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D J Grignon

Publications and source records attributed to D J Grignon.

At least 55 records · Page 3Linked to original sources
PubMed1998

Platelet-type 12-lipoxygenase in a human prostate carcinoma stimulates angiogenesis and tumor growth.

Previously, we found a positive correlation between the expression of platelet-type 12-lipoxygenase (12-LOX) and the progression of human prostate adenocarcinoma (PCa; Gao et al., Urology, 46: 227-237, 1995). To determine the role of 12-LOX in PCa progression, we generated stable 12-LOX-transfected PC3 cells, which synthesize high levels of 12-LOX protein and 12(S)-hydroxyeicosatetraenoic acid metabolite. In vitro, 12-LOX-transfected PC3 cells demonstrated a proliferation rate similar to neo controls. However, following s.c. injection into athymic nude mice, 12-LOX-transfected PC3 cells formed larger tumors than did the controls. Decreased necrosis and increased vascularization were observed in the tumors from 12-LOX-transfected PC3 cells. Both endothelial cell migration and Matrigel implantation assays indicate that 12-LOX-transfected PC3 cells were more angiogenic than their neo controls. These data indicate that 12-LOX stimulates human PCa tumor growth by a novel angiogenic mechanism.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1998

Prognostic indicators in patients with seminal vesicle involvement following radical prostatectomy for clinically localized prostate cancer.

PURPOSE: We identify prognostic factors in patients with seminal vesicle involvement and negative lymph nodes following radical prostatectomy for clinically localized prostate cancer. MATERIALS AND METHODS: A total of 93 patients who underwent radical prostatectomy and had seminal vesicle invasion without lymph node metastasis were evaluated. Patients who underwent neoadjuvant/adjuvant hormonal or radiation therapy were excluded from study. Preoperative serum prostate specific antigen (PSA), biopsy and radical prostatectomy specimen Gleason score, surgical margin status, presence of extraprostatic extension and evidence of biochemical disease progression were determined prospectively. Biochemical failure was defined as a single serum PSA elevation greater than 0.4 ng./ml. RESULTS: The presence of positive surgical margins (p = 0.001), and Gleason score 7 or higher from preoperative biopsies (p = 0.03) and from the radical prostatectomy specimen (p = 0.01) were significant predictors of disease progression at a median followup of 43.3 months. Patients with preoperative PSA less than 10 ng./ml. had a better disease-free survival (p = 0.07). On multivariate analysis, after adjusting for biopsy Gleason score, prostatectomy Gleason score and serum PSA, positive surgical margins remained a statistically significant predictor of disease progression (p = 0.002). CONCLUSIONS: Surgical margin status is an independent predictor of disease recurrence in patients with seminal vesicle involvement and negative lymph nodes following radical prostatectomy. Serum PSA 10 ng./ml. or greater and specimen Gleason score 7 or greater also were adverse prognostic factors in these patients. Conversely, patients with negative surgical margins and lymph nodes have a better prognosis than previously expected, despite seminal vesicle invasion.

Aged↗
PubMed1998

High flow malignant priapism with isolated metastasis to the corpora cavernosa.

Malignant priapism is a rare disease with only 88 reported cases. We present a case of a patient with priapism secondary to isolated metastasis to corpora cavernosa from bladder tumor. Metastasis to penis usually represents evidence of a more widespread disease in 80% to 90% of the patients. Rarely, as in this case, the metastasis is solitary.

Aged↗
PubMed1998

Papillary and metanephric adenomas of the kidney.

Papillary renal adenomas are the commonest neoplasms of the renal tubular epithelium, occurring in up to 40% of adults. If these criteria are met, the diagnosis of adenoma can be made with confidence: (1) papillary, tubular, or tubulopapillary architecture; (2) diameter less than or equal to 5 mm; and (3) does not histologically resemble clear cell, chromophobe, or collecting duct renal cell carcinomas. They are composed of epithelial cells with variable amounts of cytoplasm with variable tinctorial qualities including clear. Metanephric adenoma and metanephric adenofibroma are closely related neoplasms that appear to be benign. Although they have a morphological resemblance to Wilms' tumor, there is some genetic evidence relating them to papillary adenoma and papillary renal cell carcinoma. Metanephric adenoma and metanephric adenofibroma occur at all ages, have a 2:1 predominance of female patients, and are associated with polycythemia. No instance of malignant behavior has been reported. The adenomatous component is composed of uniform small cells arranged in tubular or papillary architectural patterns. The fibromatous component is moderately cellular and composed of bland spindle cells.

Adenofibroma↗
PubMed1998

A similar pattern of chromosomal alterations in prostate cancers from African-Americans and Caucasian Americans.

A combination of genetic and epigenetic factors may explain the disproportionate incidence and mortality of prostate cancer among African-American males (AAMs) as compared with Caucasian American males (CAMs). We wished to determine whether primary prostate cancers from AAMs and CAMs harbor different patterns or frequencies of chromosomal alterations. Comparative genomic hybridization (CGH) was performed on clinically localized, untreated primary prostate cancers from 16 AAMs and 16 CAMs. Detailed statistical analysis was used to delineate gains and deletions with high sensitivity and specificity and to compare the frequency and pattern of alterations between the two groups of tumors. The two groups of patients had indistinguishable preoperative serum prostate-specific antigen levels, and the two groups of tumors had similar pathological stages and grades. Chromosomal gains and deletions occurred in regions known to be frequently altered in prostate cancer. Specifically, the most frequent alterations were deletions of regions on chromosomes 13q, 5q, 16q, and 8p and gains of regions on 8q and 5q. When tumors from AAMs and CAMs were compared, the frequencies of alteration (deletion, gain, or no alteration) were similar across 98.9% of the length of the genome. The patterns of alterations of the most frequently altered chromosomes were also similar between tumors from AAMs and CAMs. We concluded that primary prostate cancers from AAMs and CAMs harbor a similar pattern and frequency of chromosomal alterations. These data support the notion that sporadic prostate cancers from AAMs and CAMs develop by similar chromosomal mechanisms. Biological differences, if present, do not occur on the chromosomal level.

Black People↗
PubMed1998

Systemic interleukin 2 therapy for human prostate tumors in a nude mouse model.

Once the regional lymph nodes become involved in prostate carcinoma, 85% of patients develop distant metastases within 5 years, and metastatic disease is difficult to treat. We have investigated the effect of systemic interleukin 2 (IL-2) treatment on metastatic prostate carcinoma using a xenograft tumor model. Cells from a PC-3/IF cell line, produced by intrafemoral injection of human PC-3 prostate carcinoma cells, were injected in the prostate of Balb/c nude mice. Prostate tumors and para-aortic lymph nodes were resected, and tumor cells were recultured and passaged in the prostate in vivo to produce new cell lines. On day 6 following prostatic injection of these cell lines, mice were treated with i.p. injections of IL-2 at 25,000-50,000 units/ day for 5 consecutive days. The effect of IL-2 on tumor progression was assessed, and histological studies were performed on prostate tumor and lymph node sections. The tumor cell lines generated by serial prostate injection were tumorigenic and metastasized to regional para-aortic lymph nodes. Tumors of 0.4 cm were obtained by day 16 and grew to 1-1.5 cm by day 40 with metastasis to para-aortic lymph nodes. Following two to three weekly courses of 5 days of 25,000-40,000 units/day of IL-2, the growth of prostate tumors was inhibited by 94%. Higher doses of 50,000 units/ day were toxic. Histologically, prostate sections showed vascular damage manifested by multifocal hemorrhages and an influx of lymphocytes and polymorphonuclear cells into disintegrating tumors and areas of necrosis containing numerous apoptotic cells. In contrast to control mice, para-aortic lymph nodes were not enlarged in responding mice. These findings suggest that systemic IL-2 therapy can induce an antitumor response in prostate tumors and control their growth and metastasis.

Animals↗
PubMed1998

Limited role of radionuclide bone scintigraphy in patients with prostate specific antigen elevations after radical prostatectomy.

PURPOSE: Bone scintigrams of patients with increasing serum prostate specific antigen (PSA) after radical prostatectomy are only rarely positive. We identify clinical parameters that would improve our ability to select patients for this imaging study. MATERIALS AND METHODS: We reviewed all bone scintigrams done at our institution between 1991 and 1996 in patients with persistently increasing serum PSA after radical prostatectomy. What prompted the clinician to obtain the bone scintigram was trigger PSA (tPSA). The rate of increase in PSA to tPSA was measured by tPSA/time from radical prostatectomy (slope 1) and tPSA/time from last undetectable PSA (slope 2). These parameters were evaluated together with standard clinicopathological data in univariate and multivariate analyses to determine the ability to predict the bone scintigram result. RESULTS: In univariate analysis tPSA (p = 0.003), slope 1 (p = 0.005) and slope 2 (p = 0.004) were useful in predicting the bone scintigram result but pathological stage, Gleason score, preoperative PSA and time to recurrence were not. In multivariate analysis the single most useful parameter in predicting the bone scintigram result was tPSA (p = 0.01). Based on a logistic regression model the probability of a positive bone scintigram was less than 5% until tPSA increased to 40 to 45 ng./ml. CONCLUSIONS: In patients with increasing serum PSA after radical prostatectomy current serum PSA is the best predictor of the bone scintigram result. Furthermore, there is limited usefulness of bone scintigraphy until PSA increases above 30 to 40 ng./ml.

Bone Neoplasms↗
PubMed1998

Expression of bcl-2, p53, and p21 in benign and malignant prostatic tissue before and after radiation therapy.

Abnormalities in genes of the apoptotic pathway might contribute to survival in prostatic cancer (PCa) cells after radiation therapy (RT). We investigated the immunohistochemical expression of the products of the p53, p21WAF1, and bcl-2 genes in pre-RT and post-RT biopsy specimens from 38 patients with locally advanced PCa. All of the 38 patients underwent a uniform protocol of RT with or without neoadjuvant hormonal therapy. Immunohistochemical staining for expression of the products of the p53, p21WAF1, and bcl-2 genes was performed on material from pre-RT and post-RT specimens. Sufficient tissue for analysis was available from 25 of the pre-RT and 38 of the post-RT biopsy specimens. In benign prostatic epithelium, RT resulted in expression of p53 (2 [8%] of 25 pre-RT specimens vs. 15 [71%] of 21 post-RT specimens; P < .001) and increased expression of bcl-2 (1 [5%] of 18 pre-RT vs. 18 [86%] of 21 post-RT; P < .001). There was no change in the expression of p21WAF1 (1 [4.5%] of 22 pre-RT vs. 4 [17%] of 23 post-RT; P = NS). Post-RT specimens were positive for PCa in 24 (63%) of 38 cases. In the PCa tissue, p53 expression was seen in 10 (42%) of 24 pre-RT and 12 (63%) of 19 post-RT samples (P = NS). A significant upregulation of p53 was seen in the subgroup of patients who did not receive neoadjuvant hormonal therapy (9 [82%] of 11 vs. 3 [38%] of 8; P = .05). No significant change in p21WAF1 (5 [21%] of 24 vs. 5 [33%] of 15; P = NS), or bcl-2 (4 [18%] of 22 vs. 3 [21%] of 14; P = NS) expression was detected. There was no significant correlation between immunohistochemical expression of apoptosis-related markers and treatment failure. We concluded that RT induced upregulation of the bcl-2 and p53 gene products in benign prostatic tissue and that this likely reflected a protective mechanism in genetically unaltered epithelium. Increased p53 expression in PCa was only seen in patients without neoadjuvant hormonal treatment, indicating that the cancer cells with abnormal p53 were at least partially protected from RT-induced cell death.

Adult↗
PubMed1998

Prostatic intraepithelial neoplasia and atypical adenomatous hyperplasia. Relationship to pathologic parameters, volume and spatial distribution of carcinoma of the prostate.

OBJECTIVE: To summarize studies that have investigated the morphologic, spatial and volumetric relationship between prostate cancer and its putative precursors, high grade prostatic intraepithelial neoplasia (HGPIN) and atypical adenomatous hyperplasia (AAH). METHODS: Studies addressing the relationship between morphologic parameters of prostate cancer (i.e., stage, grade, volume and anatomic distribution) and both HGPIN and AAH are reviewed. Similar data based on our institutional experience with surgical and autopsy series of step-sectioned, totally embedded prostate glands are also presented. RESULTS: Most investigators have demonstrated significant associations between HGPIN and carcinoma in terms of coexistence, "zonal" origin and physical proximity. The two lesions have a high tendency to be present simultaneously; both originate predominantly in the peripheral zone and are often found within the same microscopic field. Reports on the relationship between HGPIN and the stage of prostate cancer are less consistent, and the associations of this lesion with cancer grade and volume are exceedingly complex. HGPIN appears to be associated with moderately to poorly differentiated, smaller, often-multifocal tumors and is less frequent in large, high grade cancers. There are data suggesting a trend-of a reciprocal relationship between more extensive and diffuse HGPIN and large-volume prostate cancers. Conversely, there is a wide spectrum of volume distribution of the two lesions in glands harboring smaller tumors. Similar data concerning AAH are limited. CONCLUSION: There are strong and consistent data supporting various aspects of the morphologic associations between HGPIN and prostate cancer. The indications that glands harboring larger tumors tend to contain less extensive HGPIN could raise the hypothesis that as carcinoma becomes larger, it may replace areas of the gland previously occupied by HGPIN. Alternatively, prostate cancer can evolve from ducts with HGPIN and gradually overgrow their precursor. There is a relative dearth of similar information concerning AAH.

Adenoma↗
PubMed1998

Pathology of premalignant lesions and carcinoma of the prostate in African-American men.

The objective of this study was to summarize data describing the morphological characteristics of the spectrum of prostatic neoplasia in African-American men and compare them to their equivalents in Caucasian men. Studies that have emphasized the documentation of pathological features of prostate cancer or its putative precursors in African Americans are reviewed and are contrasted with comparable data concerning Caucasians. The author's experience is also presented. There is significant overlap between the pathological features of prostate cancer in African Americans and Caucasians in their clinical associations. The main pathological parameter reported with consistency to differ between the two groups is the observation that African-American patients present with a more advanced stage of the disease compared with Caucasian patients. Reports on differences in the grade and volume of the disease are less consistent. Comparative data on "preclinical," autopsy-type cancers and those concerning premalignant lesions indicate a similar prevalence of autopsy cancers between the two races while the prevalence and extent of high-grade prostatic intraepithelial neoplasia is higher in African-American men compared with Caucasian men. The difference is more evident in younger individuals. In conclusion, there are indications that African-American men with clinically localized prostate cancer tend to have a more advanced pathological stage at the time of radical prostatectomy compared with Caucasian men. Our data also indicate a higher prevalence of a putative precursor for clinically evident prostate cancer, high-grade prostatic intraepithelial neoplasia in African-American men. The earlier onset and extensiveness of this lesion may contribute to the higher incidence of clinically evident prostate cancer in African Americans.

Adenocarcinoma↗
PubMed1998

Matrix metalloproteinase-9 expression in bladder washes from bladder cancer patients predicts pathological stage and grade.

The matrix metalloproteinases (MMPs), in particular the gelatinases (MMP-2 and MMP-9) have been associated with tumor cell invasion and metastasis in many human cancers. Here we examined the expression of proMMP-2 (gelatinase A) and proMMP-9 (gelatinase B) proteins in the cellular component of bladder washes obtained from 65 patients. Twenty-six patients had active bladder cancer, 24 had a history of bladder cancer but no evidence of active disease at the time of cystoscopy (recurrence-free), and 15 patients had lesions other than bladder cancer (controls). The results were correlated with the cytological findings of the bladder wash and the histopathological results of the tumor resection when performed. In patients with active transitional cell carcinoma of the bladder, 71 and 38% had expression and overexpression of the latent form of MMP-9 (proMMP-9), respectively. In contrast, neither latent nor active MMP-2 could be detected in any of the samples examined, regardless of tumor status. Overexpression of proMMP-9 correlated with higher grade (P = 0.003) and pathological stage (P = 0.04) of disease in the active bladder cancer group. No significant gelatinase expression was detected in the recurrence-free and control cases. Compared with urine cytology, proMMP-9 expression had an overall higher sensitivity for bladder cancer identification (71 versus 54%, P = 0.11). Detection of proMMP-9 in bladder washes may be a novel approach for the identification of patients with more aggressive forms of bladder cancer.

Adult↗
PubMed1997

Growth of human nondiploid primary prostate tumor epithelial cells in vitro.

Research into molecular and cellular defects underlying prostate cancer would be advanced by in vitro models of prostate tumor cells representing patient tumors. We have propagated, in serum-free medium, epithelial cell cultures derived from nondiploid prostate tumors and normal human prostate. The serial passage tumor cells exhibited nondiploid karyotype and transformed phenotypes of focus formation and anchorage-independent growth. In contrast, the normal prostate cells showed diploid karyotype and lacked transformed phenotypes. Both the tumor and normal cells were positive for prostate-specific antigen and cytokeratins 18 and 19 and negative for keratin 15. These results demonstrate that the nondiploid prostate tumors and normal prostate epithelial cell cultures retained their respective in vivo properties and should allow studies to elucidate molecular alterations involved in human prostate cancer.

Biomarkers↗
PubMed1997

Diagnostic and prognostic markers for human prostate cancer.

BACKGROUND: The incidence and mortality of prostate cancer are increasing at alarming rates, partially due to an aging population. Early detection of prostate cancer, using clinically sensitive procedures and/or tumor markers (e.g., prostate-specific antigen [PSA]), is of prime importance. However, the choice of therapeutic interventions for prostate cancer at the time of diagnosis is largely dependent on clinical and pathologic staging and prediction of the degree of aggressiveness of the disease. Clinically applicable prognostic markers are urgently needed to assist in the selection of optimal therapy. METHODS: Literature review of the potential diagnostic and prognostic markers for human prostate cancer. RESULTS: Well-established tissue prognostic indicators, including histologic grade, margin positivity, pathologic stage, intraglandular tumor extent, and DNA ploidy, are not reviewed in this paper. Recently, a number of novel markers have been identified. In this paper, we begin with a discussion of a number of well-established as well as investigational diagnostic markers and then focus on evaluation of prognostic markers. Diagnostic markers that have prognostic value and investigational prognostic markers are also discussed. CONCLUSIONS: Currently, only PSA is utilized for early diagnosis and monitoring of prostate cancer. A number of potential prognostic markers warrant further investigation. Multimarker analysis is implicated.

Acid Phosphatase↗
PubMed1997

p53 status and prognosis of locally advanced prostatic adenocarcinoma: a study based on RTOG 8610.

BACKGROUND: The p53 tumor suppressor gene (also known as TP53) is one of the most frequently mutated genes in human cancer. Several studies have shown that p53 mutations are infrequent in prostate cancer and are associated with advanced disease. PURPOSE: We assessed the prognostic value of identifying abnormal p53 protein expression in the tumors of patients with locally advanced prostate cancer who were treated with either external-beam radiation therapy alone or total androgen blockade before and during the radiation therapy. METHODS: The study population consisted of a subset of patients entered in Radiation Therapy Oncology Group protocol 8610 ("a phase III trial of Zoladex and flutamide used as cytoreductive agents in locally advanced carcinoma of the prostate treated with definitive radiotherapy"). Immunohistochemical detection of abnormal p53 protein in pretreatment specimens (i.e., needle biopsies or transurethral resections) was achieved by use of the monoclonal anti-p53 antibody DO7; specimens in which 20% or more of the tumor cell nuclei showed positive immunoreactivity were considered to have abnormal p53 protein expression. Associations between p53 protein expression status and the time to local progression, the incidence of distant metastases, progression-free survival, and overall survival were evaluated in univariate (logrank test) and multivariate (Cox proportional hazards model) analyses. Reported P values are two-sided. RESULTS: One hundred twenty-nine (27%) of the 471 patients entered in the trial had sufficient tumor material for analysis. Abnormal p53 protein expression was detected in the tumors of 23 (18%) of these 129 patients. Statistically significant associations were found between the presence of abnormal p53 protein expression and increased incidence of distant metastases (P = .04), decreased progression-free survival (P = .03), and decreased overall survival (P = .02); no association was found between abnormal p53 protein expression and the time to local progression (P = .58). These results were independent of the Gleason score and clinical stage. A significant treatment interaction was detected with respect to the development of distant metastases: Among patients receiving both radiation therapy and hormone therapy, those with tumors exhibiting abnormal p53 protein expression experienced a reduced time to the development of distant metastases (P = .001); for patients treated with radiation therapy alone, the time to distant metastases was unrelated to p53 protein expression status (P = .91). CONCLUSIONS: Determination of p53 protein expression status yield significant, independent prognostic information concerning the development of distant metastases, progression-free survival, and overall survival for patients with locally advanced prostate cancer who are treated primarily with radiation therapy. IMPLICATIONS: The interaction of radiation therapy plus hormone therapy and abnormal p53 protein expression may provide a clinical link to experimental evidence that radiation therapy and/or hormone therapy act, at least in part, by the induction of apoptosis (a cell death program) and suggests that this mechanism may be blocked in patients whose tumors have p53 mutations.

Adenocarcinoma↗
PubMed1997

Human prostate carcinoma cells produce extracellular heparanase.

The degradation of heparan sulfate proteoglycan (HSPG) in basement membranes (BM) has been previously suggested to be accomplished by an endoglycosidase activity called heparanase which has not been isolated outside of platelets. HSPG degradation by heparanase has been associated with tumor cell invasion, angiogenesis, and growth factor function. In this study, we identify heparanase activity biochemically and immunologically in malignant human prostate carcinoma cells (PC-3M), linking platelet heparanase probes with the tumor heparanase activity observed. Concentrated conditioned medium from PC-3M cells was analyzed by a heparin-Sepharose affinity column. Three peaks eluted with 0.15, 0.35, and 0.5 M NaCl. Each peak was analyzed by incubation with 3H-labeled heparin as well as [3H]HSPG from EHS tumor BM. The 0.5 M peak material degraded [3H]-heparin by 17.2%, with little additional degradation by the other peaks in comparison to the conditioned medium from which they were obtained. Likewise, the same amount of the 0.5 M peak accounted for the majority of degradation (30.8%) of 3H-labeled HSPG. Interestingly, for the same amount of 0.5 M peak material, significantly more HSPG was degraded than heparin under the same conditions. In addition, carrageenan-lambda, an inhibitor of glycanase, completely inhibited the degradation of heparin and heparan sulfate proteoglycan by the 0.5 M peak. Using antibody to the N-terminus domain of platelet heparanase, a 60-kDa protein was identified by immunoblot in 0.5 M peak material. Additionally, immunohistochemical staining of human prostate carcinoma specimens showed granular staining at or near the cell membrane and near the luminal surface using antibody to the N-terminus and C-terminus domains of platelet heparanase. In summary, human prostate carcinoma cells show heparanase activity in conditioned medium that degrades heparin and BM HSPG and is detected by antibody to platelet heparanase. In addition, the membrane-associated staining in tissue sections of prostate cancer strongly correlates with the biochemical and immunological detection in conditioned medium of human PC-3M cells.

Chromatography, Affinity↗
PubMed1997

Prostate cancer: indicators of aggressiveness.

In spite of the slow progression rates common to most prostate cancers, it is well recognized that a subset of patients will experience a more aggressive course with many losing their lives to this malignancy. As the number of patients diagnosed with prostate cancer continues to increase, there is a growing pressure to refine and supplement the three most important prognostic parameters for this disease (tumor pathologic stage, its histologic differentiation (Gleason score) and the level of prostate specific antigen). While this review emphasizes the value of these factors in stratifying patients into risk groups, it also explores the prognostic significance of additional commonly used and evolving non-traditional markers (DNA ploidy, proliferation, tumor angiogenesis, and the status of tumor suppressor genes).

Adenocarcinoma↗
PubMed1997

Clinicopathologic and interphase cytogenetic analysis of papillary (chromophilic) renal cell carcinoma.

Trisomy 7 and 17 with deletion of Y is typical of papillary renal cell adenoma (PRCA), and additional alterations occur in the putative genetic progression toward papillary renal cell carcinoma (PRCC). Our study correlated aneuploidy with clinicopathologic features in PRCCs. We used fluorescence in situ hybridization to assess copy number for chromosomes 7, 8, 10, 12, 16, 17, and Y in 16 PRCCs and surrounding benign tubular parenchyma from 15 patients by use of alpha satellite (centromere) probes on deparaffinized tissue sections. We then compared the pattern of monosomy/nullisomy or trisomy/polysomy/hemidisomy to clinicopathologic parameters. Nine tumors (58% Group 1) showed the numeric aberrations typical of PRCAs and PRCCs, with gains of 7 and 17 and loss of Y. We also identified four trisomies of 12 and 16 and one of 8 in Group 1. The remaining seven cases (Group 2) were cytogenetically atypical. Two displayed borderline loss of chromosome 7, although trisomy 17 was present in both. Five had trisomy 7, but none exhibited chromosome 17 alterations, and two exhibited a gain of Y. Neoplasms in Group 2 were less often multicentric than were Group 1 tumors, and they contained foamy macrophage infiltrates less often. One chromophilic carcinoma with abundant clear cells and another with oncocytic features exhibited Group 2 chromosomal profiles. One patient (nuclear grade 4) died from disease, and 14 had no evidence of carcinoma at the last follow-up. We concluded that PRCCs represent a histologically and genotypically heterogeneous group of tumors. If PRCAs consistently exhibit +7, +17, and -Y, it is uncertain whether PRCCs always evolve directly from such lesions. The presence of genotypic heterogeneity might reflect histologic variants of PRCCs, which overlap with other types of RCC. PRCC is generally an indolent neoplasm, despite a high frequency of chromosomal aneuploidy.

Adult↗