The dedifferentiation of prostate carcinoma

Brawn, Peter N.

doi:10.1002/1097-0142(19830715)52:2<246::aid-cncr2820520210>3.0.co;2-q

Cited by 88 publications

(30 citation statements)

References 4 publications

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“…The process of dedifferentiation has been demonstrated clinically and experimentally within primary tumours (Foulds, 1954;Kastendieck & Altenahr, 1976;Nowell, 1976;Brawn, 1983;Barnett, 1984;Leonard & Smyth, 1985;Poste, 1986). It would not be unusual to expect a similar process to occur within metastases.…”

Section: Discussionmentioning

confidence: 98%

“…The M.D. Anderson method was used without difficulty in the original study, which documented dedifferentiation of prostate carcinoma (Brawn, 1983). The task of determining whether metastases were entirely or predominantly differentiated or were entirely or predominantly undifferentiated was less complicated than grading prostate carcinoma.…”

Section: Methodsmentioning

confidence: 99%

“…Dedifferentiation has been demonstrated experimentally and clinically within primary tumours but not, as yet, within metastases (Foulds, 1954;Kastendieck & Altenahr, 1976;Nowell, 1976;Brawn, 1983;Barnett & Eccles, 1984;Leonard & Smyth, 1985;Poste, 1986). In order to determine whether dedifferentiation occurs within metastases the current study compared the histology of metastatic prostate carcinoma in staging lymphadenectomies to the histology of widely disseminated prostate carcinoma at autopsy.…”

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The dedifferentiation of metastatic prostate carcinoma

Brawn

Speights²

1989

Br J Cancer

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Summary Two hundred consecutive staging lymphadenectomies with metastatic prostate adenocarcinoma and 100 consecutive autopsies with widely disseminated metastatic prostate adenocarcinoma were identified. The metastases from 41% of the staging lymphadenectomies were entirely differentiated (gland forming) and an additional 43% were predominantly (50% or more) differentiated. In contrast, the metastases from 70% of the autopsies were entirely undifferentiated (non-gland forming) and an additional 18% were predominantly undifferentiated. Further, five patients with completely or predominantly differentiated metastases in staging lymphadenectomies were found to have widespread completely or predominantly undifferentiated metastases at autopsy 4-7 years later. These findings suggest that dedifferentiation occurs within metastases and that dedifferentiation within metastases may be important in understanding the widespread dissemination of metastatic prostate carcinoma.Dedifferentiation is characterised by a progression from a more differentiated to a less differentiated histological appearance with time. Dedifferentiation has been demonstrated experimentally and clinically within primary tumours but not, as yet, within metastases (Foulds, 1954;Kastendieck & Altenahr, 1976;Nowell, 1976;Brawn, 1983;Barnett & Eccles, 1984;Leonard & Smyth, 1985;Poste, 1986). In order to determine whether dedifferentiation occurs within metastases the current study compared the histology of metastatic prostate carcinoma in staging lymphadenectomies to the histology of widely disseminated prostate carcinoma at autopsy. Materials and methodsEight hundred and fifty-seven consecutive staging lymphadenectomies were performed on patients with a diagnosis of prostate carcinoma. Criteria for staging lymphadenectomy were: (1) confirmed histological diagnosis of prostate carcinoma in needle biopsy or transurethral resection of prostate; (2) prostate carcinoma clinically confined to the prostate, or 6cm or less in size if extending beyond the capsule of the prostate; and (3) no evidence of metastases preoperatively. Two hundred of these 857 staging lymphadenectomies had metastatic prostate carcinoma in pelvic lymph node(s) (obturator, hypogastric, external iliac, internal iliac or common iliac lymph nodes).One hundred consecutive autopsies with widely disseminated metastatic prostate carcinoma were identified. Widely disseminated metastatic prostate carcinoma was defined as metastases beyond lymph nodes and/or bone. Invasions from the prostate into adjacent tissue or organs were not considered to be metastases.Metastases were determined to be of prostatic origin by: (1) the histological appearance of the metastases; (2) a comparison of the histological appearance of the primary tumour and the metastases; (3) the gross description of the prostate; and (4) serum acid phosphatase levels. If doubt remained sections of the tumour were stained with a Prostatic Specific Antigen Immunohistology kit (HistoGeMTM) (Hadji et al., 1981).The current study examin...

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Section: Discussionmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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The dedifferentiation of metastatic prostate carcinoma

Brawn

Speights²

1989

Br J Cancer

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“…An early study of Brawn in 1983 22 reported dedifferentiation between 2 subsequent TURP specimens with an interval of 3-11 years, in 65% of 54 patients; in the remaining 33% no substantial difference in differentiation grade was found (Anderson score was used). In this study, the majority of patients received hormone therapy, which may artificially produce the appearance of a higher prostate cancer grade.…”

Section: Discussionmentioning

confidence: 99%

Gleason score, age and screening: Modeling dedifferentiation in prostate cancer

Draisma

Postma

Schröder

et al. 2006

Intl Journal of Cancer

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Tumor differentiation as measured by the Gleason score is highly predictive of the course of prostatic cancer after diagnosis. Since the introduction of the prostate-specific antigen (PSA) test tumors are diagnosed with a favorable tumor stage and differentiation grade. Does screening with PSA just detect more tumors with favorable characteristics or is dedifferentiation actually being prevented by early detection and consequent treatment? The latter option implies that tumors dedifferentiate in the preclinical screen-detectable phase. To model the natural history of prostate cancer, we analyzed the age-specific distribution of clinical stage and Gleason score of 2,204 tumors diagnosed in the ERSPC-Rotterdam trial. We fitted 2 MISCAN simulation models to the observed data: Model I where tumors dedifferentiate before becoming screen-detectable and Model II where dedifferentiation occurs during the screen-detectable preclinical phase. The hypothesis of dedifferentiation during the screen-detectable phase was tested by a goodness of fit test of both models. In ERSPC-Rotterdam, we observed a significantly more favorable distribution of Gleason scores in screen-detected cancers compared to cancers found in the control arm, and in cancers detected in the second round compared to cancers detected in the first round of screening. Also, a significant association between Gleason score and age at diagnosis was found, most notably in cancers detected in the first round of screening. These findings were reproduced by Model II and less so by Model I, with a significant difference in goodness of fit between the 2 models (p < 0.001).This study provides epidemiological evidence of dedifferentiation as a major mechanism of progression in prostate cancer. Tumors dedifferentiate during the screen-detectable phase and consequently screening with PSA and early treatment can possibly prevent dedifferentiation. ' 2006 Wiley-Liss, Inc.Key words: prostatic neoplasms; Gleason score; screening; computer simulation; aging In the western world the incidence of prostate cancer is increasing because of the general availability of serum tests for prostate specific antigen (PSA) and aging of the population.1 Early detection by PSA testing and curative treatment of prostate cancer may result in a decrease in mortality from prostate cancer, 2 but definite evidence for this effect is not yet given. Nevertheless, trial results show that TNM stage and Gleason score of screen-detected tumors compare favorably to those of clinically diagnosed tumors in the control arms of the trials 3,4 ; in particular Gleason score is predictive for treatment success and survival. 5 It is tempting to deduce that early detection by screening and treatment could prevent tumor growth and dedifferentiation. However, the favorable characteristics of screen-detected cancers might be due to length bias sampling: tumors with favorable characteristics probably grow more slowly and have more chance of being detected; moreover, these tumors might never give rise to clinical sym...

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“…However, this has been contradicted by Brawn and others (Brawn, 1983;McNeal et al, 1986;MacNeal et al, 1988a). coworkers (1986, 1988a) examined prostatectomy specimens whereas Brawn (1983) graded repeat TUR biopsies and found that 65% of his patients showed a higher malignancy grade with time. Gleason did only include some occasional re-biopsies in his study.…”

Section: Gradementioning

confidence: 94%

Hormone resistant prostatic adenocarcinoma. An evaluation of prognostic factors in pre- and post-treatment specimens

Berner

Nesland²,

Wæhre³

et al. 1993

Br J Cancer

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Pre- and post-treatment specimens from 47 patients with hormone resistant prostatic carcinoma were compared with each other regarding histological grade and immunoreactivity for p53 protein, neuron specific enolase and c-erbB-2 protein. Significantly more specimens expressed a high malignancy grade when the tumour had become hormone resistant than at the time of initial diagnosis (Gleason P: < 0.0001, WHO P:0.0003). p53 protein immunoreactivity increased significantly with disease progression (P:0.006), while tissue PSA immunoreactivity was reduced in post-treatment specimens (P:0.011). p53 protein expression did not correlate with histological grade or PSA expression and seems to be an independent parameter which participates late in the neoplastic transformation. Thirty-two percent of the tumours were neuron specific enolase positive, but this parameter did not correlate with development of hormone resistance. c-erbB-2 protein reactivity was not recognised. Images Figure 1

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The dedifferentiation of prostate carcinoma

Cited by 88 publications

References 4 publications

The dedifferentiation of metastatic prostate carcinoma

The dedifferentiation of metastatic prostate carcinoma

Gleason score, age and screening: Modeling dedifferentiation in prostate cancer

Hormone resistant prostatic adenocarcinoma. An evaluation of prognostic factors in pre- and post-treatment specimens

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