tbuckley/cabot-search huggingface dataset:
Revisiting Nursing’s Effect on Surgical Quality and Cost
Authors: Amir A. Ghaferi, Christopher R. Friese
Journal: JAMA Surgery (2016)

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Reduced Antineoplastic Activity in Mice of Cisplatin Administered With High Salt Concentration in the Vehicle&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: S Aamdal, O Fodstad, O Kaalhus, A Pihl
Journal: JNCI Journal of the National Cancer Institute (1984)

The effect of high NaCl concentration in the vehicle on the toxic and antineoplastic activities of cisplatin [cis-dichloro-diammineplatinum(II)] (CDDP) was reinvestigated in mice. The toxicity, as measured by the survival of mice given CDDP iv, was reduced by 50-60% when the NaCl concentration in the vehicle was raised from 0.9 to 4%. In ascitic P388 leukemia the antineoplastic activity of CDDP given ip was not reduced significantly. However, in all other systems studied the antitumor activity was reduced when the CDDP was dissolved in high NaCl solution. The tumor models studied included systemic P388 and L1210 leukemias, Lewis lung carcinoma, and 5 human tumor xenografts. The human tumors were studied by the subrenal capsule assay. In the case of a malignant melanoma and a malignant fibrous histiocytoma, the effect also was demonstrated in the subcutaneous nude mouse model. In one of the malignant melanomas a 50% increase in the CDDP dose did not compensate for the reduced antitumor activity caused by the high NaCl concentration in the vehicle. These results, which stand in contrast to current views, question the experimental basis for the use of high-NaCl vehicles in the "high-dose" CDDP regimens.
Does participating in clinical trials change the experience of dying for patients with cancer?
Authors: C. A. Thompson, T. Shanafelt, J. Sloan, P. Novotny, A. Tan, C. Loprinzi, T. Moynihan
Journal: Journal of Clinical Oncology (2005)

8066 Background: Many patients with incurable malignant disease are offered the opportunity to enroll in clinical trials, despite the low probability of a cure. Little is known, however, about how the experience of dying for individuals enrolled in clinical trials compares to the experience for individuals not participating in a clinical trial. Methods: We performed a retrospective review of all Olmsted County residents who died of cancer in 2002 and were cared for in the Mayo Clinic Department of Oncology. Information extracted from medical records included: age, location of death, cause of death, type of cancer, study participation, treatment interventions in the last 2 months of life (chemotherapy, surgery, hospitalization, intubation, cardiac resuscitation, dialysis, radiation), code status at time of death, and hospice care. We compared study participants to non-participants using Wilcoxon rank and Fisher’s exact tests. Seventy-two patients were included. Within two months of death, 12 patients were enrolled in a study, and the others were treated with standard of care. Results: Patients enrolled in a clinical trial at the time of death were more likely to have a full code status (45.5% vs. 18.3%, p=0.0257), receive chemotherapy (66.7% vs. 30%, p=0.0158), and dialysis (8.3% vs. 0%, p=0.0243) in the last 2 months of life than those treated with standard care. Trends toward a higher likelihood of surgery (33% vs. 13%; p=0.09) and endotracheal intubation (25% vs. 9%; p=0.09) were also observed. There was no difference in age at diagnosis or death, number of days in hospital or ICU, cancer specific death, location of death, radiation, invasive procedure, cardiopulmonary resuscitation, antibiotic use, or participation in hospice. Conclusions: This pilot study suggests that patients enrolled in clinical trials do have a different end-of-life experience than those not on study. No differences, however, were observed in hospice participation, number of days in hospital, and location of death. This suggests that patients should be offered enrollment in clinical trials without fear of negatively affecting their end-of-life care. No significant financial relationships to disclose.
Abstract 10857: Long-term Cause-specific Mortality of One-year Survivors of Subarachnoid Haemorrhage - A Population-based Prospective Study
Authors: Miika Korja, Karri Silventoinen, Tiina Laatikainen, Pekka Jousilahti, Veikko Salomaa, Jaakko Kaprio
Journal: Circulation (2012)
Localization of Kaposi's Sarcoma–Associated Herpesvirus in Bone Marrow Biopsy Samples From Patients With Multiple Myeloma
Authors: Jonathan W. Said, Matthew R. Rettig, Karen Heppner, Robert A. Vescio, Gary Schiller, Hong J. Ma, Daniel Belson, Alison Savage, I. Peter Shintaku, H. Phillip Koeffler, Hiroya Asou, Geraldine Pinkus, Jack Pinkus, Matthew Schrage, Eric Green, James R. Berenson
Journal: Blood (1997)
Risk of osteoporosis/osteopenia among women with breast cancer receiving anti-cancer therapy (ACT)
Authors: S. P. Boyce, B. A. Mincey, M.-S. Duh, M. Marynchenko, M. K. Raut, J. Brandman, E. A. Perez
Journal: Journal of Clinical Oncology (2005)

665 Background: ACT with hormonal and chemotherapy agents are a routine part of the management of breast cancer and have been reported to decrease bone mineral density, a major determinant of bone loss. Moreover, studies based on small populations have shown an increased bone loss risk in women treated for breast cancer. This retrospective study assesses the association between ACT and osteoporosis/osteopenia risk on a large population of women with nonmetastatic breast cancer. Methods: From the anonymous health claims of 2 million employees and their beneficiaries, 14,604 women who had ≥ 2 breast cancer claims without bone metastases were identified between 1/98 and 3/03. Of these, 8,762 (mean age: 62 ± 11 years) received ACT and 5,842 (mean age: 63 ± 12 years) did not (control group). The mean follow-up period was 31 months for both groups. The endpoint was prevalence of osteoporosis/osteopenia. The association between ACT and bone loss was examined in both univariate and multivariate analyses. Multivariate logistic regression analysis isolated the effect of ACT on bone loss by controlling for other covariates. Results: Patients who received ACT had an elevated risk of developing osteoporosis/osteopenia (odds ratio (OR)=1.18; 95% CI=1.05–1.33) relative to the control group. Multivariate analysis, controlling for age, duration of follow-up, comorbidities, income, health plan and region, indicated that patients who received ACT had a 30% higher risk for osteoporosis/osteopenia (OR=1.29; 95% CI= 1.13–1.46). Other significant risk factors were increasing age (compared to patients 55 years of age or less, 56–65 yrs: OR=1.90 95% CI= 1.59–2.26; 66–75 yrs: OR=2.03; 95% CI= 1.65–2.48; 76+ yrs: OR=1.28; 95% CI= 1.01–1.62), and patient comorbidities (OR=1.09 for one unit increase in Charlson comorbidity index; 95% CI= 1.06–1.11). Conclusions: This large employed population-based study corroborates smaller studies in finding that treatment with ACT in women with nonmetastatic breast cancer is associated with an increased risk for osteoporosis/osteopenia. Monitoring and intervention for bone loss is therefore recommended for this population. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Novartis Novartis Novartis
Validation of an inverse association between programmed death ligand 1 (PDL1) and genes in the vascular endothelial growth factor (VEGF) pathway in primary clear cell renal cell (ccRCC).
Authors: Richard Wayne Joseph, Mansi Parasramka, Daniel Serie, Jeanette Eckel-Passow, E Aubrey Thompson, Christine M. Lohse, Thai Huu Ho, Erik P. Castle, Robert Houston Thompson, Bradley C. Leibovich, John Cheville, Alexander S. Parker
Journal: Journal of Clinical Oncology (2013)

4567 Background: Trials combining anti-PDL1 and anti-VEGF therapies for clear cell renal cell carcinoma (ccRCC) are underway; however the relationship between the expression of PDL1 and genes in the VEGF pathway is poorly understood. Using the Affymetrix platform, we observed an inverse association between the expression of PDL1 and key genes in the VEGF pathway. Herein, we validate this inverse association using an independent set of 100 primary ccRCC tumors. Methods: From our registry database we sampled 100 ccRCC tumors with varying PDL1 protein expression (0%-100%) determined by immunohistochemistry (IHC). We extracted RNA from FFPE slides and performed RT-PCR to quantify gene expression of PDL1, VEGF, VEGFR1, and VEGFR2. All genes were normalized to the POLR2a gene. We evaluated the association of PDL1 protein expression and VEGF gene expression using Spearman rank correlation. In addition, we employed a linear mixed effects model to compare the fold-change in expression of VEGF genes between PDL1 low (0-5%, n=68) and PDL1 high (&gt;5%, n=32) tumors. Results: As expected, PDL1 protein expression positively correlates with PDL1 geneexpression (corr=0.42, p&lt;0.001). Validating our array data, PDL1 protein expression inversely correlates with expression of key VEGF genes: VEGF (corr=-0.23, p=0.01), VEGFR1 (corr=-0.34, p&lt;0.001), and VEGFR2 (corr=-0.23, p=0.01). In our dichotomized analysis, we noted significantly higher expression of VEGF genes in the PDL1 low compared to the PDL1 high group: VEGF (fold change=1.82, p&lt;0.001), VEGFR1 (FC=2.63, p&lt;0.001), and VEGFR2 (FC=2.13, p=0.001). Conclusions: We independently validate an inverse association between the expression of PDL1 and key genes in the VEGF pathway in primary ccRCC. If validated further in larger studies, the existence of an immune evasive and an angiogenic phenotype within ccRCC could inform current clinical trials targeting these two pathways. Ultimately, whether VEGF signaling affects PDL1 expression, or whether angiogenic or immune evasive phenotypes predict response to anti-PDL1, anti-VEGF, or a combination of the two therapies remains unclear.
A photopolymerized composite hydrogel and surgical implanting tool for a nucleus pulposus replacement
Authors: Andreas Schmocker, Azadeh Khoushabi, Daniela A. Frauchiger, Benjamin Gantenbein, Constantin Schizas, Christophe Moser, Pierre-Etienne Bourban, Dominique P. Pioletti
Journal: Biomaterials (2016)
A multivariate analysis on histopathologic prognostic factors for predicting outcome of node-positive endometrial carcinoma
Authors: H. Watari, Y. Todo, M. Takeda, Y. Ebina, R. Yamamoto, N. Sakuragi
Journal: Journal of Clinical Oncology (2004)

5064 Background: Prognosis of advanced endometrial cancer patients (stage IIIc and IV) is poor. In order to clarify the histopathologic prognostic factors of node-positive endometrial cancer, we performed the following analysis. Methods: A retrospective review of 55 node-positive endometrial cancer patients (44 in stage IIIc and 11 in stage IV) among 303 patients treated between 1982 and 2002 at Hokkaido University Hospital was performed. All Patients underwent primary surgical treatment including pelvic and para-aortic lymphadenectomy followed by adjuvant chemotherapy consisting of intravenous cisplatin, doxorubicin, and cyclophoshamide. Survival analyses were performed by the Kaplan-Meier curves and the log-rank test. Independent prognostic factors were determined by multivariate Cox regression analysis. Results: Multivariate analysis revealed that FIGO (1988) stage and lymph-vascular space invasion (LVSI) of the tumor were found to be independently related to poor survival . The estimated 5-year survival rate of stage IIIc patients with or without moderate/prominent LVSI was 50.9 % and 93.3 %, respectively. The difference of survival rate was statitstically significant (p=0.0024). The estimated 5-year survival rate of stage IV patients was 20.0%. In stage IIIc patients, multivariate analysis showed that LVSI alone was found to be an independent prognostic factor for survival. Prognosis of stage IIIc patients could be stratified into three groups by the number of positive para-aortic lymph node (PAN) with an estimated 5-year survival rate of 86.4% for no positive PAN (n=23), 60.4% for 1 positive PAN (n=13), 20.0% for >=2 positive PAN (n=8). The difference of survival rate between no or one positive PAN and >=2 PAN was statistically significant (p=0.0007 for no positive PAN vs >=2 PAN, p=0.0319 for one positive PAN vs >=2 positive PAN). Conclusions: LVSI was an independent prognostic factor for stage IIIc patients and their prognosis was stratified by the number of positive PAN. Postoperative therapy and follow-up modality need to be individualized according to LVSI and the number of positive PAN for stage IIIc patients. No significant financial relationships to disclose.
Amonafide and ara-C treatment for secondary acute myeloid leukemia (sAML)
Authors: H. P. Erba, D. A. Rizzieri, M. R. O'Donnell, A. S. Lundberg, A. M. Ajami, A. D. Rampersad, R. L. Capizzi
Journal: Journal of Clinical Oncology (2007)

7065 Background: sAML portends a poor prognosis due to disease (unfavorable cytogenetics and multidrug resistance (MDR) phenotype) and patient (pt) characteristics (elderly w/comorbid illnesses). Amonafide, a topoisomerase II inhibitor, is not a substrate for the MDR efflux pump, P-glycoprotein (see Chau et al, ASCO 2007). Phase 1 trials of amonafide alone or together with ara-C reported a 50% CR rate (10/20) in pts with sAML (Allen et al, ASCO 2006). The dose-limiting toxicities of amonafide were manageable. Methods: In a Phase II trial pts with sAML (prior MDS or leukemogenic therapy, i.e., tAML) received amonafide 600 mg/m 2 /day on days 1–5 and CIV ara- C 200 mg/m 2 /day on days 1–7. A 2 nd course could be given if day 14 marrow showed persistent leukemia. CR pts received either stem cell transplant or intermediate/high dose ara-C depending on age. An independent Data Safety Monitoring Board and central morphology review participated in the study. Primary endpoint was CR rate. Results: Enrollment has been completed. 44 % of 80 pts achieved CR. Details are available for the 1 st 40 pts: median age 63 yrs (range 26 –87); prior MDS, 57%; tAML, 43%; unfavorable cytogenetics, 40%. 16/40 (40%) achieved CR (15 CR+1CRp). Subgroup CR analysis: MDS→AML without and with prior therapy for MDS (mostly azacytidine), 64% &amp; 33%; tAML, 29%; intermediate and unfavorable cytogenetics, 58% and 18%; &lt;60yrs, 42%; ≥60yrs, 39%. With a median follow up of 39 weeks, the median duration of CR is 28 weeks (range 20+ to 40+ weeks), with 8 of 16 patients in continuous CR. Median overall survival for CR patients has not been reached (range 1–47+ weeks). Death in first 28 days from consequences of hypoplasia was 17.5%. Grade 3, 4 non-heme adverse events occurring in &gt; 10% pts were hypotension 23%, pneumonia 18%, dyspnea 13%, and diarrhea 13%. Data on all patients will be updated. Conclusions: Amonafide and ara-C is well tolerated in patients with poor prognosis sAML. A 64% CR was achieved in pts with untreated MDS→AML. Lower CR occurred with prior therapy for MDS, tAML and unfavorable cytogenetics. Age ≥60 yrs did not affect CR. Amonafide and ara-C may be a promising alternative for patients with sAML, especially those with over-expression of P-glycoprotein. No significant financial relationships to disclose.
Ultrastructural Features of Basophil and Mast Cell Granulopoiesis in Blastic Phase Philadelphia Chromosome-Positive Leukemia
Authors: J L Parkin, R W McKenna, R D Brunning
Journal: JNCI Journal of the National Cancer Institute (1980)

Ultrastructural and ultracytochemical studies were performed on blood and bone marrow specimens from 18 patients with Philadelphia chromosome-positive blastic leukemia; 7 patients were in blast transformation following a typical history of chronic myelogenous leukemia and 11 patients presented with “acute leukemia.” The patients were divided into 2 morphologic groups on the basis of light microscopic and cytochemical observations. In group 1, which consisted of 11 patients, the proliferating cells were “lymphoid” in appearance and demonstrated many cytochemical, biochemical, and immunologic features similar to those of the lymphoblasts of non-T, non-B acute lymphoblastic leukemia. In group II, which consisted of 7 patients, the proliferating cells were myeloid in appearance. On the basis of ultrastructural observations, the 11 group I patients were divided into 2 subgroups, A and B. Subgroup IA, consisting of 5 patients, was characterized by blasts that demonstrated no differentiating features. In subgroup IB, consisting of 6 patients, 20–30% of the leukemic cells contained inclusions that resembled leukemic mast cell or basophil granules. The leukemic cells in the 7 group II patients manifested myeloid characteristics by light microscopy and prominent basophil and mast cell granulopoiesis by electron microscopy. Abnormalities of other myeloid cell lines were also observed in both the lymphoid and myeloid groups of patients.
Caffeine inhibits TGFβ activation in epithelial cells, interrupts fibroblast responses to TGFβ, and reduces established fibrosis in<i>ex vivo</i>precision-cut lung slices
Authors: Amanda L Tatler, Josephine Barnes, Anthony Habgood, Amanda Goodwin, Robin J McAnulty, Gisli Jenkins
Journal: Thorax (2016)

Caffeine is a commonly used food additive found naturally in many products. In addition to potently stimulating the central nervous system caffeine is able to affect various systems within the body including the cardiovascular and respiratory systems. Importantly, caffeine is used clinically to treat apnoea and bronchopulmonary dysplasia in premature babies. Recently, caffeine has been shown to exhibit antifibrotic effects in the liver in part through reducing collagen expression and deposition, and reducing expression of the profibrotic cytokine TGFβ. The potential antifibrotic effects of caffeine in the lung have not previously been investigated. Using a combined in vitro and ex vivo approach we have demonstrated that caffeine can act as an antifibrotic agent in the lung by acting on two distinct cell types, namely epithelial cells and fibroblasts. Caffeine inhibited TGFβ activation by lung epithelial cells in a concentration-dependent manner but had no effect on TGFβ activation in fibroblasts. Importantly, however, caffeine abrogated profibrotic responses to TGFβ in lung fibroblasts. It inhibited basal expression of the α-smooth muscle actin gene and reduced TGFβ-induced increases in profibrotic genes. Finally, caffeine reduced established bleomycin-induced fibrosis after 5 days treatment in an ex vivo precision-cut lung slice model. Together, these findings suggest that there is merit in further investigating the potential use of caffeine, or its analogues, as antifibrotic agents in the lung.
5-fluorouracil in head and neck cancer patients: A population pharmacokinetics study.
Authors: C. Mercier, C. Yang, L. Dahan, J. Ciccolini, D. Bagarry, J. F. Seitz, R. G. Favre, B. Lacarelle, F. Duffaud
Journal: Journal of Clinical Oncology (2010)

e13098 Background: 5-fluorouracil (5FU) plays an important role in induction or in radiochemotherapy in head and neck cancer patients (pts). The saturable 5FU elimination pattern driven by DPD in the liver leading to nonlinear pharmacokinetics (PK) profile is a major cause of life-threatening toxicities. We have previously developed a U/UH2 ratio method to determine DPD status as a means to custom 5FU dosage, thus reducing toxicity without affecting efficacy. The present work aims at identifying the effect of covariates on 5FU disposition and developing a new model for describing 5FU PK. Methods: This study was carried out on 22 pts (18 men and 4 women, all having signed informed consent) treated for head and neck cancer with a dose of 5FU (3.3±1.4 g) individualized using their U/UH2 ratio (determined prior any 5FU administration). 5FU concentrations (T0, T5 min before and T15, T30, T45 min after the end of infusion) were determined by UV-HPLC. Population and individual PK parameters were computed using NONMEM v5 software. Covariates analysis including U/UH2 ratio were performed with Xpose 3.01 using GAM, bootstrap of the GAM methods, and tree-based modeling. Models' comparisons used objective function, Akaike criterion, and residual analysis. Results: In our pts, 5FU's PK was best described by a linear, one compartment model using FOCE interaction method and a mixed error model. The main covariate impacting on 5FU clearance was body surface area (BSA). Surprisingly, a significant impact of DPD status on 5FU elimination was found in 64% pts only, an observation that could be explained by the fact that pts with impaired DPD function had all reduced dosage, thus skipping the saturable elimination issue and limiting the impact of erratic DPD on drug PK. However, impact of DPD status was found to be greater than age or sex, two demographic covariates usually associated with increased risk of developing toxicities upon 5FU intake. Conclusions: In pts with U/UH2 based 5FU dosing strategy, drug PK becomes linear as saturation of DPD-mediated catabolic pathway is prevented by the preliminary identification of deficient pts and subsequent dose reduction. When the DPD issue is addressed preliminary, BSA is a relevant covariate to adjust 5FU dosage. No significant financial relationships to disclose.
Comparative analysis of intra- and interpopulation genetic diversity in Bufo bufo, using allozyme, single-locus microsatellite, minisatellite, and multilocus minisatellite data.
Authors: K T Scribner, J W Arntzen, T Burke
Journal: Molecular Biology and Evolution (1994)

Estimates of genetic diversity within, and of variation among, semi-isolated populations of the common toad (Bufo bufo) were derived and compared across four classes of nuclear genetic markers, including allozymes, microsatellites, and single and multilocus minisatellites. Estimates of multilocus heterozygosity and the number of alleles per locus derived from allozymes were lower than for each class of variable number of tandem repeat (VNTR) markers. The degree of interpopulation genetic divergence as determined by genetic distance was generally concordant across all markers, although interpopulation variance in allozyme allele frequency (as measure by F-statistics) was greater than that documented for each VNTR locus. For both classes of VNTR loci, migration appeared to have less influence than mutation on the extent of interpopulation divergence. Analyses suggest that singly and multiply detected VNTR loci may be highly informative for population-level analyses addressing questions concerning population subdivision and breeding structure.
Abstract 15221: The Prevalence of Valvular Heart Disease in Community Patients With Suspected Heart Failure
Authors: Anna Marciniak, Dominic Elton, Keli Glover, Ian Campbell, Rajan Sharma
Journal: Circulation (2013)

Background: Valvular heart disease is recognized as an important cause of morbidity and mortality. Early diagnosis is therefore essential as there are serious consequences for undiagnosed patients....