Search PubMed⌕ Search

Biomedical subjects

M Chen

Publications and source records attributed to M Chen.

At least 451 records · Page 25Linked to original sources
PubMed1997

The amino terminus of JAK3 is necessary and sufficient for binding to the common gamma chain and confers the ability to transmit interleukin 2-mediated signals.

JAK3 is a protein tyrosine kinase that specifically associates with the common gamma chain (gammac), a shared subunit of receptors for interleukin (IL) 2, 4, 7, 9, and 15. Patients deficient in either JAK3 or gammac presented with virtually identical forms of severe combined immunodeficiency (SCID), underscoring the importance of the JAK3-gammac interaction. Despite the key roles of JAK3 and gammac in lymphocytic development and function, the molecular basis of this interaction remains poorly understood. In this study, we have characterized the regions of JAK3 involved in gammac association. By developing a number of chimeric JAK3-JAK2 constructs, we show that the binding specificity to gammac can be conferred to JAK2 by transferring the N-terminal domains of JAK3. Moreover, those JAK3-JAK2 chimeras capable of binding gammac were also capable of reconstituting IL-2 signaling as measured by inducible phosphorylation of the chimeric JAK3-JAK2 protein, JAK1, the IL-2 receptor beta chain, and signal transducer and activator of transcription 5A. Subsequent deletion analyses of JAK3 have identified the N-terminal JH7-6 domains as a minimal region sufficient for gammac association. Furthermore, expression of the mutant containing only the JH7-6 domains effectively competed with full-length JAK3 for binding to gammac. We conclude that the JH7-6 domains of JAK3 are necessary and sufficient for gammac association. These studies offer clues toward a broader understanding of JAK-mediated cytokine signaling and may provide a target for the development of novel therapeutic modalities in immunologically mediated diseases.

3T3 Cells↗
PubMed1997

Isolation and characterization of two divergent infectious molecular clones of HIV type 1 longitudinally obtained from a seropositive patient by a progressive amplification procedure.

Isolation of infectious molecular clones has been valuable to our understanding of HIV-1-induced pathogenesis. Two infectious molecular clones of HIV-1 were isolated longitudinally from a seropositive subject at different stages of the disease, using a standard bacteriophage lambda vector and a novel progressive amplification procedure. We found the progressive amplification procedure was simpler and more specific than the conventional plaque hybridization assay. The two infectious HIV-1 clones had distinct cell tropism and cytopathic properties. The HIV-1 clone obtained at the asymptomatic stage of the disease was macrophage tropic and had a non-syncytium-inducing property. In contrast, the HIV-1 clone obtained at the stage of AIDS development was dual tropic for T cells and macrophages and induced syncytia. A detailed analysis of the restriction sites of the two clones showed 9 of 21 sites to be unique. These unique restriction sites were predominantly localized in the envelope region. Furthermore, the nucleotide sequence analysis of the entire gp120 region supported the results from the restriction analysis and showed that these two clones are closely related, and the differences are restricted to the variable domains. The difference in amino acid sequences in the V3 region may explain the observed differences in T cell tropism and syncytium-inducing properties. Availability of two distinct infectious molecular clones from the same patient at different stages of the disease may be useful in studies on the mechanism of HIV-1 pathogenesis.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Interactions of the amino-terminal noncollagenous (NC1) domain of type VII collagen with extracellular matrix components. A potential role in epidermal-dermal adherence in human skin.

Type VII collagen, the major component of anchoring fibrils, consists of a central collagenous triple-helical domain flanked by two noncollagenous domains, NC1 and NC2. The NC1 domain contains multiple submodules with homology to known adhesive molecules including fibronectin type III-like repeats and the A domain of von Willebrand factor. In this study, we produced the entire NC1 domain of human type VII collagen in the stably transfected human kidney 293 cell clones and purified large quantities of the recombinant NC1 protein from serum-free culture media. The recombinant NC1 formed interchain disulfide-bonded dimers and trimers and was N-linked glycosylated. Tunicamycin inhibited the cellular secretion of NC1, suggesting that N-linked glycosylation may play a role in NC1 secretion. The recombinant NC1 was indistinguishable from the authentic NC1 obtained from human amnions or WISH cells with respect to N-linked sugar content, electrophoretic mobility, rotary shadow imaging, and binding affinity to type IV collagen. Purified recombinant NC1, like authentic NC1, also bound specifically to fibronectin, collagen type I, and a laminin 5/6 complex. Both monomeric and trimeric forms of NC1 exhibited equal affinity for these extracellular matrix components, suggesting that the individual arms of NC1 can function independently. The multiple interactions of NC1 with other extracellular matrix components may support epidermal-dermal adhesion.

Amnion↗
PubMed1997

Modulation of type VII collagen (anchoring fibril) expression by retinoids in human skin cells.

We examined the effects of retinoids on the expression of type VII collagen, a major component of anchoring fibrils, in human keratinocytes and amnion cells (WISH). All-trans retinoic acid (RA) (5 X l0(-6) M) decreased the steady-state levels of type VII collagen mRNA by at least 80% after 18 h. The inhibition was evident within 6 h after the addition of RA, maximal at 18 h, and was dose-dependent. Reduction of type VII mRNA expression also occurred when cell cultures were incubated with retinol, retinal, and 13-cis RA. Retinoid-mediated inhibition of type VII collagen mRNA expression was observed in keratinocytes growing in either serum-free keratinocyte growth medium (KGM) or KGM supplemented with 1.4 mM Ca2+. Cycloheximide blocked RA-mediated inhibition of type VII collagen mRNA, demonstrating the need for de novo protein synthesis. The mRNA levels for fibronectin and glyceraldehyde phosphate dehydrogenase were not affected by the retinoids, suggesting selective inhibition on type VII collagen expression. In addition, the decrease in type VII collagen mRNA was accompanied by a parallel decrease in secretion of the 290 kDa, type VII collagen alpha chains.

Amnion↗
PubMed1997

Microcolinearity in sh2-homologous regions of the maize, rice, and sorghum genomes.

Large regions of genomic colinearity have been demonstrated among grass species by recombinational mapping, but the degree of chromosomal conservation at the sub-centimorgan level has not been extensively investigated. We cloned the rice and sorghum genes homologous to the sh2 locus of maize on bacterial artificial chromosomes (BACs), and observed that a homologue of the maize a1 gene was also present on each of these BACs. In sorghum, we found a direct duplication of a1 homologues separated by about 10 kb. In maize, sh2 and a1 are approximately 140 kb apart and transcribed in the same direction, with sh2 upstream of a1. In rice and sorghum, this arrangement is fully conserved. However, the sh2 and a1 homologues are separated by about 19 kb in both rice and sorghum. We found low-copy-number and repetitive DNAs between the sh2 and a1 homologues of sorghum and rice. The sh2 and a1 homologues cross-hybridized, but the repetitive DNA and most low-copy-number sequences between these genes did not. These results indicate that maize, sorghum, and rice have conserved gene order and composition in the sh2-a1 region, but have acquired extensive qualitative and quantitative differences in the sequences between these genes.

Base Sequence↗
PubMed1997

The thrombin receptor second cytoplasmic loop confers coupling to Gq-like G proteins in chimeric receptors. Additional evidence for a common transmembrane signaling and G protein coupling mechanism in G protein-coupled receptors.

Thrombin activates human platelets and other cells in part by cleaving an unusual G protein-coupled receptor. Thrombin cleavage of this receptor's amino-terminal exodomain unmasks a new amino terminus. This then binds intramolecularly to the body of the receptor to trigger transmembrane signaling and activation of Gi- and Gq-like G proteins. Toward identifying the domains responsible for thrombin receptor-G protein interactions, we examined the signaling properties of chimeric receptors in which thrombin receptor cytoplasmic sequences replaced the cognate sequences in the Gs-coupled beta2-adrenergic receptor (beta2AR) or the Gi-coupled dopamine D2 receptor (D2R). In Xenopus oocytes, a chimeric beta2AR bearing the thrombin receptor second cytoplasmic (C2) loop gained the ability to trigger intracellular Ca2+ release in response to adrenergic agonist, whereas a beta2AR bearing the cognate C2 loop from the D2R did not. Similarly, in COS-7 cells, a chimeric D2R bearing the thrombin receptor C2 loop gained the ability to trigger phosphoinositide hydrolysis in response to dopaminergic agonist, apparently by coupling to a Gq-like G protein. No detectable Gs coupling was seen. Thus, the thrombin receptor C2 loop was able to confer Gq-like coupling in several different receptor contexts. These observations suggest that the thrombin receptor C2 loop specifies Gq coupling by directly contacting Gq or by contributing to a structure required for Gq coupling. The ability of the thrombin receptor C2 loop to function in the context of the D2R and beta2AR strongly suggests that the transmembrane switching and G protein activation strategies used by the thrombin receptor must be very similar to those used by the D2R and beta2AR despite the thrombin receptor's strikingly different liganding mechanism.

Animals↗
PubMed1997

Interaction of transcription factors RFX1 and MIBP1 with the gamma motif of the negative regulatory element of the hepatitis B virus core promoter.

The negative regulatory element (NRE) of the hepatitis B virus (HBV) core promoter contains three subregions which act synergistically to suppress core promoter activity. One of these subregions, NRE gamma, is active in both HeLa cervical carcinoma cells and Huh7 hepatoma cells and was found to be bound by a protein factor present in both cell types. Here we show that the transcription factor RFX1 can bind to NRE gamma and transactivate the core promoter through this site. Mutations which abrogated the gene-suppressive activity of NRE gamma prevented RFX1 from binding to NRE gamma. In addition, RFX1 can bind simultaneously, most likely as a heterodimer, with the transcription factor MIBP1 to NRE gamma. In the absence of a cloned MIBP1 gene for further studies, we hypothesize that RFX1 acts with MIBP1 to negatively regulate the core promoter activity through the NRE gamma site. The ability of RFX1 to transactivate the core promoter raises the possibility that RFX1 may play a dual role in regulating HBV gene expression.

Animals↗
PubMed1997

Impaired induction of c-fos/c-jun genes and of transcriptional regulatory proteins binding distinct c-fos/c-jun promoter elements in activated human T cells during aging.

The activation of transcriptional factor c-Fos/c-Jun AP-1 is essential for normal T cell responsiveness and is often impaired in T cells during aging. In the present study, we investigated whether aberrancies in the regulation of c-fos/c-jun at the mRNA or protein level might underlie the age-associated impairments of AP-1 in human T cells. Whereas T cells from young subjects stimulated with cross-linked anti-CD3epsilon mAb OKT3 plus PMA or with the lectin PHA plus PMA demonstrated considerable increases in c-Fos protein expression, the expression of c-Fos but not c-Jun was markedly reduced in stimulated T cells from certain elderly subjects. In addition, RNase protection assays revealed that anti-CD3/PMA-stimulated T cells from a substantial proportion of elderly subjects exhibited decreased levels of c-fos and/or c-jun mRNA compared to T cells from young subjects. Using electrophoretic mobility shift assays, the levels of nuclear regulatory proteins recognizing the AP-1 consensus TRE motif, the proximal c-jun TRE-like promoter element, and the c-fos serum response element (SRE) were determined in resting and stimulated T cells. Although the stimulation of T cells from young subjects resulted in coordinated increases of nuclear protein complexes binding the AP-1 TRE, c-jun TRE, and c-fos SRE DNA sequence motifs, age-related reductions in the activation of AP-1 were accompanied by decreased levels of c-jun TRE and c-fos SRE binding complexes. Furthermore, the nuclear protein complexes binding the SRE motif induced in activated T cells of young and elderly subjects contained serum response factor and Elk-1 pointing toward age-related defects in the activation of transcriptional regulatory proteins distinct from c-jun/AP-1. These results suggest that underlying aberrancies in the induction of c-fos/c-jun as well as their nuclear regulatory proteins may contribute to the age-related impairments of AP-1 activation in human T cells.

Adult↗
PubMed1997

Effects of subchronic exposure of monochloramine in drinking water on male rats.

A subchronic rat study with paired-water control was conducted to resolve the question of whether monochloramine at 200 ppm in drinking water can cause reduced body weight gain and other changes observed in earlier investigations. Male Sprague-Dawley rats (93 +/- 5 g) were divided into three groups of 10 rats each: the treatment group was fed drinking water containing 200 ppm monochloramine, the control group was fed bicarbonate-buffered water ad libitum, and the paired-water control rats were given a daily volume of bicarbonate-buffered water equal to that consumed by the monochloramine treatment group. Compared to the control group, rats in the treatment group consumed an average of 42% less fluid and 16% less food over the 13-week treatment period and had 15-20% lower final body weight gain. Similar degrees of reduction in food consumption and body weight gain were observed in the paired-water rats. A decreased liver to body weight ratio occurred in the treatment and paired-water groups. Increased inorganic phosphate, albumin, total protein, and urea nitrogen were detected in sera from both the treatment group and the paired-water groups. The paired-water animals had lower levels of white blood cells and lymphocytes, while the paired-water and monochloramine-treated groups had reduced monocyte counts. Except for a slightly increased response to Con A observed in splenic lymphocytes of the monochloramine-treated rats (versus the paired-water), no significant changes were found in mitogen responsiveness to T cell, B cell, and B plus T cell mitogens or in splenic natural killer (NK) cell activities. There were no significant changes in serum levels of IgG, IgA, and IgM. The following biochemical parameters showed no significant variations among the three groups: serum thyroxin, liver phase I (PROD, EROD, and MROD) and phase II (UDPGT and GST) drug-metabolizing enzyme activities; serum and liver thiobarbituric acid-reactive substances (TBARS); bronchoalveolar lavage fluid protein and N-acetylgluosaminidase (NAGA) activity; and urinary ascorbic acid, protein, and NAGA activity. Histopathological examination revealed minimal to mild adaptive changes in the liver of the paired-water and monochloramine-treated rats and in the thyroid of the monochloramine-treated animals. No treatment-related cytological changes were found in red cells and bone marrow. The results indicate that the reduced body weight gain and the minor biochemical, hematological, immunological, and histopathological changes associated with subchronic exposure to 200 ppm monochloramine in drinking water (equivalent to an intake of 21.6 mg/kg/day) were largely related to the reduced water intake and food consumption and not caused by monochloramine.

Animals↗
PubMed1997

Palmitoyl-L-carnitine modifies the myocardial levels of high-energy phosphates and free fatty acids.

Long-chain acylcarnitines, such as palmitoyl-L-carnitine (PALCAR), are known to accumulate in the myocardium during ischemia. We examined whether exogenous PALCAR modifies the myocardial levels of high-energy phosphates (HEP) and free fatty acids (FFA) in the heart, and whether d-cis-diltiazem and l-cis-diltiazem, an optical isomer having less potent Ca2+ channel blocking action than d-cis-diltiazem, attenuate the PALCAR-induced myocardial changes. Rat hearts were perfused aerobically at a constant flow according to the Langendorff's technique, while being paced electrically. PALCAR (5 microM) decreased the tissue levels of adenosine triphosphate and creatine phosphate and increased the tissue level of adenosine monophosphate, and produced mechanical dysfunction. In addition, PALCAR (5 microM) increased markedly the tissue levels of FFA, especially those of arachidonic and palmitoleic acids, and the release of creatine kinase (CK) from the myocardium. These alterations in the myocardial levels of HEP and FFA induced by PALCAR were significantly attenuated by d-cis-diltiazem (15 microM) or l-cis-diltiazem (15 microM). Both drugs also attenuated the PALCAR-induced CK release. The present study demonstrates that PALCAR modifies the tissue levels of HEP and FFA in the heart and that both d-cis- and l-cis-diltiazem protect the myocardium against the PALCAR-induced changes through mechanisms other than Ca2+ channel blocking action.

Adenine Nucleotides↗
PubMed1997

Intubation of the ileocecal valve made easy.

Intubation of the ileocecal valve and terminal ileoscopy is useful clinically, especially in conjunction with diagnostic colonoscopy in patients with suspected or established inflammatory bowel disease or lower gastrointestinal tract bleeding. We describe a simple method of successful intubation of the ileocecal valve to facilitate ileoscopy. This method also confirms successful completion of colonoscopy, because the ileocecal valve is the most relevant endoscopic landmark of the cecum.

Endoscopy, Gastrointestinal↗
PubMed1997

High resolution magnetic resonance imaging of the calcaneus: age-related changes in trabecular structure and comparison with dual X-ray absorptiometry measurements.

A high-resolution magnetic resonance imaging (MRI) protocol, together with specialized image processing techniques, was applied to the quantitative measurement of age-related changes in calcaneal trabecular structure. The reproducibility of the technique was assessed and the annual rates of change for several trabecular structure parameters were measured. The MR-derived trabecular parameters were compared with calcaneal bone mineral density (BMD), measured by dual X-ray absorptiometry (DXA) in the same subjects. Sagittal MR images were acquired at 1.5 T in 23 healthy women (mean age: 49.3 +/- 16.6 [SD]), using a three-dimensional gradient echo sequence. Image analysis procedures included internal gray-scale calibration, bone and marrow segmentation, and run-length methods. Three trabecular structure parameters, apparent bone volume (ABV/TV), intercept thickness (I.Th), and intercept separation (I.Sp) were calculated from the MR images. The short- and long-term precision errors (mean %CV) of these measured parameters were in the ranges 1-2% and 3-6%, respectively. Linear regression of the trabecular structure parameters vs. age showed significant correlation: ABV/TV (r2 = 33.7%, P < 0.0037), I.Th (r2 = 26.6%, P < 0.0118), I.Sp (r2 = 28.9%, P < 0.0081). These trends with age were also expressed as annual rates of change: ABV/TV (-0.52%/year), I.Th (-0.33%/year), and I.Sp (0.59%/year). Linear regression analysis also showed significant correlation between the MR-derived trabecular structure parameters and calcaneal BMD values. Although a larger group of subjects is needed to better define the age-related changes in trabecular structure parameters and their relation to BMD, these preliminary results demonstrate that high-resolution MRI may potentially be useful for the quantitative assessment of trabecular structure.

Absorptiometry, Photon↗
PubMed1997

Lysophosphatidylcholine induces Ca2+-independent cellular injury attenuated by d-propranolol in rat cardiomyocytes.

In isolated rat cardiomyocytes, exogenous lysophosphatidylcholine (LPC) (15 microM) increased the intracellular Ca2+ concentration (Ca2+]i) from 72 +/- 5 to 3042 +/- 431 nM accompanied by cell injury as indicated by the hypercontracture of the cells and the increase in creatine phosphokinase (CPK) release. In order to understand whether the cell injury induced by LPC was a consequence of the elevation of [Ca2+]i, the effect of LPC was examined in the Ca2+-free solution containing EGTA. Under the Ca2+ -free conditions, LPC did not increase [Ca2+]i, whereas it still inflicted injury on the cells in terms of cell-shape change and CPK release to the same degree as that under the Ca2+-present condition. Addition of ryanodine (10 microM) failed to prevent the changes in cell-shape and CPK release induced by LPC under both Ca2+-free and Ca2+-present conditions. Preincubation of the myocytes with d-propranolol (50 microM) inhibited the LPC-induced changes in cell-shape and CPK release under both Ca2+ -free and Ca2+ -present conditions (p < 0.05). Our study provides clear evidence that the cellular injury induced by LPC could be independent of the increase in [Ca2+]i, and the Ca2+-independent cellular injury induced by LPC could be attenuated by d-propranolol, although the mechanism remains unknown.

Adrenergic beta-Antagonists↗
PubMed1997

Leonticins D-H, five triterpene saponins from Leontice kiangnanensis.

Five new triterpene saponins, leonticins D-H, were isolated from the tubers of Leontice kiangnanensis. Based on a combination of chemical degradation and spectroscopic analysis (negative ion FAB mass spectrometry and 2D NMR experiments), their structures were characterized as 3-O-alpha-L-arabinopyranosyl-caulophyllogenin 28 -O-alpha-L-rhamnopyranosyl-(1-->4)-beta-D-glucopyranosyl-(1-->6-beta-D- glucopyranoside, 3-O-[beta-D-glucopyranosyl -(1-->3)]-[beta-D-glucopyranosyl- (1-->2)]-alpha-L-arabinopyranosyl-oleanolic acid 28-O-alpha-L-rhamnopyranosyl- (1-->4)-beta-D-glucopyranosyl-(1-->6)-beta-D-glucopyranoside, 3-O-[beta-D-glucopyranosyl-(1-->3)]-[beta-D-glucopyranosyl-(1-->2)]-alph a-L -arabinopyranosyl-hederagenin 28-O-alpha-L-rhamnopyranosyl-(1-->4)-beta-D- glucopyranosyl-(1-->6)-beta-D-glucopyranoside, 3-O-beta-D-xylopyranosyl- (1-->3)-beta-D-galactopyranosyl-(1-->4)-beta-D- glucopyranosyl-(-->3)-alpha-L-arabinopyranosyl-echinocystic acid 28-O-alpha-L-rhamnopyranosyl-(1-->4)-beta-D- glucopyranosyl-(1-->6)-beta-D-glucopyranoside, respectively.

Carbohydrate Conformation↗
PubMed1997

New steroidal anti-inflammatory antedrugs: methyl 3,20-dioxo-9 alpha-fluoro-11 beta,17 alpha,21-trihydroxy-1,4-pregnadiene-16 alpha-carboxylate and methyl 21-acetyloxy-3,20-dioxo-11 beta, 17 alpha-dihydroxy-9 alpha-fluoro-1,4-pregnadiene-16 alpha-carboxylate.

Focused efforts have been made to increase local-to-systemic activity ratios of potent anti-inflammatory steroids for local and/or topical applications. The approach taken in the present investigation is based upon the concept of "antedrug," defined as a locally active compound that exerts its action at the application site but rapidly undergoes a predictable biotransformation to an inactive metabolite that is readily excreted upon entry into the systemic circulation. In continuing efforts to synthesize potent, anti-inflammatory steroids without systemic glucocorticoid activities, 9 alpha-fluoro-methyl 11 beta, 17 alpha, 21-trihydroxy-3,20-dioxo-pregna-1,4-diene-16 alpha-carboxylate (FP16CM) and its 21-acetate derivative (FP16CMAc) have been synthesized and screened. Novel antedrugs were evaluated for antiinflammatory activity in the acute croton oil-induced ear edema bioassay, adverse systemic effects in the 5-day croton oil model, receptor binding, and concomitant L-tyrosine-2-oxoglutarate aminotransferase (EC 2.6.1.5) (TAT) enzyme induction in HTC cells in culture. Following a single topical application in the croton oil-induced ear edema bioassay, treatment with all compounds resulted in dose-dependent inhibition of edema. From these dose-response profiles, the following ID50 values (nmol resulting in a 50% reduction of edema) were calculated: 817, 540, 266, and 67 for hydrocortisone (HC), prednisolone (P), FP16CM, and FP16CMAc, respectively. Calculated relative potencies, setting HC = 1.0, were P, 1.5; FP16CM, 3.1, and FP16CMAc, 12.2. Results of the 5-day rat croton oil ear edema bioassay indicated that, in contrast to the parent compound P, the novel steroidal antedrugs did not significantly alter body weight gain, thymus weights, or plasma corticosterone levels. Relative binding potencies for cytosolic HTC glucocorticoid receptors were 1.0, 20.1, 5.4, and 2.5 for HC, P, FP16CM, and FP16CMAc, respectively. As predicted by the antedrug concept, FP16CM and FP16CMAc were very weak agonists for induction of TAT in HTC cells. Collectively, results of these investigations suggest that modification of P, which included addition of the 9-fluoro and 16-methoxycarbonyl group alone or in conjunction with a 21-acetoxy moiety, increase topical anti-inflammatory activity without significant adverse systemic effects. These new antedrugs may be useful as anti-inflammatory steroids for local applications.

Administration, Topical↗
PubMed1997

Calculated prostate cancer volume: the optimal predictor of actual cancer volume and pathologic stage.

OBJECTIVES: A new clinical pretreatment quantity called the calculated prostate cancer volume has been defined. The correlation between the calculated parameter and the actual prostate cancer volume, and its ability to predict for pathologic Stage T3 disease in patients with clinically localized disease, is tested. METHODS: Prostate cancer volume measurements were obtained using a 3-dimensional computerized morphometric reconstruction technique on 104 whole-mounted radical prostatectomy specimens. The calculated prostate cancer volume was determined based on pretreatment clinical parameters (prostate-specific antigen [PSA], biopsy Gleason score, and prostate ultrasound volume). Linear regression was used to determine the Pearson correlation coefficients (r) between the PSA, the calculated prostate cancer volume, and the measured prostate cancer volume. Logistic regression multivariable analysis evaluating the predictive value of the pretreatment PSA, biopsy Gleason score, clinical stage, and calculated prostate cancer volume in predicting pathologic Stage T3 disease in patients with clinically organ-confined disease was performed. RESULTS: The calculated prostate cancer volume (r 0.71 to 0.96) was superior to PSA (r 0.12 to 0.67) in predicting the measured prostate cancer volume over a wide range (0.02 to 9.5 cm3) of cancer volumes. The calculated prostate cancer volume was the only significant predictor (P = 0.02) of pathologic Stage T3 disease in patients with clinical Stage T1 to T2 disease on multivariable analysis. CONCLUSIONS: The calculated volume of prostate cancer is superior to PSA in predicting both the pathologic prostate cancer volume and pathologic Stage T3 disease in patients with clinical Stage T1 and T2 disease. Therefore, it may be useful in determining the optimal candidates for radical prostatectomy.

Humans↗