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PubMed1983

Presence of adherent cytotoxic cells and non-adherent natural killer cells in progressive and regressive Marek's disease tumors.

Marek's disease virus-induced progressive tumors and Marek's disease transplantable local regressive tumors were dispersed by treatment with collagenase and cells were examined in vitro for cytotoxic effector functions against target cells of tumor lines. Both types of tumors had adherent and non-adherent cytotoxic cells. The cytotoxicity of adherent cells was detected in an 18-hour but not in a 4-hour 51Cr-release assay. The adherent effector cells from progressive tumors were inactivated by pretreatment with carbonyl iron and carrageenan whereas the adherent effector cells from the regressive tumors were refractory to these treatments. In the progressive tumors, the 18-hour cytotoxic activity of cells of tumors and of spleens of tumor-bearing chickens was compared; the activity was higher in the tumor than in spleen. The nonadherent cell cytotoxicity detectable in a 4-hour 51Cr-release assay was associated with anti thymocyte serum-resistant natural killer cells. The incidence and levels of natural killer cell reactivity were greater in the regressive tumors than in the progressive tumors. In the regressive tumors, the natural cytotoxicity levels were higher in the tumor than in the spleen of tumor-bearing chickens. The differences in characteristics of adherent cytotoxic cells in virus-induced progressive tumors and transplantable regressive tumors and elevated levels of NK cells in regressive but not in progressive tumors may indicate a role for intratumoral immunity in tumor regression.

Animals↗

PubMed1989

The progression rate of late radiation effects in normal tissue and its impact on dose-response relationships.

The progression of late skin telangiectasia after radiotherapy has been studied prospectively in patients for 1, 2 and 5 fractions per week and various dose levels. The degree of telangiectasia was scored on an arbitrary scale. Skin telangiectasia was found to be a continuously progressing endpoint both in the individual patient and in terms of the number of patients who achieved a certain degree of damage. The rate of progression was dose-dependent. Dose-response analysis were performed at 3, 5 and 9 years follow-up for various endpoints: telangiectasia score greater than or equal to 1, score greater than or equal to 2 and score greater than or equal to 3. Iso-effective doses (ED50S) for score greater than or equal to 1 at 3 years, score greater than or equal to 2 at 5 years and score greater than or equal to 3 at 9 years were very similar. In an iso-effect analysis it is therefore worthwhile and time-saving to include the minimal detectable damage in the endpoint (e.g. using score greater than or equal to 1), even if this mild damage is of no clinical significance, and the dose in the endpoint (e.g. using score greater than or equal to 1), even if this mild damage is of no clinical significance, and the dose response become somewhat less steep than for more severe damage. The fact that the progression rate is dose-dependent has impact on dose-response analysis. Dose-response analysis for score greater than or equal to 3 at various follow-up times showed a very flat curve at 3 years compared to 5 and 9 years. The steepness of the dose-response curves was similar at 5 and 9 years. A minimum follow-up of 5 years is therefore necessary for reliable estimation of the late complication rates in a comparison of two dosage schedules using this endpoint. The implication of the continuous progression of telangiectasia is that the dose-response curves are shifted to the left with follow-up. The ED50 is dramatically reduced between 3 and 5 years. The ED50 is also significantly reduced between 5 and 9 years' follow-up, in spite of no change in the steepness of the dose-response curve during this period. Consequently, the time of response is the most fundamental parameter in any iso-effect analysis with progressive endpoints and the late complication rates always have to be specified at a fixed time of follow-up.

Dose-Response Relationship, Radiation↗

PubMed1995

Progression of cancer.

Carcinoma constitution originates in the hetero duplication mitoses which divide non-maturable stem cells into two different types of daughter cells: maturable and non-maturable cancerous stem cells. Throughout the progression of such mitoses the organoid continuity of the cancer depends only on the non-maturable daughter stem cells, not on the maturable ones. This type of cancer can be considered non-progressive or to be in the incubation stage, as it only enables cancer tissue to preserve its organoid continuity without allowing progressive growth. However, when an occasional mitotic phase of the hetero-duplication mitotic progression undergoes genuine cell-phase duplication mitosis, this non-progressive or incubation stage of cancer is converted to a progressive type of cancer. This conversion is dependent on the reappearance of the complete mitotic condition of the mitotic maturation promoting system (MMPS) containing an abnormal supplement. Thus, a thorough investigation of the abnormal supplement and the reappearance of the complete mitotical condition is an essential part of research efforts to prevent and eradicate cancer.

Cell Division↗

PubMed1993

Various intensities of leisure time physical activity in patients with coronary artery disease: effects on cardiorespiratory fitness and progression of coronary atherosclerotic lesions.

OBJECTIVES: This study was designed to define the effect of different levels of leisure time physical activity on cardiorespiratory fitness and progression of coronary atherosclerotic lesions in unselected patients with coronary artery disease. BACKGROUND: It has been shown in various studies that regression of coronary atherosclerotic lesions can be achieved by means of lipid-lowering drugs, reduction of fat consumption and physical exercise. METHODS: Patients were prospectively randomized either to an intervention group (n = 29) participating in regular physical exercise or to a control group (n = 33) receiving usual care. Energy expenditure in leisure time physical activity was estimated from standardized questionnaires and from participation in group exercise sessions. After 12 months of participation, repeat coronary angiography was performed; coronary lesions were measured by digital image processing. RESULTS: After 1 year, patients in the intervention group achieved an increase in oxygen uptake at a ventilatory threshold of 7% (p < 0.001) and peak exercise of 14% (p < 0.05), whereas a significant decrease was observed in patients in the control group. To achieve significant improvement in cardiorespiratory fitness, approximately 1,400 kcal/week had to be expended in the form of leisure time physical activity (p < 0.001). The mean energy expended in such activity was 1,876 +/- 163 kcal/week in the intervention group and 1,187 +/- 97 kcal/week in the control group (p < 0.001). In the intervention group, regression of coronary artery disease was noted in 8 patients (28%), progression of disease in 3 (10%) and no change in coronary morphology in 18 (62%). In contrast, coronary artery disease progressed at a significantly faster rate in patients in the control group (progression in 45%, no change in 49% and regression in 6%) (p < 0.001 vs. intervention). When the two groups were combined, the lowest level of leisure time physical activity was noted in patients with progression of disease (1,022 +/- 142 kcal/week) as opposed to patients with no change (1,533 +/- 122 kcal/week) or regression of disease (2,204 +/- 237 kcal/week) (p < 0.005). CONCLUSIONS: Measurable improvement in cardiorespiratory fitness requires approximately 1,400 kcal/week of leisure time physical activity; higher work loads are necessary to halt progression of coronary atherosclerotic lesions (1,533 +/- 122 kcal/week), whereas regression of coronary lesions is observed only in patients expending an average of 2,200 kcal/week in leisure time physical activity, amounting to approximately 5 to 6 h/week of regular physical exercise.

Coronary Angiography↗

PubMed1992

Regulation of breast cancer cell cycle progression by growth factors, steroids and steroid antagonists.

The control of human breast cancer cell proliferation in vitro is known to involve complex interactions between steroid hormones, peptide hormones and growth factors. Little is known, however, of the mechanisms by which these factors, alone or in combination, control cell cycle progression and the expression of specific genes involved in cell cycle control. A pre-requisite for such studies is a cellular system in which non-proliferating or slowly proliferating cells can be maintained in a defined environment and stimulated to progress through the cell cycle by addition of hormones and growth factors. Such a system has been developed for T-47D human breast cancer cells: quiescent or slowly proliferating cells maintained in a serum-free medium can be stimulated to increase their rate of cell cycle progression upon a single addition of insulin, IGF-I, EGF, TGF alpha or bFGF. Oestradiol alone was ineffective but caused a significant increase in % S phase cells when added in the presence of insulin. Progestins, in the presence of absence of insulin, had a biphasic effect with an initial increase in cell cycle progression followed by cell cycle arrest. Both antioestrogens and the antiprogestin, RU 486, in the absence of oestrogen or progestin, were potent inhibitors of insulin-induced proliferation. Increases in cell cycle progression were invariably accompanied by acute increases in c-fos and c-myc mRNA levels. Induction of c-myc by oestrogen and progestin was inhibited by antioestrogens and RU 486, respectively. These data illustrate that the culture of breast cancer cells in a serum-free, chemically defined environment provides an excellent model in which to define the role of individual factors involved in breast cancer growth control. The biological data derived from this system provide a basis for identifying and characterizing genes involved in the control of cell cycle progression in human breast cancer.

Breast Neoplasms↗

PubMed2006

The effect of glucose on the progression of the nuclear maturation of pig oocytes.

The progression of the nuclear maturation of oocytes is a useful marker for the estimation of the subsequent developmental competence of oocytes. In this study, we examined the effect of energy substrates in an in vitro maturation medium on the progression of the nuclear maturation of oocytes. In experiment 1, the supplementation of the maturation medium with 0, 5 and 10 mM of glucose lead to increase in the total cell number of the blastocysts. In experiments 2 and 3, the maturation phase was divided into two stages (germinal vesicle (GV) stage: 0-20 h and nuclear maturation stage: 20-44 h), and the effects of glucose or pyruvate added at each stage on the kinetics of nuclear maturation were examined. The addition of glucose at the nuclear maturation stage rather than at the GV stage of maturation effected greater acceleration in the progression of nuclear maturation. However, the addition of pyruvate at both stages had the same effect on the progression of nuclear maturation was the same. In addition, when glucose was added to the medium containing pyruvate, an additive effect on the progression of nuclear maturation was observed (experiment 4). In experiment 5, the inhibitors of glucose-6-phosphate dehydrogenase (G6PD), dehydroepiandrosterone (DHEA) and 6-aminonicotinamide (6-AN) decreased the rate of the final maturation of oocytes and reduced the difference between the rates of the final maturation of oocytes cultured with glucose and those cultured with pyruvate. In the experiment 6, when the activator of G6PD, brilliant cresyle blue (BCB), was added to the maturation medium, the progression of nuclear maturation was significantly accelerated. The results of this study suggested that in addition to the role of an energy substrate, glucose or its metabolites play a role in nuclear maturation. This role was more pronounced at the second stage of maturation (transition from GV breakdown (GVBD) to M2), probably due to the metabolism of glucose via the pentose phosphate pathway (PPP) rather than the glycolysis pathway.

6-Aminonicotinamide↗

PubMed2004

Progressive behavioural changes in the spatial open-field in the quinolinic acid rat model of Huntington's disease.

Huntington's disease (HD) is a progressive neurodegenerative disorder, characterized by severe degeneration of basal ganglia, motor abnormalities, impaired cognitive functions and emotional disturbances. Intrastriatal injection of the excitotoxin quinolinic acid (QA), an N-methyl-D-aspartate receptor agonist, appears to reproduce in rats some of the clinical features of human HD, included motor and behavioural deficits. Aim of this study was to assess whether the behavioural alterations described in the QA rat model of HD progressed over time. We analysed the effects of bilateral striatal injection of QA (300 nmol/1 microl) to adult rats in the spatial open-field test, a nonaversive task in which exploratory activity and responses to both spatial rearrangement of familiar objects and object novelty are measured. Rats were tested 2 weeks, 2 and 6 months after the QA lesion. Lesioned rats showed progressive alterations in performance in this task. Whereas sham and QA rats did not markedly differ 2 weeks post-lesion, lesioned rats were significantly more active than controls 2 and 6 months after surgery. Specifically, frequency and duration of rearing and wall rearing increased progressively over time, while grooming was enhanced at 2 months post-lesion only. Spatial and object novelty discrimination was not affected. These results show that a single injection of QA excitotoxin can induce behavioural changes that progress over time. The main implication of these findings is that, besides genetic mice models of HD, QA-lesioned rats may represent a suitable mean to test the ability of new drugs to slow down disease progression.

Animals↗

PubMed2005

Docetaxel and cyclooxygenase-2 inhibition with celecoxib for advanced non-small cell lung cancer progressing after platinum-based chemotherapy: a multicenter phase II trial.

PURPOSE: To assess the overall and progression-free survival, response rate, and toxicity of combined docetaxel and celecoxib in the treatment of patients with non-small cell lung cancer progressing after initial chemotherapy for advanced disease. PATIENTS AND METHODS: Patients with non-small cell lung cancer and either measurable or evaluable disease experiencing progression after one or more platinum-based chemotherapy regimens given for advanced or metastatic disease, ECOG performance status 0-2, and adequate hematologic and biochemistry parameters were eligible for study inclusion; exclusion criteria included symptomatic brain metastases and full dose anti-coagulation. Therapy consisted of docetaxel 75 mg/m(2) every 21 days for a maximum of six cycles and celecoxib 400 mg orally twice daily commencing 7 days prior to docetaxel and continuing until disease progression. RESULTS: A total of 41 patients were enrolled of whom 39 were deemed eligible and received at least one course of docetaxel. The mean age of enrolled patients was 60.5 years (range, 44-77); 67% were men and 79% white. All but one patient had an Eastern Clinical Oncology Group (ECOG) performance status of 0 or 1. Most (72%) had been treated with a prior taxane. Overall survival was 11.3 months (95% confidence interval [CI]: 7.9, 15.7) and progression-free survival 19.6 weeks (95% CI: 13.5, 25.0). A response rate of 10.2% (95% CI: 3%, 24%) for all eligible and treated patients was found. Grade 3 or 4 neutropenia occurred in 10/39 patients (25.6%); one death due to neutropenic sepsis occurred. No grade 3 or 4 renal or hepatic toxicities were documented. CONCLUSION: Treatment with combination celecoxib and docetaxel is a safe regimen with a toxicity profile similar to that of docetaxel alone. Survival data are encouraging compared to historical controls and may prolong time to disease progression compared with single-agent docetaxel.

Administration, Oral↗

PubMed2006

Calpastatin overexpression prevents progression of S-1,2-dichlorovinyl-l-cysteine (DCVC)-initiated acute renal injury and renal failure (ARF) in diabetes.

Previously we have shown that 90% of streptozotocin (STZ)-induced type-1 diabetic (DB) mice survive from acute renal failure (ARF) and death induced by a normally LD(90) dose (75 mg/kg, i.p.) of the nephrotoxicant S-1,2-dichlorovinyl-l-cysteine (DCVC). This remarkable protection is due to a combination of slower progression of DCVC-initiated renal injury and increased compensatory nephrogenic tissue repair in the DB kidneys. BRDU immunohistochemistry revealed that the DB condition led to 4-fold higher number of proximal tubular cells (PTC) entering S-phase of cell cycle. In the present study, we tested the hypothesis that DB-induced augmentation of PTC into S-phase is accompanied by overexpression of the calpain-inhibitor calpastatin, which endogenously prevents the progression of DCVC-initiated renal injury mediated by the calpain escaping out of damaged PTCs. Immunohistochemical detection of renal calpain and its activity in the urine, over a time course after treatment with the LD(90) dose of DCVC, indicated progressive increase in leakage of calpain into the extracellular spaces of the injured PTCs of the non-diabetic (NDB) kidneys as compared to the DB kidneys. Calpastatin expression was minimally detected in the NDB kidneys, using immunohistochemistry, over the time course. On the other hand, consistently higher number of tubules in the DB kidney showed calpastatin expression over the time course. The lower leakage of calpain in the DB kidneys was commensurate with constitutively higher expression of calpastatin in the S-phase-laden PTCs of these mice. To test the protective role of newly divided/dividing PTCs, DB mice were given the anti-mitotic agent colchicine (CLC) (2 mg/kg and 1.5 mg/kg, i.p., on days 8 and 10 after STZ injection) prior to challenge with a LD(90) dose of DCVC, which led to 100% mortality by 48 h. Mortality was due to rapid progression of DCVC-initiated renal injury, suggesting that newly divided/dividing cells are instrumental in mitigating the progression of DCVC-initiated renal injury in DB. The anti-mitotic effect of CLC in DB kidney is associated with lower expression of calpastatin and higher leakage of calpain in the injured tubules. These findings suggest that constitutively higher cell division in the DB kidney is associated with overexpression of calpastatin, which reduces the progression of DCVC-initiated renal injury mediated by calpain on the one hand and accelerates nephrogenic tissue repair on the other, thereby restoring renal structure and function.

Acetylcysteine↗

PubMed1996

Intraoperative progress reports decrease family members' anxiety.

The researcher used a four-group quasi-experimental posttest design to examine the effect of intraoperative progress reports on 200 family members' anxiety. Group one (ie, control group) received standard perioperative care, which did not include intraoperative progress reports. Group two received in-person progress reports from perioperative nurses. Group three received an "attention" protocol (ie, checklist explaining hospital routines, waiting room procedures). Group four received progress reports delivered by telephone. The researcher compared family members' state anxiety scores, mean arterial pressures (MAPs), and heart rates measured halfway during their relatives' surgical procedures, measuring these dependent variables after providing the interventions. The in-person intraoperative progress report group reported lower state anxiety scores (P < .001) and had significantly lower MAPs and heart rates (P < .05) than the other three groups. In-person progress reports appear to be the most beneficial perioperative nursing intervention for reducing family members' anxiety during the intraoperative waiting period.

Adolescent↗

PubMed2002

Blindness and glaucoma: a comparison of patients progressing to blindness from glaucoma with patients maintaining vision.

PURPOSE: To compare patients becoming legally blind from glaucoma with those who did not go blind. DESIGN: Retrospective, cohort, and case-control study. METHODS: A retrospective community-based longitudinal study of residents of Olmsted County, Minnesota, who were newly diagnosed with open-angle glaucoma between 1965 and 1980 and followed through 1998. A case-control study was performed comparing patients progressing to legal blindness from glaucoma with aged-matched and visual field-matched patients not progressing to blindness. RESULTS: Fifty-six of 290 patients progressed to legal blindness in at least one eye over the 34-year period of the study. Most who progressed to blindness had moderate to advanced visual field loss at the time of diagnosis of glaucoma. Those becoming legally blind had mean intraocular pressures (IOP) on therapy lower than or similar to patients who did not go blind, although the variability of IOP was higher in the blind group. Different susceptibilities to IOP were apparent, as some eyes with initially normal disks and visual fields became blind at an IOP of 20 mm, while others did not worsen. Changes in medical therapy after progression of visual field damage were less effective in lowering IOP in the group becoming blind than in the nonblind group. CONCLUSIONS: Patients at greatest risk of blindness had visual field loss at the time of diagnosis of glaucoma. Different susceptibilities to IOP were apparent, with some patients becoming blind at pressures that others tolerated without significant progression. This suggests that continued monitoring of visual fields and reassessment of target IOP levels when field damage occurs are fundamental in the management of glaucoma.

Aged↗

PubMed1991

Correlation between intraocular pressure control and progressive glaucomatous damage in primary open-angle glaucoma.

Fifty-five patients with primary open-angle glaucoma and early glaucomatous damage who had medical therapy and laser trabeculoplasty were followed up for four to 11 years or until progressive glaucomatous damage was documented. Factors associated with the stability or progression of glaucoma were evaluated. Eyes with mean intraocular pressure higher than 21 mm Hg during the follow-up period uniformly had progressive glaucomatous changes. Conversely, eyes with mean intraocular pressure less than 17 mm Hg remained stable, and approximately half of the eyes with mean intraocular pressure between 17 and 21 mm Hg had progressive glaucomatous changes. Patients who remained stable were slightly younger than those with progressive glaucomatous changes (P less than .05), but initial optic nerve head appearance, initial visual field findings, number of medicines used, medical history, and patient gender or race were not statistically associated with stability or progression of the glaucoma. These findings reinforce the importance of intraocular pressure control in primary open-angle glaucoma and the need to identify other markers that help determine the proper level of intraocular pressure for individual patients.

Adult↗

PubMed2001

Progressive, age-related behavioral impairments in transgenic mice carrying both mutant amyloid precursor protein and presenilin-1 transgenes.

This study provides a comprehensive behavioral characterization during aging of transgenic mice bearing both presenilin-1 (PS1) and amyloid precursor protein (APP(670,671)) mutations. Doubly transgenic mice and non-transgenic controls were evaluated at ages wherein beta-amyloid (Abeta) neuropathology in APP+PS1 mice is low (5-7 months) or very extensive (15-17 months). Progressive cognitive impairment was observed in transgenic mice for both water maze acquisition and radial arm water maze working memory. However, transgenicity did not affect Y-maze alternations, circular platform performance, standard water maze retention, or visible platform recognition at either age, nor did transgenicity affect anxiety levels in elevated plus-maze testing. In sensorimotor tasks, transgenic mice showed a progressive increase in open field activity, a progressive impairment in string agility, and an early-onset impairment in balance beam. None of these sensorimotor changes appeared to be contributory to any cognitive impairments observed, however. Non-transgenic mice showed no progressive behavioral change in any measure evaluated. Given the age-related cognitive impairments presently observed in APP+PS1 transgenic mice and their progressive Abeta deposition/neuroinflammation, Abeta neuropathology could be involved in these progressive cognitive impairments. As such, the APP+PS1 transgenic mouse offers unique opportunities to develop therapeutics to treat or prevent Alzheimer's Disease through modulation of Abeta deposition/neuroinflammation.

Aging↗

PubMed1995

Progression of premature thelarche to central precocious puberty.

To evaluate whether girls with premature thelarche progress to central precocious puberty (CPP) and to analyze their clinical and hormonal characteristics, we retrospectively examined 100 girls with premature thelarche who were followed for several years. Fourteen of the patients with characteristics diagnostic of premature thelarche (isolated breast development before age 8 years, bone age advancement within 2 SD of normal, normal growth velocity, follicle-stimulating hormone-predominant response to luteinizing hormone-releasing hormone) progressed during follow-up to precocious or early central puberty (progressive breast size increase, bone age acceleration, and significant decrease in predicted adult height). The chronologic age of this group of 14 girls was 5.1 +/- 2.0 years at the onset of premature thelarche and 7.8 +/- 0.6 years (mean +/- SD) after progression to central early or precocious puberty. Pelvic ultrasonography showed significant differences in measurements between the time of diagnosis of premature thelarche and progression to CPP. Nine of these patients required treatment, three with cyproterone acetate and six with luteinizing hormone-releasing hormone analogs, and all responded as expected for classic CPP. At baseline evaluation, no clinical or hormonal characteristics could be established that separated the 14 children who progressed to precocious or early puberty from the 86 girls who did not. We conclude that premature thelarche is not always a self-limited condition and may sometimes accelerate the timing of puberty.

Age Determination by Skeleton↗

PubMed1989

Superficial bladder cancer treated with bacillus Calmette-Guerin: a multivariate analysis of factors affecting tumor progression.

A multivariate analysis was performed on data from 221 patients with superficial bladder tumors (papilloma in 30, grade II to III stage Ta in 51, grade II to III stage Tis in 111 and grade II to III stage T1 in 29) who were treated with intravesical bacillus Calmette-Guerin and followed for a minimum of 24 months or until progression. The purpose of this analysis was to identify prognostic variables predictive of tumor progression defined as muscle invasion, metastasis or endoscopically uncontrolled superficial bladder carcinoma involving the bladder and/or prostatic urethra. Variables examined before bacillus Calmette-Guerin, and at 3 and 6 months after bacillus Calmette-Guerin included age, sex, race, purified protein derivative reaction, duration of disease, tumor category, tumor grade, multifocality, results of cytology, flow cytometry, cystoscopy, biopsy, prior chemotherapy and bacillus Calmette-Guerin treatment regimen. Significant variables (Cox regression analysis, p less than 0.07) for tumor progression were before bacillus Calmette-Guerin--stage T1 tumors and duration of disease less than 1 year, at 3 months after bacillus Calmette-Guerin--stage T1 tumor, duration of disease less than 1 year, positive cytology studies and multifocality, and at 6 months after bacillus Calmette-Guerin--stage T1 tumor, positive cytology and positive biopsy other than stage T1 tumors. Prognostic risk groups were best defined at 6 months after bacillus Calmette-Guerin, the probability of tumor progression thereafter being at 1, 3 and 5 years, respectively, as follows: for risk group 1 (T1 tumor)--71, 100 and 100 per cent, for risk group 2 (positive biopsy other than T1 plus positive cytology)--25, 79 and 100 per cent, for risk group 3 (either positive biopsy other than stage T1 or positive cytology studies)--18, 40 and greater than 81 per cent, and for risk group 4 (negative biopsy and negative cytology studies)--2, 11 and 26 per cent, respectively. Evaluation of patients with superficial bladder carcinoma at 6 months after intravesical bacillus Calmette-Guerin therapy identifies the probability of tumor progression. Patients at high risk for tumor progression require alternative treatment strategies, whereas low risk patients can be observed for further therapy if necessary.

BCG Vaccine↗

PubMed1989

Flow cytometry as a predictor of response and progression in patients with superficial bladder cancer treated with bacillus Calmette-Guerin.

Simultaneous bladder wash flow cytometry, voided urinary cytology and cystoscopic examinations were performed at 3-month intervals during a median of 18 months (range 5.5 to 50 months) in 65 patients receiving intravesical bacillus Calmette-Guerin treatment for superficial bladder cancer. Of the 65 patients treated 36 (56 per cent) had a complete response, 12 (18 per cent) had no response and 17 (26 per cent) had progression. Results of examinations at 6 months suggested that a negative bladder wash flow cytometry (29 of 36 patients, r equals 0.73, p less than 10(-7) is a strong predictor of response to bacillus Calmette-Guerin, comparable with cytological (r equals 0.60, p less than 10(-7) or cystoscopic (r equals 0.38, p less than 0.005) examinations alone or combined with cytology (r equals 0.74, p less than 10(-7)). At 6 months a positive bladder wash flow cytometry (r equals 0.44, p less than 0.0005) is as strong a predictor of disease progression as a positive cystoscopic examination (r equals 0.43, p less than 0.0005). The combination of bladder wash flow cytometry and voided urinary cytology is not superior to positive bladder wash flow cytometry alone. Median estimated interval to progression for these patients treated with bacillus Calmette-Guerin was 38 months. In the subgroup with positive bladder wash flow cytometry at 6 months the median interval to progression was 30 months. With a negative bladder wash flow cytometry at 6 months the probability of survival free of progression at 30 months was 85 per cent (p less than 0.01). Thus, negative bladder wash flow cytometry at 6 months is a strong predictor of response to bacillus Calmette-Guerin and also survival free of progression.

Administration, Intravesical↗

PubMed1988

Tumor volume versus percentage of specimen involved by tumor correlated with progression in stage A prostatic cancer.

Previous studies from this institution have shown that in untreated stage A prostate cancer when 5 per cent of the specimen or less was involved by tumor (stage A1) only 2 per cent of the patients had progression at 4 years. Of the specimens with greater than 5 per cent cancer (stage A2) 33 per cent had progression at 4 years. More recently, we have shown that 16 per cent of the men with stage A1 disease who remained at risk for 8 years or longer after diagnosis had progression of disease despite a small percentage of the specimen involved by tumor. To address whether the actual volume of tumor resected may be a better predictor of progression than the percentage of the specimen involved by tumor the data from these studies were re-evaluated. We demonstrated that at 4 and 8 years of followup the percentage of the specimen and resected tumor volume were strongly associated with tumor progression, with the percentage of the specimen showing a stronger association especially at 4 years. Our study reaffirms the use of the percentage of resected tissue involved by tumor as a means to distinguish between stages A1 and A2 prostate cancer. Although at 8 years the distinction between stages A1 and A2 disease is blurred, this staging classification still is useful to identify those tumors with a relatively indolent course and a minimal short-term risk of progression from those that are more aggressive.

Adenocarcinoma↗

PubMed2001

Assessment of frequency of progression to hypertension in non-hypertensive participants in the Framingham Heart Study: a cohort study.

BACKGROUND: Patients with optimum (<120/80 mm Hg), normal (120-129/80-84 mm Hg), and high normal (130-139/85-89 mm Hg) blood pressure (BP) may progress to hypertension (>140/90 mm Hg) over time. We aimed to establish the best frequency of BP screening by assessing the rates and determinants of progression to hypertension. METHODS: We assessed repeated BP measurements in individuals without hypertension (BP<140/90 mm Hg) from the Framingham Study (4200 men, 5645 women; mean age 52 years) who attended clinic examinations during 1978-94. The incidence of hypertension (or use of antihypertensive treatment) and its determinants were studied. FINDINGS: A stepwise increase in hypertension incidence occurred across the three non-hypertensive BP categories; 5.3% (95% CI 4.4-6.3%) of participants with optimum BP, 17.6% (15.2-20.3%) with normal, and 37.3% (33.3-41.5%) with high normal BP aged below age 65 years progressed to hypertension over 4 years. Corresponding 4-year rates of progression for patients 65 years and older were 16.0% (12.0-20.9), 25.5% (20.4-31.4), and 49.5% (42.6-56.4), respectively. Obesity and weight gain also contributed to progression; a 5% weight gain on follow-up was associated with 20-30% increased odds of hypertension. INTERPRETATION: High normal BP and normal BP frequently progress to hypertension over a period of 4 years, especially in older adults. These findings support recommendations for monitoring individuals with high normal BP once a year, and monitoring those with normal BP every 2 years, and they emphasise the importance of weight control as a measure for primary prevention of hypertension.

Adult↗