 +/- 6.7 (range 48-75) years were studied, and it was found that most are closed-type cells (95.8%) and that there is a gradual fall both in their total number and the number per square millimeter (p = 0.03) with advancing age. There were microscopic foci of high-grade prostatic intraepithelial neoplasia (PIN) in 59.3% of the patients and occult carcinomas in 28.1%, but no statistical relationship was found between these lesions and the number of NCs (p = 0.35 and p = 0.9, respectively). The gradual increase in NCs in the peripheral zone of normal prostates as of adolescence, reported in the literature, would appear to support a possible androgenic action on these cells. Our finding of a decrease in patients with foci of PIN and carcinoma from the fifth decade suggests that this decrease in NCs may make the prostate more susceptible to carcinogenic factors.

Adenocarcinoma↗
PubMedDate not supplied

Frequency and location of mitoses in prostatic intraepithelial neoplasia (PIN).

The aim of our study was to assess the frequency and location of mitoses in routine haematoxylin- and eosin-stained sections of prostatic intraepithelial neoplasia (PIN) and then to compare the patterns with those in benign prostatic hyperplasia (BPH) and prostatic invasive adenocarcinoma (PAC). The frequency of mitoses in the epithelial cell layers increased from BPH through PIN up to PAC. The proportions of mitoses in PIN lesions of low grade (PINlow) and high grade (PINhigh) were greater than in BPH (mean 0.001%; standard error, SE, 0.001%), the values decreasing from the basal layer towards the lumenal. In PINlow, the mean category values were 0.087% (SE 0.04%) in the basal, 0.046% (SE 0.033%) in the intermediate and 0.024% (SE 0.024%) in the lumenal position. In PINhigh, the mean category values were 0.194% (SE 0.178%) in the basal position, 0.075% (SE 0.06%) in the intermediate and 0.049% (SE 0.033%) in the lumenal position. The proportions of mitoses in adenocarcinoma with cribriform pattern decreased from the basal towards the lumenal layer, as for PIN: 0.154% (SE 0.096%) in the basal position, 0.072% (SE 0.044%) in the intermediate and 0.064% (SE 0.04%) in the lumenal position. In the solid/trabecular adenocarcinomas, the mean category value in the cell layer adjacent to the stroma was 0.22% (SE 0.111%), whereas in the other cell layers it was 0.074% (SE 0.045). In small and large acinar adenocarcinomas, the proportions of mitoses were 0.058% (SE 0.024%) and 0.068% (SE 0.019%), respectively. In conclusion, the evaluation of mitotic frequency and location in haematoxylin- and eosin-stained sections gives accurate information on how the mitotic activity in PIN compares with BPH and PAC.

Adenocarcinoma↗
PubMed2006

Prostatic intraepithelial neoplasia and adenocarcinoma in mice expressing a probasin-Neu oncogenic transgene.

NEU (ERBB2) and other members of the epidermal growth factor receptor (EGFR) family have been implicated in human prostate cancer (CAP) development and progression to an androgen-independent state, but the extent of involvement and precise role of this signaling pathway remain unclear. To begin addressing such open questions in an animal model, we have developed a transgenic line in which an oncogenic Neu cDNA (Neu*) driven by the probasin gene promoter is overexpressed in the mouse prostate and causes development of prostatic intraepithelial neoplasia (PIN) that progresses to invasive carcinoma. Expression profiling using microarrays, which was selectively validated and extended by immunophenotyping of Neu*-induced PIN and CAP, led to the identification of some novel biomarkers and also revealed increased expression of Egfr, Erbb3 and phosphorylated androgen receptor. In view of this information from our mouse model, which can be used to analyze further the role of Erbb signaling in prostatic tumorigenesis, we examined human prostate cancer tissue arrays by immunohistochemistry. Based on statistical analyses of the results, we propose the testable hypothesis that ERBB3, shown to be expressed in 86% of the human CAP cases that we examined, is the pivotal element of the Erbb pathway promoting tumorigenesis by heterodimerization with NEU or EGFR, while a NEU/EGFR dimer does not appear to play a significant role in CAP.

Adenocarcinoma↗
PubMed1995

Interphase cytogenetics of prostatic adenocarcinoma and precursor lesions: analysis of 25 radical prostatectomies and 17 adjacent prostatic intraepithelial neoplasias.

Twenty-five radical prostatectomy specimens were screened for the presence of numerical chromosome changes within the adenocarcinoma as well as 17 adjacent prostatic intraepithelial neoplasias (PIN) by means of interphase in situ hybridization (ISH) to routinely processed tissue sections. To this end a defined alfoid repetitive DNA probe set was used, specific for the centromeres of chromosomes 1, 7, 8, 10, 15, and Y. The cytogenetic information was correlated with histopathological and clinical features as well as with DNA ploidy. Numerical aberrations of at least one chromosome were shown in 13 of 25 cases (52%). Alterations of chromosome 8 and loss of the Y chromosome were the most frequent findings (both 20%), followed by loss of chromosomes 15 (16%) and 10 (12%). Gain of chromosome 7 was seen in 8% of cases. No aberrations of chromosomes 7, 8, 10, and 15 were found in the adjacent PIN lesions, whereas loss of the Y chromosome in both PIN and tumor occurred in two cases. Also, (low level) aneuploidy was observed in 76% of these PIN lesions. Ploidy of the carcinomas as assessed by ISH correlated well with ploidy measured by DNA flow cytometry (FCM; P < 0.02). Due to the more specific correspondence between ISH and tumor pathology, pathologic grade correlated with ISH aneuploidy (P < 0.05), whereas FCM ploidy did not. Furthermore, genetic heterogeneity within a tumor was seen, as judged by the focal appearance of chromosomal aberrations. Chromosomal alterations occurred in all grades and stages, although loss of chromosome 10, gain of chromosome 7, and aberrations of chromosome 8 tended to predominate in more advanced cancers.

Adenocarcinoma↗
PubMed2001

Identification of potential diagnostic markers of prostate cancer and prostatic intraepithelial neoplasia using cDNA microarray.

The identification of novel genes or groups of genes expressed in prostate cancer may allow earlier diagnosis or more accurate staging of the disease. We describe the assembly and use of a 1877-member microarray representing cDNA clones from a range of prostate cancer stages and grades, precursor lesions and normal tissue. Using labelled cDNA from tumour samples obtained from TURP or radical prostatectomy, analysis of expression patterns identified many up-regulated transcripts. Cell lines were found to over-express fewer genes than diseased tissue samples. 17 known genes were found to over-express more than 4-fold in 4 or more cancers out of 15 cancers. Only 2 genes were over-expressed in 6 out of 15 cancers or more, whilst no genes were consistently found to be over-expressed in all cancer samples. Novel prostate cancer associations for several well characterized genes or full length cDNAs were identified, including PLRP1, JM27, human UbcM2, dynein light intermediate chain 2 and human homologue of rat sec61. Novel associations with high-grade PIN include: breast carcinoma fatty acid synthase and cDNA DKFZp434B0335. We shortlist and discuss the most significant over-expressed genes in prostate cancer and PIN, and highlight expression differences between malignant and benign samples.

Aged↗
PubMed2006

Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study.

Green tea catechins (GTCs) proved to be effective in inhibiting cancer growth in several experimental models. Recent studies showed that 30% of men with high-grade prostate intraepithelial neoplasia (HG-PIN) would develop prostate cancer (CaP) within 1 year after repeated biopsy. This prompted us to do a proof-of-principle clinical trial to assess the safety and efficacy of GTCs for the chemoprevention of CaP in HG-PIN volunteers. The purity and content of GTCs preparations were assessed by high-performance liquid chromatography [(-)-epigallocathechin, 5.5%; (-)-epicatechin, 12.24%; (-)-epigallocatechin-3-gallate, 51.88%; (-)-epicatechin-3-gallate, 6.12%; total GTCs, 75.7%; caffeine, <1%]. Sixty volunteers with HG-PIN, who were made aware of the study details, agreed to sign an informed consent form and were enrolled in this double-blind, placebo-controlled study. Daily treatment consisted of three GTCs capsules, 200 mg each (total 600 mg/d). After 1 year, only one tumor was diagnosed among the 30 GTCs-treated men (incidence, approximately 3%), whereas nine cancers were found among the 30 placebo-treated men (incidence, 30%). Total prostate-specific antigen did not change significantly between the two arms, but GTCs-treated men showed values constantly lower with respect to placebo-treated ones. International Prostate Symptom Score and quality of life scores of GTCs-treated men with coexistent benign prostate hyperplasia improved, reaching statistical significance in the case of International Prostate Symptom Scores. No significant side effects or adverse effects were documented. To our knowledge, this is the first study showing that GTCs are safe and very effective for treating premalignant lesions before CaP develops. As a secondary observation, administration of GTCs also reduced lower urinary tract symptoms, suggesting that these compounds might also be of help for treating the symptoms of benign prostate hyperplasia.

Administration, Oral↗
PubMed1999

[Influence of prostatic intraepithelial neoplasia on blood levels of PSA and free PSA percentage].

OBJECTIVE: To analyze the influence of prostatic intra-epithelial neoplasia (PIN) on serum total PSA levels and free PSA percentage. MATERIAL AND METHODS: Total and free PSA concentrations (IRMA Tandem and Tandem free PSA, Hybritech Inc) were determined in 349 patients with normal DRE and PSA greater than 4 ng/ml, undergoing prostatic biopsy by sextant and in 81 patients with prostate cancer in clinical stage T1c N0 M0 undergoing radical prostatectomy. In the group of patients undergoing prostatic biopsy, benign hyperplasia was diagnosed in 284 (81.6%) patients, 234 (82.4%) were PIN free, 41 (14.4%) with low grade PIN and 9 (3.2%) with high grade PIN. Cancer was diagnosed in 65 patients (18.6%), 30 of whom (46.2%) had associated high grade PIN. High grade PIN was detected in 62 (76.5%) patients in the group undergoing radical prostatectomy. RESULTS: No statistically significant differences were detected among total PSA and free PSA percentage serum concentrations relative to the detection of associated PIN, regardless of its degree, in patients undergoing prostatic biopsy. Cancer detection was the single most significant contributing variable. In patients undergoing radical prostatectomy, high degree PIN did not influence significantly. The greatest contribution in this group was the pathological stage. CONCLUSIONS: PSA serum concentration and PSA percentage are not influenced by the existence of PIN. High degree PIN is strongly associated to cancer. Accordingly, repeat biopsies are warranted in any patient presenting such lesions.

Adult↗
PubMed2000

Bcl-2 proto-oncogene expression in low- and high-grade prostatic intraepithelial neoplasia.

OBJECTIVE: To determine the incidence of bcl-2 protein expression in low- and high-grade prostatic intra-epithelial neoplasia (PIN) lesions, and to explore the role of bcl-2 in prostatic tumorigenesis. Materials and methods Immunoreactivity for bcl-2 was examined in 10 samples of benign prostatic hyperplasia (BPH), 13 of primary prostatic adenocarcinoma, 15 of high-grade PIN and 18 of low-grade PIN. All immunostaining results were scored for the approximate percentage of positive tumour cells and relative immunostaining intensity (score range 0-12). RESULTS: In all BPH samples, bcl-2 staining was detected consistently in the basal cell layer of the ducts and acini, but no staining was ever apparent in luminal cells. The immunoreactivity for bcl-2 was heterogeneous in the prostatic carcinomas and bcl-2 protein expression was present in six samples. In these six bcl-2-positive tumours, the mean (range) staining score was 1.15 (1-6). There was detectable expression of bcl-2 in low- and high-grade PIN in all cell layers; immunoreactivity was present in 10 of 15 high-grade PIN lesions, with a mean (range) score of 1.14 (1-4), and in 12 of 18 samples of low-grade PIN, with a mean (range) score of 1.77 (1-6). CONCLUSIONS: The high incidence of bcl-2 protein expression in low- and high-grade PIN lesions suggests that bcl-2 protein expression is associated with early prostate tumorigenesis.

Gene Expression↗
PubMed1996

Platelet-derived growth factor A and B chains and the alpha and beta receptors in prostatic intraepithelial neoplasia.

BACKGROUND: The objective of this study was to evaluate the expression of platelet-derived growth factor (PDGF A, PDGF B) and their receptors (PDGF alpha, PDGF beta) in prostatic intraepithelial neoplasia (PIN) and adenocarcinoma. METHODS: Peroxidase-antiperoxidase immunoperoxidase labeling was used to detect the extent of antibody labeling in 29 different high grade PIN specimens. RESULTS: PDGF A and PDGF alpha were uniformly expressed in glandular epithelial and stromal cells, whereas PDGF B was not expressed by either tissue. However, PDGF beta was lightly expressed in a uniform manner by both the glandular epithelial and stromal cells. CONCLUSIONS: The data suggest that an autocrine loop may exist in which the epithelial cells of high-grade PIN express PDGF AA and PDGF alpha to modulate growth of precancerous lesions.

Carcinoma in Situ↗