tbuckley/cabot-search huggingface dataset:
Health needs assessment: Needs assessment: from theory to practice
Authors: A. Stevens, S. Gillam
Journal: BMJ (1998)

This is the third in a series of six articles describing approaches to and topics for health needs assessment, and how the results can be used effectively

The purpose of needs assessment in health care is to gather the information required to bring about change beneficial to the health of the population. It is generally, but not universally, accepted that this takes place within the context of finite resources.1 “Health gain” can therefore be achieved by reallocating resources as a result of identifying four factors:

The subjects of healthcare needs assessment are the populations and patients who are recipients or potential beneficiaries of health care. Populations, of course, include individual patients. The assessment of individuals' needs may form part of the assessment of a population's needs, but it may be costly and it risks ignoring individuals with needs who do not present themselves for health care. Table 1 shows the circumstances favouring individual needs assessment for planning purposes.

View this table:

Table 1 
Factors determining basis for assessing healthcare needs



The priority attached to different needs, whether of populations or of individuals, raises philosophical problems. For example, should the principal criterion be the benefit that could potentially be obtained for each individual, or the severity of their presenting condition?2 In other words, should greater priority (a greater assessed need) be attributed to the need for surgery of a patient with early stage colorectal cancer or to the need for hospice care of a terminally ill lung cancer patient? In practice the former, the approach that favours the greater …
A Case of Cerebral Metastases of Unknown Origin
Authors: TARIK BELHOCINE, STEPHANIE BOLLE, JEAN-LOUIS ALBERINI, FREDERIC DAENEN, ISABELLE RUTTEN, PIERRE RIGO
Journal: Clinical Nuclear Medicine (2001)

BELHOCINE, TARIK M.D.; BOLLE, STEPHANIE M.D.; ALBERINI, JEAN-LOUIS M.D.; DAENEN, FREDERIC M.D.; RUTTEN, ISABELLE M.D.; RIGO, PIERRE Ph.D. Author Information
Abstract 103: A prospective study of plasma inflammatory markers and risk of colorectal cancer in men.
Authors: Mingyang Song, Kana Wu, Shuji Ogino, Charles S. Fuchs, Edward L. Giovannucci, Andrew T. Chan
Journal: Cancer Research (2013)

Abstract Chronic inflammation may mediate risk of colorectal cancer (CRC); however, the association between circulating inflammatory markers and risk of CRC has been inconsistent. We prospectively evaluated the association of plasma C-reactive protein (CRP), interleukin-6 (IL-6), and the soluble tumor necrosis factor receptor 2 (sTNFR-2) with incident CRC among 18,225 men in the Health Professionals Follow-up Study who provided blood samples in 1994. Through 2008, we documented 274 CRC cases and matched up to 2 controls by age and date of blood draw. We used conditional logistic regression to estimate relative risks (RRs) and confidence intervals (CIs). Compared to men in the lowest quartile of plasma IL-6 (Q1), men in the highest quartile (Q4) had a multivariate RR for CRC of 1.54 (95% CI, 0.99-2.40; Ptrend = .02). However, after excluding cases diagnosed within 2 years of blood draw, the association was substantially attenuated (Q4 versus Q1, RR = 1.26, 95% CI = 0.78-2.05; Ptrend = .21). In analyses restricted to cases diagnosed at least 2 years after blood draw, the association of IL-6 with CRC appeared to differ by body mass index such that the significantly positive association was only present among lean individuals (Pinteraction = .03). We did not observe any significant association between CRP or sTNFR-2 and CRC. Taken together, plasma inflammatory markers are not generally associated with risk of CRC among men. However, the possibility that plasma IL-6 is associated with increased risk of CRC among lean men requires further investigation. Citation Format: Mingyang Song, Kana Wu, Shuji Ogino, Charles S. Fuchs, Edward L. Giovannucci, Andrew T. Chan. A prospective study of plasma inflammatory markers and risk of colorectal cancer in men. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 103. doi:10.1158/1538-7445.AM2013-103
PHASE II TRIAL OF THE PHOSPHATIDYINOSITOL-3 KINASE (PI3K) INHIBITOR BUPARLISIB (BKM120) IN RECURRENT GLIOBLASTOMA CONDUCTED BY THE IVY FOUNDATION EARLY PHASE CLINICAL TRIALS CONSORTIUM
Authors: P. Y. Wen, P. Y. Wen, W. K. A. Yung, I. K. Mellinghoff, S. Ramkissoon, B. Alexander, M. Rinne, H. Colman, A. M. Omuro, L. M. DeAngelis, M. R. Gilbert, J. DeGroot, T. F. Cloughesy, E. Q. Lee, L. Nayak, A. S. Chi, T. Batchelor, S. M. Chang, M. D. Prados, D. A. Reardon, K. L. Ligon
Journal: Neuro-Oncology (2014)

BACKGROUND: The PI3K pathway is activated in most GBMs and represents a potential therapeutic target. Buparlisib is an oral, pan-Class I PI3K inhibitor that enters the brain at therapeutic concentrations and inhibits the growth of U87 and human glioma tumor sphere models. METHODS: The Ivy Consortium conducted a phase II study of buparlisib in recurrent GBM patients with activation of the PI3K pathway (mutation, homozygous deletion or loss of IHC of PTEN, PIK3CA or PIK3RI mutations, or detectable pAKT). Additional eligibility criteria included radiologic progression, 1st or 2nd relapse, >18 yrs, KPS >60, adequate bone marrow and organ function, no prior bevacizumab or enzyme-inducing antiepileptic drugs. Patients received buparlisib 100mg daily. The study consisted of 2 concurrent cohorts. In Cohort 1 (up to 15 patients) buparlisib was given for 8-12 days prior to surgery for recurrent disease. Patients underwent FDG PET, pharmacokinetic studies, and tumor was obtained for drug concentrations and pharmacodynamic effects. In Cohort 2, 50 patients with unresectable GBM received buparlisib with a primary endpoint of PFS6. RESULTS: 13 patients were enrolled into cohort 1, 50 into cohort 2. Treatment was fairly well-tolerated with no grade 4 toxicities. Grade 3 toxicities were asymptomatic lipase elevation (6), rash (4), hyperglycemia (3), fatigue (4), elevated ALT/AST (2), and 1 each with depression, anxiety, hypophosphatemia, thrombocytopenia and lymphopenia. Analysis of tumor specimens from Cohort 1 showed reduction of pAKT by IHC in 4/6 (67%) of evaluable patients. The combined cohorts showed minimal efficacy with median PFS of 1.8 months and median OS of 10.9 months. Best response was stable disease. Only 1 patient in each cohort achieved PFS6. Of the first 40 patients who underwent exome sequencing, there were 4 PIK3CA (10%), 2 PIK3R1 (5%) and 13 PTEN (33%) mutations. Patients with PTEN loss and or PI3K mutations paradoxically had a worse outcome. CONCLUSIONS: Buparlisib is well-tolerated in patients with recurrent GBM and achieves adequate tumor concentration to inhibit pAKTS473. However, single agent efficacy was minimal. Final correlation of tumor genotype with outcome will be presented. SECONDARY CATEGORY: n/a.
P0075 : Health-related quality of life is improved after liver transplantation and is related to disease acceptance, helplessness and perceived disease benefits
Authors: W. Develtere, L Onghena, X. Rogiers, R.I. Troisi, F. Berrevoet, A. Vanlander, A. Geerts, H. Van Vlierberghe, X. Verhelst, C. Poppe
Journal: Journal of Hepatology (2015)
Activation of EVI1 transcripts with chromosomal translocation joining the TCRVβ locus and the EVI1 gene in human acute undifferentiated leukemia cell line (Kasumi-3) with a complex translocation of der(3)t(3;7;8)
Authors: K Suzukawa, T Kodera, S Shimizu, T Nagasawa, H Asou, N Kamada, M Taniwaki, J Yokota, K Morishita
Journal: Leukemia (1999)
Abstract 2098: Reducing sequence artefacts from FFPE DNA for cancer diagnostics
Authors: Hongdo Do, Alexander Dobrovic
Journal: Cancer Research (2012)

Abstract Non-reproducible sequence artefacts have been frequently detected in DNA extracted from formalin-fixed and paraffin-embedded (FFPE) tissues. Studies of ancient DNA reveal that deamination of cytosine to uracil is a major cause of DNA damage. We hypothesised that similar lesions may occur in FFPE DNA and examined the role of uracil lesions on generation of transitional G:C to A:T artefacts in FFPE DNA by treatment with uracil DNA glycosylase (UDG). High resolution melting (HRM)-based assays were used for rapid and cost-effective screening of artefacts. The artefact rate was assessed by limited copy number-HRM (LCN-HRM) in FFPE DNA samples in which multiple G:C to A:T artefacts were found. The effect of UDG treatment on detection of true sequence changes was examined by testing mutational hotspots at the EGFR, KRAS and AKT1 genes. A high HRM positive rate as judged by the formation of heteroduplexes was found in FFPE DNA by LCN-HRM. This was markedly reduced after treatment with UDG. UDG treatment specifically suppressed the formation of artefacts in FFPE DNA and did not affect the detection of true KRAS codon 12 and EGFR exon 19 and 20 mutations. In conclusion, this study reports for the first time that uracil lesions due to cytosine deamination is one of the major causes of artefacts in FFPE DNA and the use of uracil-DNA-glycosylase that removes uracil lesions on DNA can lead to a significant reduction of artefacts. This finding will thus greatly improve biomarker studies using DNA samples derived from FFPE tissues, which has immediate implications especially to diagnostic settings. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2098. doi:1538-7445.AM2012-2098
Abstract 4701: DNA-adducts levels and chromosomal aberrations in relation to smoking history and topography in smokers
Authors: Ramona G. Dumitrescu, Yun-Ling Zheng, Yang Yang, Francoise Seillier-Moiseiwitsch, Stephanie M. Spernak, Christopher Loffredo, David H. Phillips, Peter G. Shields
Journal: Cancer Research (2010)

Abstract Introduction: Tobacco smoking is the major cause of morbidity and mortality in developed countries. Important determinants of tobacco carcinogen exposure include the smoking history and smoking topography. Tobacco carcinogens-induced DNA adducts and chromosomal aberrations have been associated with cancer development. It is unknown if the choice of cigarettes and smoking topography lead to differences in carcinogen-DNA adduct levels and chromosomal aberrations. Methods: We studied 207 population-based smokers (97 Caucasians and 110 African Americans). The subjects smoked two cigarettes, one hour apart, and the smoking topography was measured. We assessed three parameters of smoke exposure (serum cotinine, nicotine boost and carbon monoxide boost) in order to collect corroborative evidence that reflect different types of exposure. Carcinogen-DNA adducts and chromosomal aberrations in lymphocytes were determined by using the 32P-postlabeling analysis and standard cytogenetic method, respectively. Results: The chance of having high level of DNA-adducts was significantly higher in males than females (OR: 1.9; 95%CI: 1.09-3.31). Weakly associations of the DNA-adducts were observed with age and race (higher in older people and African-Americans smokers) (OR: 1.7; 95%CI: 0.97-2.90; OR: 1.5; 95%CI: 0.87-2.60). DNA-adducts were significantly associated with the baseline and post cigarette CO level for the first (p-value=0.001; 0.007 respectively) and second cigarette (p-value=&amp;lt;0.001; 0.001 respectively), with the total number of puffs for the second cigarette (p-value=0.04) and with the cumulative topography (p-value=0.03). Marginal associations were observed for the changes in CO2 pre and post cigarettes (p-value=0.08), the average inter-puff interval and the total puff volume for the second cigarette (p-value=0.06; 0.07 respectively). The changes in CO2 pre and post first and second cigarette were significantly associated with the mean number of chromosomal aberrations per cell (p-value=0.05; 0.01 respectively). Conclusion: In this study we observed potentially important associations of smoking topography with both DNA adduct levels and chromosomal aberrations. Larger study sets will be necessary to clarify the magnitude of these associations and to account for baseline differences related to gender, age, and race. Such an approach could provide useful information for understanding differential susceptibility to lung cancer among smokers. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4701.
A3.10 IL-6 Receptor Blockade Enhances CD39+ Regulatory T-Cell Development in Rheumatoid Arthritis and in Experimental Arthritis
Authors: Allan Thiolat, Jerome Biton, Luca Semerano, Yves-Marie Pers, Pierre Portales, Delphine Lemeiter, Patrice Decker, Christian Jorgensen, Marie-Christophe Boissier, Pascale Louis-Plence, Natacha Bessis
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background and Objectives</h3> Studies have demonstrated the clinical efficacy of tocilizumab, a humanised anti-IL-6 receptor (R) antibody (Ab), in patients with rheumatoid arthritis (RA). The rational for blocking IL-6 in this disease mainly lays on the pro-inflammatory role of this cytokine in the disease. However, only few works have studied the consequences of anti-IL-6R treatment on Tregs cells and mainly focuses on their frequency. Our objective was to elucidate anti-IL-6R mode of action on Tregs in RA patients treated with tocilizumab and in a RA model. <h3>Methods</h3> Mice with collagen-induced arthritis (CIA) were treated at day 0 by MR16–1 (a rat anti-mouse IL-6 receptor monoclonal Ab provided by Chugai Pharmaceutical Co. LTD, Japan) and the evolution of CD4<sup>+</sup> FoxP3<sup>+</sup> Tregs during arthritis course was assessed at key time points (day 8–18–28 and 42 after CIA induction) by studying their number, frequency and phenotype (expression of GITR, ICOS, Helios, CD62L, CTLA-4 and CD39) in lymph nodes (LN), thymus and spleen by flow cytometry. Numerical analysis of Th17 and Th1 cells was also performed by flow cytometry. Twenty patients with severe and active RA were recruited and treated with 8 mg/kg of tocilizumab monthly. Peripheral blood was recovered at day 0, as well as 1 and 3 month, and Th17and Tregs were analysed by flow cytometry. <h3>Results</h3> Clinical and histological evaluation of arthritides in mice treated with anti-mouse IL-6R mAb showed, as expected, a less severe disease as compared to control Ig treated mice. Th17 frequency was unchanged, but Tregs frequency was enhanced in the LN of MR16–1 treated mice. In the thymus, we observed an enhanced frequency of Tregs CD4<sup>+</sup>CD8<sup>−</sup>FoxP3<sup>+</sup>. Tregs phenotype was also modified in treated mice, with an increased frequency of CD39<sup>+</sup> Tregs (LN and spleen), suggesting an enhanced ATP hydrolysis immunosuppressive activity of Tregs. In RA patients, Th17 frequencies were not modified by tocilizumab therapy and did not differ between responders and non-responders. Interestingly, CD39<sup>+</sup> Treg cell among CD4<sup>+</sup> cells frequencies were significantly higher in responders than in non-responders after 3 months of tocilizumab therapy. <h3>Conclusions</h3> Tregs, but not Th17, are modified by anti-IL-6R treatment in both CIA and RA. These results support a beneficial effect in RA of treatments responsible for CD39<sup>+</sup> Tregs enhancement and emphasise the relevance of the monitoring cell populations after cytokine blockade used to treat arthritis.
Abstract 4398: MEK inhibitors prevent rebound reactivation of ERK signaling by the RAF inhibitor PLX4032 and enhance its antitumor activity
Authors: Christine A. Pratilas, Eric W. Joseph, Madhavi Tadi, Maytal Gabay, Wai Wong, Elisa De Stanchina, Gideon Bollag, Neal Rosen
Journal: Cancer Research (2011)

Abstract Activation of ERK signaling occurs in the majority of melanomas and tumors with BRAF mutation are especially sensitive to its inhibition with MEK or RAF inhibitors. The latter inhibit ERK signaling only in tumors with V600E mutant BRAF and activate the pathway in cells with WT BRAF. These data implied that RAF inhibitors would have a wider therapeutic index than MEK inhibitors with a greater therapeutic effect, but could also cause toxicity by activating the ERK pathway in normal tissue. These predictions were born out in clinical trials, in which the RAF inhibitor PLX4032 caused tumor regression in most patients with metastatic melanoma with mutant BRAF, but also caused squamous cell carcinoma of the skin in one third of patients. Unfortunately, these responses are rarely complete and the median time to relapse is approximately nine months. We now find that prolonged treatment of BRAF mutant cells with PLX4032 is associated with a rebound of ERK phosphorylation from its nadir that is associated with an increase in the transcriptional output of the pathway and could therefore limit the therapeutic effects of the drug. In this new steady state, ERK phosphorylation and output are sensitive to MEK inhibitors but not readdition of RAF inhibitors. The rebound of ERK signaling is associated with upstream activation in the RAS pathway. We therefore determined the effects of combined RAF and MEK kinase inhibition in a panel of melanoma cells with mutant BRAF. Combined inhibition delayed pathway rebound and resulted in more prolonged suppression of ERK output, enhanced cell death, and tumor growth inhibition compared to treatment with the RAF inhibitor alone. These results suggest that combined RAF and MEK kinase inhibition may be a useful strategy to improve the extent and duration of responses to RAF inhibitors and minimize toxicity caused by ERK activation in normal tissue. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4398. doi:10.1158/1538-7445.AM2011-4398
Use of Dynamic Images to Detect Artifacts in Dual-Isotope Parathyroid Adenoma Imaging
Authors: RAGHUVEER HALKAR, JAMES GALT, ULKUM BILKAY, JOHNATHAN VANSANT
Journal: Clinical Nuclear Medicine (2000)

A 47-year-old woman with a clinical history and biochemical profile of primary hyperparathyroid disease underwent dual-isotope imaging to localize hyperfunctioning parathyroid tissue. The subtraction image showed a focal area of uptake inferior to the left lower pole of the thyroid consistent with a parathyroid adenoma. Another focal area of increased uptake in the left infraclavicular area raised the possibility of an ectopic parathyroid adenoma. However, on the dynamic 1-minute-per-frame Tc-99m MIBI images showed that the uptake in this area steadily decreased from frame 1 to frame 20, indicating that this was most probably tracer stasis in the left subclavian vein. A single parathyroid adenoma was removed from the inferior pole of the thyroid region, and the patient’s biochemical values returned to normal. This report highlights the importance of reviewing the dynamic images.
1235 SEVERE STEATOSIS IS ASSOCIATED WITH A HAEMODYNAMICALLY SIGNIFICANT INCREASE IN INTRAHEPATIC RESISTANCE IN ASSOCIATION WITH BOTH ENDOTHELIAL DYSFUNCTION AND MORPHOLOGICAL ALTERATIONS IN A RAT MODEL
Authors: S. Francque, W. Laleman, L. Verbeke, C. Van Steenkiste, C. Casteleyn, W. Kwanten, C. Van Dijck, M. D'Hondt, A. Ramon, W. Vermeulen, B. De Winter, E. Van Marck, P. Pelckmans, P. Michielsen
Journal: Journal of Hepatology (2012)
Ovarian Cancer: Latest Gains Establish New Battle Fronts
Authors: C. McNeil
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Ovarian Cancer: Latest Gains Establish New Battle Fronts Get access Caroline McNeil Caroline McNeil Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 12, 21 June 1995, Pages 871–873, https://doi.org/10.1093/jnci/87.12.871 Published: 21 June 1995
P168 Rifabutin is a useful alternative to rifampicin in the treatment of active TB/HIV co-infection
Authors: R. Singh, N. Marshall, C. J. Reynolds, R. A. M. Breen, C. J. Smith, L. Swaden, S. Bhagani, S. Hopkins, M. A. Johnson, M. C. I. Lipman
Journal: Thorax (2010)

<h3>Introduction</h3> Effectiveshort course anti-tuberculosis treatment (TB Rx) requires use of a rifamycin, typically rifampicin (RIF). However, in patients with TB/HIV co-infection it has significant drug interactions; and rifabutin (RBT) is often substituted in those taking anti-retrovirals (ARVs). Recent data suggest that the recommended dosage of RBT may be inadequate with concomitant ARVs, leading to an increased risk of subsequent rifamycin resistance after apparent successful treatment. <h3>Aims</h3> We undertook a retrospective, single-site review of TB/HIV treatment to determine the impact of rifamycin selection on prevalence of serious (ACTG grade III or IV) adverse events (AE), TB treatment completion and TB recurrence. <h3>Methods</h3> The characteristics and treatment outcomes, stratified by rifamycin type and ARV use for all adults with TB/HIV co-infection receiving rifamycin-based therapy as part of active TB Rx from 1997 to 2008 were examined. Rifamycin choice and dosage was in line with BHIVA guidance for TB/HIV therapy—in general RIF being used with a non-nucleoside inhibitor ARV combination and RBT with boosted protease inhibitors. <h3>Results</h3> 143 HIV-positive individuals received rifamycin-based TB Rx during the study period (64 RIF, 56 RBT and 24 RIF/RBT in treatment switch—see Abstract P168 Table 1). 103/143 (72%) patients had culture positive disease, of whom 4 had isoniazid drug resistance. 106/143 (74%) patients used ARVs during TB Rx. Patients on ARVs who had RIF either alone, or switched from RIF to RBT during TB Rx had a higher incidence of serious AE compared to those prescribed RBT alone (p=0.002). There was no difference in the percentage of patients who completed prescribed TB Rx between the RIF and RBT groups (p=0.6). After a median follow-up of 3.2 years from start of TB Rx, 4 patients relapsed, all with a drug sensitive organism. <h3>Conclusion</h3> Within our study population, rifabutin is a useful alternative to rifampicin in the treatment of active TB/HIV co-infection and does not appear to lead to subsequent rifamycin resistance after successful therapy. We find no evidence in this analysis to change the advice within the current national TB/HIV guidelines.
The Appearance of Pulmonary Mucormycosis on FDG PET/CT
Authors: Chun-Jiang Dang, Ya-Jun Li, Feng-Hua Zhan, Xiao-Ming Shang
Journal: Clinical Nuclear Medicine (2012)

Pulmonary mucormycosis is a life-threatening opportunistic mycosis that is difficult to diagnose early. We report the case of a 56-year-old woman who complained of intermittent fever in the afternoon and productive cough and pain on the right side of the chest. Her clinical condition deteriorated despite antibiotherapy. FDG PET/CT showed a heterogeneous soft tissue mass at the lower part of the right lung with obvious FDG uptake in the peripheral part of the mass. Mucormycosis was proven by histopathology and fungal culture from the transbronchial lung biopsy materials.