bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trends in prostate cancer mortality among black men and white men in the United States
Authors: Chu Kenneth C. , Tarone Robert E. , Freeman Harold P. 
Published: March 2003

AbstractBACKGROUNDProstate cancer mortality rates in the United States declined sharply after 1991 in white men and declined after 1992 in black men. The current study was conducted to investigate possible mechanisms for the declining prostate cancer mortality rates in the United States.METHODSThe authors examined and compared patterns of prostate cancer incidence, survival rates, and mortality rates among black men and white men in the United States using the 1969–1999 U.S. prostate cancer mortality rates and the 1975–1999 prostate cancer incidence, survival, and incidence‐based mortality rates from the Surveillance, Epidemiology, and End Results (SEER) Program for the U.S. population. The SEER data represent approximately 10% of the U.S. population.RESULTSProstate cancer incidence and mortality rates showed transient increases after 1986, when the U.S. Food and Drug Administration approved the use of prostate specific antigen (PSA) testing. The age‐adjusted prostate cancer mortality rates for men age 50–84 years, however, have dropped below the rate in 1986 since 1995 for white men and since 1997 for black men. In fact, for white men ages 50–79 years, the 1998 and 1999 rates were the lowest observed since 1950. Incidence‐based mortality rates by disease stage revealed that the recent declines were due to declines in distant disease mortality. Moreover, the decrease in distant disease mortality was due to a decline in distant disease incidence, and not to improved survival of patients with distant disease.CONCLUSIONSSimilar incidence, survival, and mortality rate patterns are seen in black men and white men in the United States, although with differences in the timing and magnitude of recent rate decreases. Increased detection of prostate cancer before it becomes metastatic, possibly reflecting increased use of PSA testing after 1986, may explain much of the recent mortality decrease in both white men and black men. Cancer 2003;97:1507–16. Published 2003 by the American Cancer Society.DOI 10.1002/cncr.11212
Barriers to the participation of African‐American patients with cancer in clinical trials
Authors: Advani Anjali S. , Atkeson Benjamin , Brown Carrie L. , Peterson Bercedis L. , Fish Laura , Johnson Jeffrey L. , Gockerman Jon P. , Gautier Marc 
Published: March 2003

AbstractBACKGROUNDAfrican‐American patients have been under‐represented in oncology clinical trials. Better understanding barriers to African‐American participation may help increase the accrual of African‐American patients onto clinical trials.METHODSTwo hundred eighteen patients with malignant disease (72 African‐American patients and 146 white patients) were recruited from the Duke Cancer Clinic and from Duke Oncology Outreach Clinics (DOORS). Patients were interviewed using a standardized survey. Questions included patients' knowledge of cancer, religious/spiritual beliefs, satisfaction with medical care, knowledge of clinical trials, reasons for participating or refusing to participate in a clinical trial, financial/transportation issues, and demographic factors, such as age and education. Data on attitudes and belief were analyzed for group differences between African‐American patients and white patients as well as between patients who were treated at the Duke Cancer Clinic and patients who were treated at DOORS clinics.RESULTSWillingness to participate in a clinical trial depended on both race and clinic site. Forty‐five percent of white patients, compared with 31% of African‐American patients, were willing to participate in a clinical trial (P = 0.05). white and African‐American patients who were treated at the Duke Cancer Clinic were more willing to participate in a trial compared with their counterparts who were treated at DOORS clinics (47% vs. 37%, respectively; P = 0.09). The greatest differences between groups (African‐American patients vs. white patients and Duke Cancer Clinic patients vs. DOORS patients) were education and income: Much greater percentages of African‐American patients and DOORS patients did not complete high school and had annual incomes < $15,000. In addition, more African‐American patients than white patients believed that God would determine whether they would be cured or would die from their disease. In a multivariate analysis, education, income, and belief that God would determine the patient's outcome also were correlated with a decreased willingness to participate in clinical trials.CONCLUSIONSFactors associated with religion, education, and income, rather than race, may be major barriers to clinical trial participation. Interventions that target education and income may increase the recruitment of African‐American oncology patients onto clinical trials. Cancer 2003;97:1499–506. © 2003 American Cancer Society.DOI 10.1002/cncr.11213
Lung carcinoma after radiation therapy in women treated with lumpectomy or mastectomy for primary breast carcinoma
Authors: Zablotska Lydia B. , Neugut Alfred I. 
Published: March 2003

AbstractBACKGROUNDPrior studies have demonstrated that women who receive adjuvant radiation therapy (RT) after mastectomy for breast carcinoma have an increased risk of a second primary lung carcinoma after 10 years, but, to the authors' knowledge, the risk associated with adjuvant RT after breast‐conserving surgery (lumpectomy) has yet to be determined. The purpose of the current study was to confirm and extend earlier findings of the effects of postmastectomy RT on second primary lung carcinoma and to investigate the impact of postlumpectomy RT on second primary lung carcinoma in the same population and to compare the results.METHODSThe authors used data from the population‐based Surveillance, Epidemiology, and End Results (SEER) program of the U.S. National Cancer Institute, encompassing approximately 10% of the U.S. population, from 1973 to 1998. Of the women with nonmetastatic invasive breast carcinoma, 194,981 had been treated with mastectomy and 65,560 were treated with lumpectomy. Cox regression analysis was used to estimate the relative risk (RR) of a second primary lung carcinoma among women treated with RT compared with those who received surgery alone as a function of time interval since treatment and laterality for both types of surgery.RESULTSAlthough no statistically significant elevation in risk for second primary lung carcinoma prior to 10 years was observed, the authors estimated a RR of 2.06 (95% confidence interval [95% CI], 1.53–2.78) and 2.09 (95% CI, 1.50–2.90) for ipsilateral lung carcinoma at 10–14 years and 15+ years after postmastectomy RT, respectively, whereas no increased risk was observed for the contralateral lung. The excess risk of ipsilateral lung carcinoma after postmastectomy RT was found for all three major histologic subtypes of lung carcinoma (adenocarcinoma, squamous cell carcinoma, and small cell carcinoma). No increased risk of lung carcinoma was observed at 10–14 years after postlumpectomy RT for either lung.CONCLUSIONSPostmastectomy RT was found to provide a moderate increase in risk for ipsilateral lung carcinoma starting 10 years after exposure; this increased risk is reported to persist to at least 20 years. Postlumpectomy RT does not appear to incur an increased risk. These findings should be reassuring to women treated with either type of RT, but the excess risk in the postmastectomy group should be considered in the choice between treatment options. Cancer 2003;97:1404–11. © 2003 American Cancer Society.DOI 10.1002/cncr.11214
Use of quality indicators to evaluate the care of patients with localized prostate carcinoma
Authors: Miller David C. , Litwin Mark S. , Sanda Martin G. , Montie James E. , Dunn Rodney L. , Resh Jennifer , Sandler Howard , Wei John T. 
Published: March 2003

AbstractBACKGROUNDThe goal of quality assurance in health care is to preserve and improve patient care. Recently, RAND developed a set of evidence‐based candidate indicators for evaluating the quality of care for patients with localized prostate carcinoma; however, the feasibility and sensitivity of these indicators have not been tested in a clinical setting. The objectives of this study were to evaluate the feasibility of measuring these quality indicators and to determine their sensitivity to change in practice patterns over time.METHODSOne hundred sixty‐eight men who presented in either 1995 or in 2000 and were treated for localized prostate carcinoma were selected randomly from the University of Michigan tumor registry. A combination of electronic data base review and explicit chart review was used to assess the feasibility of measuring compliance for each indicator. For each indicator in which assessment was feasible, compliance with the RAND indicators was determined for patients in both years. Multivariate regression analysis was used to adjust for potential confounding effects of disease stage, tumor grade, prostate specific antigen (PSA) level, patient age, and therapy.RESULTSBased on review of available clinical data, measurement of compliance was feasible for 19 of 22 RAND candidate quality indicators (86%). For five indicators, significant differences in documentation (compliance) were detected between 1995 and 2000 (P < 0.05). Treatment received and higher PSA levels were associated independently with documentation of compliance for several indicators (P < 0.05).CONCLUSIONSMeasurement of the majority of the RAND quality indicators for the treatment of patients with localized prostate carcinoma was feasible, and improvements in several indicators were observed between 1995 and 2000. Demonstration of such variation, even within a single institution, suggests that the indicators are sufficiently sensitive to detect differences in practice patterns. Cancer 2003;97:1428–35. © 2003 American Cancer Society.DOI 10.1002/cncr.11216
Levels of hypoxia‐inducible factor‐1α independently predict prognosis in patients with lymph node negative breast carcinoma
Authors: Bos Reinhard , van der Groep Petra , Greijer Astrid E. , Shvarts Avi , Meijer Sybren , Pinedo Herbert M. , Semenza Gregg L. , van Diest Paul J. , van der Wall Elsken 
Published: March 2003

AbstractBACKGROUNDHypoxia‐inducible factor‐1 (HIF‐1) is a transcription factor that plays an important role in tumor growth and metastasis by regulating energy metabolism and inducing angiogenesis to survive cellular hypoxia. Increased levels of HIF‐1α, the O2‐regulated subunit of HIF‐1, were noted during breast carcinogenesis. In this study, the prognostic value of HIF‐1α expression and its correlation with various clinicopathologic variables in patients with invasive breast carcinoma were investigated.METHODSExpression levels of HIF‐1α, HER‐2/neu, estrogen receptor, and progesterone receptor were analyzed in 150 patients with early‐stage breast carcinoma by immunohistochemistry. HER‐2/neu gene amplification was investigated with automated fluorescent in situ hybridization. The mitotic activity index, histologic grade, and tumor type were assessed in hematoxylin and eosinstained specimens. Clinical data included disease‐free survival, overall survival, lymph node status, and tumor size. The data were analyzed with two‐sided univariate and multivariate tests, with P values < 0.05 considered significant.RESULTSHigh levels of HIF‐1α had an association of borderline significance with decreased overall survival (P = 0.059) and disease‐free survival (P = 0.110) that was ascribed completely to the subgroup of women with lymph node negative tumors (n = 81 patients; P = 0.008 and P = 0.004, respectively). HER‐2/neu immunoreactivity (P < 0.001) and gene amplification (P < 0.001), vascular endothelial growth factor expression (P = 0.016), and Ki‐67 expression (P < 0.001) were correlated strongly with HIF‐1α positivity, although none of those factors had an independent effect on survival.CONCLUSIONSIncreased levels of HIF‐1α were associated independently with shortened survival in patients with lymph node negative breast carcinoma. Therefore, the use of immunohistochemical assessment of HIF‐1α as a new predictor of poor outcome may improve clinical decision‐making regarding adjuvant treatment of patients with lymph node negative breast carcinoma. Cancer 2003;97:1573–81. © 2003 American Cancer Society.DOI 10.1002/cncr.11246
Fatigue in ovarian carcinoma patients
Authors: Holzner Bernhard , Kemmler Georg , Meraner Verena , Maislinger Andrea , Kopp Martin , Bodner Thomas , Nguyen‐Van‐Tam Dominic , Zeimet Alain G. , Fleischhacker W. Wolfgang , Sperner‐Unterweger Barbara 
Published: March 2003

AbstractBACKGROUNDAlthough fatigue is a commonly reported symptom in cancer patients it is rarely investigated, especially in patients with ovarian carcinoma. The main focus of the current study was to assess fatigue in these patients and to investigate the impact of fatigue and other clinical and psychosocial variables on their quality of life (QOL).METHODSNinety‐eight ovarian carcinoma survivors (average age of 57.4 ± 12.5 years) were included in the study. All women had received cancer therapy but had not been treated for at least 6 months. The average time elapsed since first diagnosis was 5.7 ± 5.5 years. Fatigue was measured with the Multidimensional Fatigue Inventory (MFI‐20) and QOL was measured with the Functional Assessment of Cancer Therapy (FACT)‐ovarian carcinoma part and the European Organization for Research and Treatment of Cancer Care Questionnaire, including the ovarian carcinoma module.RESULTSThirty‐two of 98 ovarian carcinoma patients (32.7%, 95% confidence interval, 23.5–42.9%) reported MFI‐20 General Fatigue scores ≥ 12.0 and therefore could be characterized as suffering from fatigue. This group of patients had a significantly lower QOL, had higher scores of anxiety and depression, and perceived that they had less social support. In a multiple regression model, mental adjustment, social support, anxiety, and depression as well as fatigue were significant predictors of QOL (FACT‐generic part total score) whereas clinical and sociodemographic variables were not.CONCLUSIONA remarkably high proportion of ovarian carcinoma survivors suffered from fatigue. Because this symptom is a key predictor of QOL, it should be given more attention in aftercare programs. Cancer 2003;97:1564–72. © 2003 American Cancer Society.DOI 10.1002/cncr.11253
Reductions in N‐acetylaspartylglutamate and the 67 kDa form of glutamic acid decarboxylase immunoreactivities in the visual system of albino and pigmented rats after optic nerve transections
Authors: Moffett John R. 
Published: March 2003

AbstractThis study compares the immunohistochemical distributions of N‐acetylaspartylglutamate (NAAG) and the large isoform of the γ‐aminobutyric acid (GABA)‐synthesizing enzyme glutamic acid decarboxylase (GAD67) in the visual system of albino and pigmented rats. Most retinal ganglion cells and their axons were strongly immunoreactive for NAAG, whereas GAD67 immunoreactivity was very sparse in these cells and projections. In retinorecipient zones, NAAG and GAD67 immunoreactivities occurred in distinct populations of neurons and in dense networks of strongly immunoreactive fibers and synapses. Dual‐labeling immunohistochemistry indicated that principal neurons were stained for NAAG, whereas local interneurons were stained for GAD67. In contrast to the distribution observed in retinorecipient zones, most or all neurons were doubly stained for NAAG and GAD67 in the thalamic reticular nucleus. Ten days after unilateral optic nerve transection, NAAG‐immunoreactive fibers and synapses were substantially reduced in all contralateral retinal terminal zones. The posttransection pattern of NAAG‐immunoreactive synaptic loss demarcated the contralateral and ipsilateral divisions of the retinal projections. In addition, an apparent transynaptic reduction in GAD67 immunoreactivity was observed in some deafferented areas, such as the lateral geniculate. These findings suggest a complicated picture in which NAAG and GABA are segregated in distinct neuronal populations in primary visual targets, yet they are colocalized in neurons of the thalamic reticular nucleus. This is consistent with NAAG acting as a neurotransmitter release modulator that is coreleased with a variety of classical transmitters in specific neural pathways. J. Comp. Neurol. 458:221–239, 2003. © 2003 Wiley‐Liss, Inc.
Inverse expression of olfactory cell adhesion molecule in a subset of olfactory axons and a subset of mitral/tufted cells in the developing rat main olfactory bulb
Authors: Treloar Helen B. , Gabeau Darlene , Yoshihara Yoshihiro , Mori Kensaku , Greer Charles A. 
Published: March 2003

AbstractThe projection of olfactory sensory neuron (OSN) axons from the olfactory epithelium (OE) to the olfactory bulb (OB) is highly organized but topographically complex. Evidence suggests that odorant receptor expression zones in the OE map to the OB about orthogonal axes. One candidate molecule for the formation of zone‐specific targeting of OSN axon synapses onto the OB is the olfactory cell adhesion molecule (OCAM). OCAM+ OSNs are restricted to three of the four zones in the OE and project their axons to the ventral OB where they form synapses with mitral/tufted (M/T) cells. To determine when this zonal connection is established, we have examined OCAM expression in rat olfactory system, during seminal periods of glomerular formation. OCAM+ axons sort out in the ventral olfactory nerve layer of the OB before glomerular formation. Surprisingly, OCAM was also expressed transiently by subsets of M/T cell dendrites located in the dorsal OB. The expression of OCAM by OSN axons and M/T dendrites was asymmetrical; in the dorsal OB, OCAM− OSN axons synapsed on OCAM+ M/T dendrites, whereas in the ventral OB, OCAM+ OSN axons synapsed on OCAM− M/T dendrites. The restricted spatial map of OCAM+ M/T cells appeared earlier in development than the zonal segregation of OCAM+ OSN axons. Thus, OCAM on M/T cell dendrites may act in a spatiotemporal window to specify regions of the developing rat OB, thereby establishing a foundation for mapping of the OE zonal organization onto the OB. J. Comp. Neurol. 458:389–403, 2003. © 2003 Wiley‐Liss, Inc.
Spatial organization of the pigeon tectorotundal pathway: An interdigitating topographic arrangement
Authors: Marín Gonzalo , Letelier Juan Carlos , Henny Pablo , Sentis Elisa , Farfán Gonzalo , Fredes Felipe , Pohl Nélida , Karten Harvey , Mpodozis Jorge 
Published: March 2003

AbstractThe retinotectofugal system is the main visual pathway projecting upon the telencephalon in birds and many other nonmammalian vertebrates. The ascending tectal projection arises exclusively from cells located in layer 13 of the optic tectum and is directed bilaterally toward the thalamic nucleus rotundus. Although previous studies provided evidence that different types of tectal layer 13 cells project to different subdivisions in Rt, apparently without maintaining a retinotopic organization, the detailed spatial organization of this projection remains obscure. We reexamined the pigeon tectorotundal projection using conventional tracing techniques plus a new method devised to perform small deep‐brain microinjections of crystalline tracers. We found that discrete injections involving restricted zones within one subdivision retrogradely label a small fraction of layer 13 cells that are distributed throughout the layer, covering most of the tectal representation of the contralateral visual field. Double‐tracer injections in one subdivision label distinct but intermingled sets of layer 13 neurons. These results, together with the tracing of tectal axonal terminal fields in the rotundus, lead us to propose a novel “interdigitating” topographic arrangement for the tectorotundal projection, in which intermingled sets of layer 13 cells, presumably of the same particular class and distributed in an organized fashion throughout the surface of the tectum, terminate in separate regions within one subdivision. This spatial organization has significant consequences for the understanding of the physiological and functional properties of the tectofugal pathway in birds. J. Comp. Neurol. 458:361–380, 2003. © 2003 Wiley‐Liss, Inc.
Differentiation of lamina I spinomedullary and spinothalamic neurons in the cat
Authors: Andrew David , Krout Karl E. , Craig A.D. (Bud) 
Published: March 2003

AbstractWe characterized spinomedullary neurons that project to the ventrolateral portion of the medulla that receives lamina I terminations in two sets of experiments in the cat. First, their distribution was examined using single unilateral iontophoretic injections of cholera toxin subunit B. The injection sites were characterized by microelectrode recordings from nociceptive‐ and thermoreceptive‐specific units, indicative of lamina I input. The spinomedullary neurons were symmetrically distributed bilaterally, predominantly (63–69%) in lamina I but also in laminae V–VIII and the thoracic lateral horn (intermediolateral cell column). In horizontal sections, spinomedullary lamina I neurons included all three main morphological types described earlier. Second, spinomedullary and spinothalamic neurons were compared in retrograde double‐labeling experiments. Different combinations of tracers were injected in the right thalamus and the left or right ventrolateral medulla (guided by recordings). The numbers of spinomedullary and spinothalamic neurons on the left side were comparable, and the segmental and laminar distributions were similar, except that a greater proportion of spinomedullary neurons originated from thoracic segments. However, the proportion of double‐labeled neurons was consistently ∼1%, indicating that spinomedullary and spinothalamic pathways arise from separate subpopulations. Spinomedullary neurons were more ventrally located within lamina I than spinothalamic neurons. A significantly greater proportion of spinomedullary neurons had fusiform somata (49% vs. 36%). These observations indicate that lamina I is the major source of spinal input to this portion of the ventrolateral medulla, that the projection includes several morphological types of inputs, and that this projection is distinct from the spinothalamic projection. These findings are consistent with the concept that lamina I projections constitute an ascending homeostatic afferent pathway relating the physiological condition of the body. J. Comp. Neurol. 458:257–271, 2003. © 2003 Wiley‐Liss, Inc.