One of the underemphasized supportive criteria for the diagnosis of prostatic cancer is the presence of retraction clefting around neoplastic glands. We analyzed a series of 152 prostatic cancer cases to determine the frequency, extent, and correlation of periacinar retraction clefting between needle core biopsies (NCB) and corresponding matched radical prostatectomy (RP) specimens. Clefting was significantly more frequent in neoplastic compared to nonneoplastic acini in NBC and RP (p<0.05). There was no significant difference in the frequency of retraction clefting in neoplastic acini between NCB and corresponding RP (p>0.05). We have also found a concordance in matched RP and NCB (Kappa=0.582). We conclude that periacinar retraction clefting appears more frequently in neoplastic acini and could serve as a reliable criterion in the diagnosis of prostatic adenocarcinoma.
Histological inflammation has a high prevalence in cancer-free prostate biopsy specimens and exerts similar effects on fPSA and f/tPSA levels as PC. Our study suggests histological prostatitis to be an important cause of decreased fPSA and f/tPSA values; therefore, when it is identified, antibiotic or anti-inflammatory therapy should be introduced to reduce the percentage of men with a continuing indication for prostate biopsy.
PurposeWe are often confronted with patients in the "gray zone" (prostate-specific antigen [PSA]<10 ng/mL) whose biopsies reveal no malignancy but only inflammation. We investigated the relationship between histological inflammation and total PSA (tPSA), free PSA (fPSA), and percentage of free PSA (f/tPSA) levels in patients without prostate cancer (PC).Materials and Methods We studied 106 men with tPSA<10 ng/mL who had undergone biopsy that was negative for PC and who had no clinical prostatitis. Inflammation observed at biopsies was scored for inflammation type in each biopsy core by use of a four-point scale and was then correlated with tPSA, fPSA, and f/tPSA.ResultsDifferent patterns of inflammation were found in each set of biopsies. Regression factor analysis was used to form two groups according to inflammation type: more chronic and more acute. Median tPSA, fPSA, and f/tPSA levels in the more chronic and more acute inflammation groups were 6.4 ng/mL, 1.09 ng/mL, and 15%, and 7.3 ng/mL, 0.79 ng/mL, and l2%, respectively. A significant difference was found in fPSA (p=0.003) and f/tPSA (p<0.001), whereas the difference in tPSA was not significant (p=0.200). Total PSA correlated with fPSA (r=0.4, p<0.001) but not with inflammation type (r=0.12, p>0.010). A correlation existed between inflammation type and fPSA (r=-0.31, p=0.001) and f/tPSA (r=-0.43, p<0.001) in that the fPSA and f/tPSA were lower in the group with more acute inflammation.ConclusionsSubclinical inflammation has a significant influence on fPSA in patients with tPSA<10 ng/mL but without PC or clinical prostatitis. Subclinical inflammation is not characterized by elevated tPSA alone but also by a decreased fPSA, a tendency similar to that in PC.
INSR H1085H C>T polymorphism seems to be associated with PC risk, whereas IRS1 G972R is not. However, because of the limited power of this study, there is a possibility that some modest effects of the IRS1 G972R polymorphism on PC risk went undetected. Neither polymorphism is associated with the degree of PC malignancy.
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