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H B Carter

Publications and source records attributed to H B Carter.

At least 73 records · Page 4Linked to original sources
PubMed1993

PSA velocity for the diagnosis of early prostate cancer. A new concept.

An evaluation of longitudinal changes in PSA in men with and without prostate disease revealed that with age, the development of prostate disease is the most important factor influencing changes in PSA. Furthermore, the PSA changes with age are significantly different in men with and without prostate disease. The PSA velocity is greater in men with prostate cancer than in men with BPH and greater in men with prostate cancer and BPH than in men without any prostate disease. Thus, evaluation of PSA changes may help distinguish between men with prostate cancer and those without the disease. This idea will need to be confirmed prospectively. Finally, estimation of PSA doubling time from changes in PSA suggests that changes reflect prostatic growth. Therefore, PSA velocity could be of benefit in identifying men with prostate cancer that is destined to progress.

Adult↗
PubMed1992

Estimation of prostatic growth using serial prostate-specific antigen measurements in men with and without prostate disease.

Prostate growth curves were estimated from serial prostate-specific antigen (PSA) measurements on frozen sera in three groups of men: (a) 16 men with no prostatic disease by urological history and examination; (b) 20 men with a histological diagnosis of benign prostatic hyperplasia (BPH) who had undergone simple prostatectomy; and (c) 18 men with a histological diagnosis of prostate cancer. The median number of repeated PSA measurements over an 8- to 26-yr period prior to histological diagnosis or exclusion of prostate disease was eight and 11 for noncancer and cancer subjects, respectively. Predicted rates of change in PSA (PSA velocity) were linear and curvilinear for control and BPH subjects, respectively. Subjects with cancer demonstrated both a linear and an exponential phase of PSA velocity. Based on time to double PSA, we estimated the epithelial doubling time for men without prostate disease to range from 54 +/- 13 yr at age 40 to 84 +/- 13 yr at age 70. For men with BPH, doubling times ranged from 2 +/- 13 yr at age 40 to 17 +/- 5 yr at age 85. Subjects with local/regional and advanced/metastatic cancer had similar PSA doubling times of 2.4 +/- 0.6 yr and 1.8 +/- 0.2 yr, respectively. These data are consistent with what is known about prostatic growth with age in men without prostate disease and BPH, and the kinetics of prostate cancer growth. Estimates of prostatic growth rate from changes in PSA may be useful clinically in management of men with prostate disease.

Aged↗
PubMed1992

Correlation of prostate cancer nuclear deoxyribonucleic acid, size, shape and Gleason grade with pathological stage at radical prostatectomy.

Using image cytometry and a video planimetry unit, various deoxyribonucleic acid (DNA) measurements, nuclear size and shape factors, and Gleason grade were correlated with capsular penetration, seminal vesicle invasion and lymph node involvement in 113 radical prostatectomy specimens. Percentage of nondiploid cells was the best DNA measurement and standard deviation of nuclear area was the best size measurement correlating with capsular penetration. However, stepwise regression analysis demonstrated that Gleason grade was the only independent predictor of capsular penetration. The only parameter that independently predicted seminal vesicle invasion in a stepwise regression analysis was percentage of tetraploid cells. The mode of optical density was the best DNA measurement for predicting lymph node involvement, although stepwise regression analysis found that Gleason grade was the only independent predictor. DNA ploidy was not as predictive of pathological stage. In summary, DNA measurements and nuclear morphometry performed on smears offered relatively little additional prediction of pathological stage over that of Gleason grade.

Adenocarcinoma↗
PubMed1992

The biology of prostate cancer: new and future directions in predicting tumor behavior.

Because the present ability to treat and cure patients with prostate cancer is limited to those patients with pathologically organ-confined disease, it has become increasingly important to diagnose this disease at an early stage when cure is most likely. Recent advances in imaging may allow the urologist and pathologist to make the diagnosis of prostate cancer much earlier in the natural course of the disease. It therefore becomes imperative to have methods available to predict which patients have a high probability of progressing so that treatment can be assigned logically and appropriately. Our current methods of prognosis determination (stage and grade) do not allow accurate assessment of tumor behavior in the majority of individual patients with prostate cancer. Therefore, more accurate quantification of nuclear and cellular changes that take place as a tumor progresses to take on the aggressive (metastatic) phenotype are urgently needed. Experimental techniques have proven useful in answering these questions in animal models and now seem ready for large-scale testing in clinical studies.

Biomarkers, Tumor↗
PubMed1991

Can stage A1 tumor extent be predicted by transurethral resection tumor volume, per cent or grade? A study of 64 stage A1 radical prostatectomies with comparison to prostates removed for stages A2 and B disease.

We studied 64 totally embedded radical prostatectomy specimens of stage A1 prostate cancer. The transurethral resection specimens were studied and compared to previously studied stages A2 and B cancer in which tumor volumes also were calculated. At radical prostatectomy 6% of the specimens had no residual cancer, 74% had minimal cancer and 20% had substantial cancer. Although most stages A2 and B tumors were larger, there was overlap among all stages. Transurethral resection tumor volume, per cent and grade were not statistically correlated with either radical prostatectomy residual tumor volume, or whether tumor was classified as minimal or substantial. Gleason sum 2 to 4 versus 5 to 7 tumor on transurethral resection showed no difference in predicting radical prostatectomy residual tumor or minimal versus substantial tumor status. Because 20% of all stage A1 cancers have substantial tumor at radical prostatectomy unpredictable by transurethral resection, radical prostatectomy remains an option for young men with stage A1 prostate cancer.

Aged↗
PubMed1991

Nonpalpable prostate cancer: detection with MR imaging.

The pathologic specimens and magnetic resonance (MR) images of 53 patients with clinically palpable prostate cancer confined to one lobe were studied to evaluate the ability of MR imaging to depict clinically nonpalpable prostate cancer. All patients had undergone imaging with a 1.5-T imager with T1- and T2-weighted sequences in both axial and sagittal planes before undergoing radical retropubic prostatectomy. At pathologic examination, only the palpable tumor was present in 30 of the 53 patients (57%), and 33 unsuspected tumors were present in an area distinct from the palpable tumor in 23 of the patients (43%). MR imaging successfully depicted 51 palpable tumors for a sensitivity of 96% and 19 of the 33 unsuspected tumors for a sensitivity of 58%. The sensitivity of MR imaging in the detection of nonpalpable, posteriorly located tumors was greater than for those located anteriorly (85% vs 15%). MR imaging was false-positive for nonpalpable tumor in 17 of 30 patients for a specificity of 43%. On the basis of these data, MR imaging has greater sensitivity in the depiction of posteriorly located cancer and is limited by a high false-positive rate in the depiction of nonpalpable tumors.

False Positive Reactions↗
PubMed1990

The prostate: an increasing medical problem.

The prostate gland is the major site of medical problems in the U.S. male. Surgery for benign prostatic hyperplasia is the most common surgical procedure performed in males, and the total cost for this surgery exceeds 1 billion dollars per year. The incidence of and mortality from prostate cancer are increasing yearly. Prostate cancer now exceeds lung cancer as the most commonly diagnosed cancer in males and is the second leading cause of male cancer deaths. Of all tumors, the prevalence of prostate cancer increases the most rapidly with age. A shift in age distribution favoring an older population will lead to an increase in the number of patients diagnosed with prostate cancer in the United States. It is estimated that by the year 2000 there will be a 37% increase in prostate cancer deaths per year and a 90% increase in prostate cancer cases per year. Although the factors responsible for the development and progression of prostate cancer to a clinically manifest form are not known, there is evidence that environmental factors may play a role. It will be important for the future to focus on the etiological factors that may lead to a decrease in the prevalence of prostatic tumors.

Adult↗
PubMed1990

Epidemiologic evidence regarding predisposing factors to prostate cancer.

In 1990, prostate cancer will be the most common cancer diagnosed in U.S. men and will be the second-leading cause of cancer mortality in these men. One in ten U.S. men will develop prostate cancer in his lifetime. Twenty thousand prostate cancer cases occur each year in men under the age of 65. The average number of years of life lost for a man dying of prostate cancer is nine. In addition, both incidence and mortality of prostate cancer are increasing. A review of the literature regarding prostate cancer is timely in light of recent studies examining possible predisposing factors for this disease. In this review, a framework for understanding genetic and environmental factors which may predispose to prostate cancer is presented. The identification of factors which predispose to clinical prostate cancer offers the possibility of lowering the incidence and mortality of prostate cancer in the United States. Epidemiologic evidence regarding possible predisposing factors to prostate cancer is reviewed.

Causality↗
PubMed1990

Effect of ambient temperature and running wheel activity on the outcome of pregnancy in CD-1 mice.

The effect of ambient temperature and running activity on fetal outcome was studied in CD-1 mice. Pregnant mice were allowed to be active in a running wheel at various ambient temperatures (26, 30, 32, 34, or 36 degrees C) for 100 min a day. The dams were killed near term, and various maternal and fetal measures made. Mean deep body temperature (measured using radio-telethermometers implanted in the abdomen) of pregnant dams was raised to 39.5 degrees C while running at an ambient temperature of 36 degrees C. Bred mice, pregnant or not, continued to increase their running activity, but pregnant mice exercised less from mid-pregnancy on. Running up to 1 km/hr had no effect on maternal weight gain, number of implantations, number of live fetuses, fetal body weight, and fetal relative brain weight. However, increasing ambient temperature was effective in decreasing maternal weight gain and fetal body weight and increasing fetal relative brain weight. Even though body temperature can be increased significantly by increasing either running rate or ambient temperature, the body temperature increase caused by running appears to have no significant influence on the outcome of pregnancy. At levels in this study, body temperature per se does not appear to be the variable on which to predict fetal effects. This is because only body temperature raised by higher ambient temperature, and not body temperature raised by increased running, was shown to effect a fetal change.

Animals↗
PubMed1990

The relationship of prostate specific antigen levels and residual tumor volume in stage A prostate cancer.

Preoperative serum prostate specific antigen correlates well with morphometrically determined prostate tumor volume in prostatectomy specimens. However, since prostate specific antigen is produced by hyperplastic as well as malignant prostatic epithelium, the contribution of hyperplastic epithelium (benign prostatic hyperplasia) to serum prostate specific antigen interferes with the ability of serum prostate specific antigen to predict tumor volume in individual patients. We wondered if the removal of benign prostatic hyperplasia tissue would increase the correlation between prostate specific antigen and tumor volume, and, thus, make prostate specific antigen a more accurate predictor of residual cancer volume after transurethral resection of the prostate. A total of 67 patients with clinical stage A cancer underwent radical retropubic prostatectomy (22, or 33%, with stage A1 and 45, or 67%, with stage A2 disease), and had pre-radical prostatectomy measurement of serum prostate specific antigen and morphometric determination of residual cancer volume in the radical prostatectomy specimen. The correlation between serum prostate specific antigen and residual cancer volume for all 67 patients was 0.66, and for stages A1 and A2 disease it was 0.64 and 0.70, respectively. All stage A1 cancer patients with a serum prostate specific antigen value of 1 ng./ml. or less had residual tumor volumes of less than 0.5 cc and all stage A cancer patients with a serum prostate specific antigen value of more than 10 ng./ml. had residual tumor volumes of greater than 0.5 cc. Of the patients 51% had levels of 1 to 10 ng./ml. and serum prostate specific antigen was not useful to predict residual tumor volume in this group. Serum prostate specific antigen measurements may be helpful in stage A1 cancer patients with levels of 1 ng./ml. or less, or greater than 10 ng./ml. in choosing the most appropriate therapy.

Antigens, Neoplasm↗
PubMed1990

Clinical evidence for and implications of the multistep development of prostate cancer.

Based upon a large body of experimental and clinical data, it is evident that multiple malignant events are necessary for a normal cell to give rise to a fully malignant cancer cell. A critical issue with regard to human prostatic carcinogenesis is the clinical significance of the large number of cancers that are present histologically in the elderly male prostate gland. A possibility is that these histological prostate cancers already have undergone all of the malignant events necessary to produce clinically manifest cancer and, thus, only further tumor growth is required to produce a clinical tumor. Alternatively, these histological cancers may have undergone some but not all of the events necessary to produce clinical disease and, therefore, despite host longevity the cancer will remain clinically silent as long as no further malignant changes occur. This issue has importance clinically with respect to the diagnosis, therapy and possible prevention of prostatic cancer. Clinical observations and the mathematical relationship between prostate cancer prevalence and host age (time) support the fact that, in addition to growth, histological prostate cancer requires further malignant events to produce clinical disease. A better understanding of the events involved in prostate cancer development will be necessary to have a greater impact on this disease in the future.

Adult↗
PubMed1990

Prostate specific antigen in the staging of localized prostate cancer: influence of tumor differentiation, tumor volume and benign hyperplasia.

To evaluate the usefulness of serum prostate specific antigen in the preoperative staging of prostate cancer we examined tumor volume and differentiation, as well as benign prostatic hyperplasia volume to determine their influence on serum antigen levels. Serum prostate specific antigen was measured in 350 men with clinically localized prostate cancer and preoperatively in 72 men with documented benign prostatic hyperplasia. Although the mean antigen levels increased with advancing pathological stage, the usefulness of prostate specific antigen to predict pathological stage for an individual patient was limited: 1 of 102 men (0.9%) with prostate specific antigen levels of less than 2.8 ng./ml. had positive lymph nodes and 5 of 5 men with levels of greater than 100 ng./ml. had either seminal vesicle or lymph node involvement. However, for the majority of men (greater than 70%) with prostate specific antigen values between these 2 extremes the antigen levels did not accurately predict pathological stage. Because serum prostate specific antigen levels correlated with morphometrically determined tumor volume (r equals 0.535, p less than 0.01) they should, in fact, be predictive of pathological stage. However, most men with prostate cancer also have varying degrees of benign prostatic hyperplasia tissue in the gland producing prostate specific antigen. We have found that serum prostate specific antigen does not correlate with the volume of benign hyperplasia within the gland (r equals 0.21, p greater than 0.05). In addition, immunohistochemical studies have suggested that the lack of correlation between pathological stage and serum prostate specific antigen might be explained by a decrease in the production of antigen with increasing histological grade. Our findings of a negative correlation (r equals -0.37, p less than 0.01) between serum prostate specific antigen levels and Gleason score adjusted for tumor volume confirmed this suggestion. Consequently, serum prostate specific antigen levels do not reflect tumor burden and pathological stage accurately in individual patients for 2 reasons: 1) the unpredictable contribution from the benign prostatic hyperplasia component of the gland and 2) the decreasing production of prostate specific antigen by higher grade lesions as tumor volume increases.

Adenocarcinoma↗
PubMed1990

Comparison of DNA ploidy and nuclear size, shape and chromatin irregularity in tissue sections and smears of prostatic carcinoma.

Image analysis measurements of nuclear size, shape, texture and DNA ploidy were compared in smears versus the corresponding 4-microns tissue sections, both prepared from radical prostatectomy specimens obtained from resections for prostatic cancer. Thirty-nine cases (78%) showed concordant DNA histograms between the smear and the tissue section. In six cases (12%), both preparations were nondiploid, but a tetraploid population was also present in one, but not both, of the preparations. In five cases (10%), there was a major discordance between the smear and the tissue section, with one preparation diploid and the other nondiploid. One source of discrepancy between the smear and tissue histograms was the overlapping of larger nuclei in tissue sections, which often precluded the analysis of the most atypical cells. Some tissue histograms were difficult to interpret due to wide coefficients of variation, irregular peaks and some shift from 2n in the diploid peaks. The best morphometric correlation (0.78) between the smears and the tissue sections was for the modal nuclear shape. Nuclear size and texture measurements showed poorer correlations. These findings suggest that cytologic preparations of prostatic carcinoma should be preferred for image analysis.

Cell Nucleus↗
PubMed1989

Evaluation of transrectal ultrasound in the early detection of prostate cancer.

To determine the ability of transrectal ultrasound to detect early localized prostate cancer, unsuspected (nonpalpable) cancer in the contralateral lobe of patients undergoing radical prostatectomy for clinically localized disease was evaluated. A total of 59 patients with palpable prostate cancer clinically confined to 1 lobe underwent transrectal ultrasound before radical prostatectomy and step-sectioning of the radical prostatectomy specimen. Transrectal ultrasound was performed with 5 or 7 MHz. real-time transrectal units. Pathological findings in these 59 cases revealed no tumor in the contralateral lobe in 34 (58%) and the presence of unsuspected tumor in 25 (42%). Transrectal ultrasound detected 13 of 25 unsuspected cancers for a sensitivity of 52%. Of 34 patients with no contralateral lobe lesion transrectal ultrasound was correct in 23 for a specificity of 68%. The positive and negative predictive values for transrectal ultrasound in this study group were 54 and 66%, respectively. There was no significant difference in the pathological size of the clinically suspected and clinically unsuspected cancers as measured by average largest dimension, and transrectal ultrasound sensitivity did not correlate with the size of the cancer. Based on careful sonopathological analysis, transrectal ultrasound may not be a good method to detect clinically unsuspected prostate cancer and the false positive rate would appear to be high.

Humans↗
PubMed1989

Prediction of metastatic potential in an animal model of prostate cancer: flow cytometric quantification of cell surface charge.

The natural history of clinically localized prostate cancer in individual patients is difficult to predict using currently available techniques. The majority of these patients will undergo treatment without knowledge of whether the tumor would have progressed during their lifetime. Because more patients are being diagnosed yearly with early stage prostate cancers it is becoming increasingly important to delineate factors that will clarify which patients have tumors with invasive potential. Using the Dunning R-3327 rat prostate animal tumor model we have previously shown that an increase in cell surface charge, as measured by individual cell electrophoresis, is associated with an increase in metastatic ability. This electrophoretic technique is limited by the small number of cells that can be analyzed during each assay. Therefore, we adapted a flow cytometric method for measurement of cell surface change, utilizing a large molecule (cationized ferritin) that binds quantitatively to the negative charges at the cell surface. With a fluorescent tag attached to the ferritin molecule, flow cytometric quantification of surface charge was possible, and this method was successful in identifying tumors with high metastatic ability in the Dunning prostate tumor model.

Animals↗
PubMed1988

Cell surface charge in predicting metastatic potential of aspirated cells from the Dunning rat prostatic adenocarcinoma model.

The transplantable Dunning R-3327 rat prostatic adenocarcinoma model has provided a series of tumor variants with broad ranges of metastatic potential. We tested whether cell surface charge might be related to metastatic potential by measuring the electrophoretic mobility of live tumor cells obtained by needle aspiration. Cells were aspirated from tumors with low metastatic potential (following subcutaneous inoculation of 10(6) tumor cells the H, G and AT-1 variants had less than 5% metastases; AT-2 had 5-20%) and were compared to the electrophoretic mobility of cells aspirated from highly metastatic tumors (MAT-LyLu, MAT-Lu, AT-3 had greater than 90% metastases). Electrophoretic mobility expressed in mu/sec/volt/cm. was measured on 100 cells from each tumor subline, and the cell surface charge expressed as a zeta potential was calculated from electrophoretic mobility using the Helmholtz-Smoluchowski equation. The average zeta potential (+/- S.E.M.) for the four sublines with low metastatic potential was (-17.4 +/- 0.4 mV) compared to the three sublines with high metastatic potential (-26.5 +/- 0.7 mV), and the differences were significant (p less than .01) using the Mann-Whitney Wilcoxon test. Using a zeta potential of -20.5 mV as the cutoff between high and low metastatic potential, the sensitivity and specificity of zeta potential in predicting metastatic potential in 140 determinations on seven tumor lines were 92% and 82.5%, respectively. The predictive value of a positive test (value greater than -20.5 mV) was 80% and the predictive value of a negative test (value less than -20.5 mV) was 93%. The results support a difference in the cell surface charge between these metastatic and nonmetastatic tumors with increasing negativity at the cell surface correlating with increased metastatic potential, but not with tumor growth rates.

Adenocarcinoma↗