tbuckley/cabot-search huggingface dataset:
Patient-Reported Outcomes Following Treatment for Localized Prostate Cancer
Authors: Freddie C. Hamdy, Jenny L. Donovan
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Impact of performance evaluation on the quality of care in non-small cell lung cancer.
Authors: Tawee Tanvetyanon, Ji-Hyun Lee, William J. Fulp, Paul B. Jacobsen
Journal: Journal of Clinical Oncology (2013)

6531 Background: Improvement in the quality of care can translate into an improvement in the patient outcome. Evaluation of care quality among oncology practices has been associated with an improvement in the care of breast or colorectal cancer patients previously. Lung cancer is the leading cause of cancer death. Recently quality of care indicators specific for non-small cell lung cancer (NSCLC) have been developed. We investigated the impact of oncology practice evaluation on care quality in NSCLC. Methods: In 2008, members of the Florida Initiative for Quality Cancer Care submitted medical records of randomly sampled, new NSCLC patients who were seen in 2006 for review as baseline practice performance. Results were then circulated among members and voluntary improvement projects independently undertaken in each practice. In 2010, a repeat evaluation was conducted of new NSCLC patients first seen in 2009 to characterize change(s). Results: 10 practices (7 private and 3 university-based) contributed 1,091 patient records for analysis: 518 in 2006 and 573 in 2009. Baseline characteristics of patients were well balanced; however, the proportion of Medicaid or unfunded patients was higher in 2009 than in 2006 (14.8% vs. 7.7%, p=0.002). Of the 7 quality indicators measured, 4 showed a significant improvement when adjusted by practice site and patient characteristics (Table). Notable improvements included the use of brain staging before chemoradiation for stage III patients, performance status documentation and the use of cisplatin for adjuvant therapy. Conclusions: Performance evaluation is associated with an improvement in selected indicators of the quality of care in NSCLC. [Table: see text]
SPECIAL DEPARTMENTS
Authors: K. Mokbel A. Athow C. Kouriefs C. Leris N. Williams R. Carpenter, Göran Liljegren
Journal: Journal of Clinical Oncology (2000)

Article Tools SPECIAL DEPARTMENTS Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2000.18.4.942 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 10673537 K. Mokbel A. Athow C. Kouriefs C. Leris N. Williams R. CarpenterxK. Mokbel A. Athow C. Kouriefs C. Leris N. Williams R. CarpenterSearch for articles by this author Göran LiljegrenxGöran LiljegrenSearch for articles by this author , for the Uppsala Örebro Breast Cancer Study GroupxSearch for articles by this author Show More St Bartholomew’s Hospital West SmithfieldLondon, United KingdomÖrebro Medical Center Hospital ÖrebroSweden https://doi.org/10.1200/JCO.2000.18.4.942 First Page Full Text PDF Figures and Tables © 2000 by American Society of Clinical OncologyjcoJ Clin OncolJournal of Clinical OncologyJCO0732-183X1527-7755American Society of Clinical OncologyResponse14022000In Reply:In our analysis, we used tumor size as a continuous variable. There was a trend for higher risk with increasing tumor size, although it was not statistically significant (P = .08). If tumor size was categorized as ≤ 10 mm or greater than 10 mm, tumors ≤ 10 mm in size had a statistically significantly lower risk of local recurrence (P = .04).The median histopathologic tumor size in the trial was 13 mm. Histopathological tumor size was used in the risk factor analysis.The results presented by Mokbel et al are interesting, but it must be cautioned that smaller institutional series may be subject to selection bias. We maintain that our hypothesis about a low-risk group should be tested in a trial or in a carefully designed cohort study.
Stimulation of natural killer (NK) cell and macrophage infiltration in pancreatic cancer with virulizin (V), an immunotherapeutic agent
Authors: M. Y. Cao, Y. Lee, D. Miao, S. Cadden, J. A. Wright, A. H. Young
Journal: Journal of Clinical Oncology (2004)

4257 Purpose: V is stimulates macrophages and monocytes in vitro and in vivo. Pancreatic cancer patients treated with V in phase I/II studies showed increased 6 and 12 months survival vs historical controls. V administration was associated with increased NK cell activity in patients showing the best response to V. Hence, NK cell function may be a mediator of V anti-tumor activity. Methods: To determine if V induces NK cell infiltration into tumors, CD-1 nude mice with Capan-1 pancreatic tumor xenografts were treated with V; tumor samples were analyzed by flow cytometry using NK cell-specific antibodies. Anti-tumor activity and NK cell infiltration were also evaluated in human tumor xenografts in CD-1 nude mice depleted of macrophages. Immunohistochemical staining of tumor xenografts was performed to further assess NK cell and macrophage activity. Results: V increased NK cell infiltration of tumors (59.4 – 116.0%). Macrophage depletion reduced both NK cell infiltration of tumors, and anti-tumor activity of V (P=0.1632). V-treated mice showed a significant increase in infiltration of F4/80+ (macrophages) and NK1.1+ (NK) cells, vs saline treated controls. Increased NK1.1+ cell infiltration occurred early in V treatment, and correlated with an early marker for tumor apoptosis. V treatment also resulted in a significant increase in the NK cell number in the spleen. Conclusion: Macrophage-mediated NK cell activation/recruitment is implicated in the mechanism of action of V.. These results suggest that V mediates a sustained infiltration of NK cells and macrophages into tumors. Low NK cell activity may be a risk factor for malignancy and metastases, and a negative prognostic indicator in pancreatic cancer. NK cell function and other immune activities are being assessed as biologic markers of clinical response in a Phase III trial in pancreatic cancer as a first line combination therapy with gemcitabine. NK cell function will be correlated with clinical response parameters. No significant financial relationships to disclose.
The Combination of a BET Inhibitor (GS-5829) and a BTK Inhibitor (GS-4059) Potentiates DLBCL Cell Line Cell Death and Reduces Expression of MYC, IL-10, and IL-6 in Vitro
Authors: Jamie Bates, Saritha Kusam, Stacey Tannheimer, Julie Chan, Yvonne Li, David Breckenridge, Daniel Tumas
Journal: Blood (2016)
Hsp90β promoted endothelial cell-dependent tumor angiogenesis in hepatocellular carcinoma
Authors: Jing Meng, Yanrong Liu, Jingxia Han, Qiang Tan, Shuang Chen, Kailiang Qiao, Honggang Zhou, Tao Sun, Cheng Yang
Journal: Molecular Cancer (2017)

Vascular endothelial growth factor receptors (VEGFRs) are the major receptors involved in endothelial cell-dependent tumor angiogenesis. There are studies account for the effects of Hsp90 on angiogenesis, but the role and mechanism of Hsp90β isoforms and NVP-BEP800, a specific inhibitor of Hsp90β, in tumor angiogenesis is rarely mentioned. Immunohistochemistry and statistical analysis was used to evaluate the correlation between Hsp90β expression, CD31 endothelial cell-dependent vessel density, and VEGFRs expression in tissue samples of 96 HCCs. Kaplan-Meier survival analysis and COX proportional hazards analysis the relation of Hsp90β and prognosis. HUVEC cells were transfected with Hsp90β or treated with NVP-BEP800, and then cell proliferation, migration, invasion and tube formation were investigated. The VEGFR1 and VEGFR2 expression was determined by Western blot and immunofluorescence. The VEGFR1 and VEGFR2 promoter activities were detected by dual luciferase report system. In vivo, the angiogenesis promotion of Hsp90β and anti-angiogenesis efficacy of NVP-BEP800 was tested in HCC xenograft models. Histological analysis was performed on tumor samples to evaluate Hsp90β, VEGFRs expression and MVD. This study investigated the correlation between Hsp90β expression and CD31+ endothelial cell-dependent vessel density. Hsp90β promoted VEGFRs expression by increasing their promoter activities. The proliferation, migration, invasion, and tube formation activities of human endothelial cells significantly increased when Hsp90β was overexpressed. NVP-BEP800 down-regulated VEGFRs expression to significantly reduce tubular differentiation, as well as endothelial cell proliferation, migration, and invasion. Furthermore, NVP-BEP800 decreased VEGFR1 and VEGFR2 promoter activities. In vivo, Hsp90β promoted VEGFRs and CD31 expression in human hepatocellular carcinoma tumor xenografts and was associated with increased tumor microvessel density. After 18 days of treatment with 30 mg/kg/day NVP-BEP800, VEGFRs and CD31 expression significantly decreased. Hsp90β induced endothelial cell-dependent tumor angiogenesis by activating VEGFRs transcription. NVP-BEP800 has potential as a therapeutic strategy for inhibiting tumor angiogenesis by decreasing endothelial cell progression and metastasis. It can help develop a therapeutic strategy for tumor treatment through the inhibition of endothelial cell progression and metastasis.
12-Lipoxygenase in hypoxia and hypoxia-induced angiogenesis.
Authors: Sriram Krishnamoorthy, Krishna Rao Maddipati, Daotai Nie, Kenneth V. Honn
Journal: Cancer Research (2004)

Proc Amer Assoc Cancer Res, Volume 45, 2004

3591 

The enzyme platelet-type 12-lipoxygenase and its metabolite 12(S)-HETE have been shown to play major roles in tumor cell proliferation, migration, metastasis and angiogenesis. We have shown previously that 12(S)-HETE increases the expression of VEGF in prostate cancer cells. We have also shown the enhanced angiogenic response in tumors generated by injecting PC3 cells overexpressing 12-lipoxygenase. In the present study we have identified the roles played by 12-lipoxygenase and 12(S)-HETE in tumor hypoxia and hypoxia mediated angiogenesis. Our experiments have revealed that treatment of PC3 prostate cancer cells with 12(S)-HETE can lead to the increased expression of HIF-1α, the master regulator of hypoxic events. This has a positive correlation with hypoxia mediated angiogenesis since HIF-1α increases the transcription of vascular endothelial growth factor (VEGF). We have also observed the increased production of VEGF by PC3 cells overexpressing 12-lipoxygenase under both hypoxic and non-hypoxic conditions. This clearly emphasizes a major role played by 12-lipoxygenase and 12(S)-HETE in tumor hypoxia mediated angiogenesis. These findings have a lot of clinical relevance since new drugs have been developed targeting this pathway.
Association between body weight and efficacy outcomes during trabectedin therapy for recurrent advanced soft tissue sarcoma (STS).
Authors: Maurizio D'Incalci, Carlos Galmarini, Ines de la Riba Alvarez, Nadia Badri, Patrick Schöffski
Journal: Journal of Clinical Oncology (2012)

10047 Background: Trabectedin is the first marine-derived antineoplastic drug approved in Europe for the treatment of patients with recurrent advanced STS. Different studies have implicated tumor-derived cytokines as mediators of cachexia in cancer patients. Preclinical studies have demonstrated that trabectedin acts on tumor microenvironment particularly reducing IL-6, which is involved in cancer-induced cachexia (Germano et al. 2011, Ligouri et al. 2011). Methods: This exploratory retrospective analysis evaluated the association between body weight increase during treatment with respect to baseline and efficacy outcomes in 319 adult patients with recurrent STS. Patients were treated in four phase II trials with trabectedin at the approved dose of 1.5 mg/m 2 , given as a 24-hour infusion every 3 weeks. An analysis of the concordance between weight increase and objective response (OR) rate, tumor control (TC) rate (OR+stable disease lasting ≥3 months), progression-free survival (PFS) and overall survival (OS) was performed. Results: Correlation between weight increase and responses was observed: 68% of patients who achieved OR and 70% of patients with TC increased their weight for a median of 1.2 kg. Remarkably, PFS (5.1 vs. 1.9 months; p&lt;0.0001, log rank) and OS (21.0 vs. 8.2 months; p&lt;0.0001, log rank) were significantly prolonged in patients who gained weight during treatment. Six and 12-months Kaplan-Meier PFS estimates and survival rates at 12, 24 and 36 months were also better in those patients. Additionally, in Cycle 1-2, a significant relationship between weight increase and improved median PFS (4.2 vs. 2.2 months; p&lt;0.0001) and OS (19.4 vs. 9.3 months; p=0.0002) was observed. This is in concordance with the tendency to gain weight starting from the first cycle of treatment. Conclusions: This analysis suggests that weight gain is associated with favorable efficacy outcomes when patients are treated with trabectedin. Further research is needed to assess the prognostic value of weight changes as a complementary source of evaluation on the long-term clinical outcomes and impact of trabectedin on tumor microenvironment.
Transfection with the ferroportin gene increases the cytotoxicity of the iron chelator deferoxamine mesylate to MCF-7 human breast cancer cells
Authors: Xianpeng Jiang, Robert Elliott, Jonathan Head
Journal: Cancer Research (2008)

AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA

899 

Iron is an essential component of ribonucleotide reductase which is involved in DNA synthesis. There are a number of genes which regulate cellular iron homeostasis. Transferrin receptors and SLC11A2 (also known as DMT1, Nramp2 and DCT1) mediate iron uptake into cells. On the other hand, ferroportin (also known as SLC40A1, IREG1 and MTP1) transports intracellular iron out of cells. In the current study, we used quantitative RT-PCR to determine the mRNA expression of iron-regulator genes in the normal human mammary epithelial MCF-12A cell line and the breast cancer MCF-7 cell line. We found that MCF-7 breast cancer cells lose their expression of ferroportin, an iron exporter gene. To further study the role of ferroportin in breast cancer, we introduced a 1725bp cDNA including the whole ferroportin coding sequence into MCF-7 cells. A pTargetTM vector without the ferroportin gene was used as the control. Cells were treated with the iron chelator deferoxamine mesylate (DFOM) and cytotoxicity was measured by 3[H]-thymidine incorporation. Ferroportin-transfected MCF-7 cells express the mRNA of ferroportin, but parent MCF-7 cells and vector-transfected MCF-7 cells do not. Transfection does not significantly change the growth of the MCF-7 cells. When we treated cells with DFOM, ferroportin-transfected MCF-7 cells (IC50: 2.4µm, 72 hours of incubation) were more sensitive to DFOM than parent and vector-transfected MCF-7 cells (IC50s: 5.5µm and 6.1µm, respectively, 72 hours of incubation). In summary, breast cancer cells lose their expression of ferroportin (an iron exporter) and ferroportin gene transfection will increases the response of MCF-7 cells to the iron chelator DFOM.
National Shortages of Generic Sterile Injectable Drugs
Authors: Julie M. Donohue, Derek C. Angus
Journal: JAMA (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Antihypertensive therapy with ACE-inhibitors and clinical outcome in metastatic renal cell carcinoma (mRCC) patients.
Authors: Maristella Bianconi, Mario Scartozzi, Luca Faloppi, Riccardo Giampieri, Alessandro Bittoni, Michela Del Prete, Luca Cecchini, Luciano Burattini, Rodolfo Montironi, Stefano Cascinu
Journal: Journal of Clinical Oncology (2013)

e15536 Background: Preclinical and clinical reports in various solid tumours, such as HCC, showed a potential enhancement of anti-angiogenic effect of TKIs treatment by the concomitant use of ACE-inhibitors. On the other hand hypertension is a common side-effect with the use of such therapeutic approach with an improved efficacy profile suggested in these patients. However data in metastatic renal cell carcinoma patients are lacking. The aim of our analysis was to evaluate the correlation between incidental use of ACE-inhibitors and clinical outcome in mRCC patients receiving first-line TKIs. Methods: 102 patients were eligible for our analysis. All patients received a TKI as a first-line treatment. ACE-inhibitors therapy was initiated prior or during the TKI administration. Results: Median OS was 32.13 months. 21 (21%) patients received ACE-inhibitors, while 81 (79%) did not. The OS was 37.5 months for patients treated with concomitant ACE-inhibitors and 17.8 months for those without such a treatment (p=0,005). No significant differences were found with other antihypertensive treatments or for the clinical variables considered. Conclusions: In our analysis the incidental use of ACE-inhibitors represents a relevant factor for clinical outcome in mRCC patients. If confirmed in larger case series the use of antihypertensive treatment, particularly ACE-inhibitors, could be considered a stratification factor.
International comparison of androgen-deprivation therapy (ADT) for the treatment of nonmetastatic (M0) prostate cancer (PC).
Authors: Kirsty Hope, Alex Graham, Jorge Arellano, Alexander Liede
Journal: Journal of Clinical Oncology (2013)

e16040 Background: ADT represents standard of care for PC patients (pts) with signs of recurrence after primary therapy (tx). Nature and extent of ADT among M0 pts is not well-characterized, and nearly all ADT-treated pts relapse to develop castration-resistant PC (CRPC) after a median 18-24 months (mos) (Felici 2012). This physician survey quantifies ADT in populations with high or increasing incidence of M0 PC (Ferlay 2010). Methods: A 45-minute online survey was completed by urology and oncology practitioners (MDs) from 19 countries. Eligibility ensured MDs were responsible for tx decisions in the care of M0 PC, and had ≥10 pts on ADT. MDs were asked about tx at different points in the PC pathway, focusing on ADT (gonadotropin-releasing hormone [GnRH] or bilateral orchiectomy [bil orch]), type and duration of GnRH (intermittent vs. continuous), concurrent tx, and pts with CRPC (high risk CRPC definitions explored). Results: In total, 441 MDs completed the survey; predominantly urologists (88%). MDs had 98,689 PC pts under their care, 76,386 (77%) M0 PC. Of M0 PC, 38% received ADT: 37% (28104) GnRH (mainly leuprorelin [47%] or goserelin [21%]) and 1.6% (1251) bil orch (Table). The 34% tx rate reported by US MDs is consistent with decreasing ADT use (Shahinian 2010), whereas rates remain higher in Europe, particularly for Eastern European pts. Across regions, 74% (20,729) of GnRH pts received ≥6 mos, 48% (13,594) continuously; of these, 71% were expected to develop CRPC, 57% of CRPC were considered high risk for bone metastasis (BM). PSA doubling time ≤6 mos was most commonly cited high risk definition. Conclusions: These findings further our understanding of ADT use among M0 PC, which differs by country, by region, with highest rates reported in Europe. ADT rates have public health implications on the number of men expected to develop CRPC and be at high risk of BM in the future. [Table: see text]
Lymphopenia: Is it a prognostic factor in metastatic non-small cell lung cancer?
Authors: Zineb Benbrahim El Mekkeoui, Samia Arifi, Lamiae Amaadour, Naima Abda, Chakib Nejjari, Mellas Nawfel, Omar El Mesbahi
Journal: Journal of Clinical Oncology (2012)

e18124 Background: Lymphopenia is frequent in advanced cancers and predicts the toxicity of chemotherapy. It is known as a poor prognostic marker in solid tumors such as metastatic breast cancer and sarcomas. However, its impact on relapse and survival in metastatic non small cell lung cancer is unknown. The aim of our study was to establish the correlation between lymphopenia and survival (disease-free survival (DFS) and overall survival (OS)) in metastatic non small cell lung cancer. Methods: We reviewed retrospectively 115 cases of metastatic non small cell lung carcinomas diagnosed between January 2007 to June 2011 at the Medical Oncology Department at Hassan II University Hospital. Complete blood counts were performed at the time of diagnosis and prior to treatment. Lymphopenia was defined as an absolute lymphocyte count (ALC) &lt; 1000 /µL. We used the Kaplan-Meier method and Cox model to estimate OS and DFS. Results: Median age was 57 ± 10 years. 83.5% of patients were men. 81% of patients were treated with platinum based chemotherapy. Twelve patients (13%) had a low ALC at diagnosis with a mean of 854 (± 100)/µL. Lymphopenia was frequent in men patients (p=0.03) and non squamous cell carcinomas (p= 0.04). However, it was not correlated to age, performance status, body mass index, number of metastatic sites involved, pleural effusion, liver metastasis, hypercalcemia, anemia and hypoalbuminemia. The median duration of follow-up was 7.4 months (range: 1-99 months). In the univariate analysis, the medians of OS and DFS were shorter but not significantly different in lymphopenic patients (OS: 7.5 versus 9 months p= 0.07 and DFS: 5 versus 6 months p= 0.12). In multivariate analysis, lymphopenia was not significantly associated with OS and DFS. Conclusions: In this study, the association between lymphopenia and unfavorable OS and DFS was not clearly demonstrated in patients with metastatic non small cell lung carcinoma. Prospective clinical trials are needed to confirm or deny the prognostic role of lymphopenia in this cancer.