tbuckley/cabot-search huggingface dataset:
Frequency of histopathologic types of soft tissue sarcoma (STS) reported from a large community-based hospital over a 20 year period
Authors: S. G. Nair, C. H. Amadio, M. Scarlato, D. A. Forman
Journal: Journal of Clinical Oncology (2006)

19507 Background: Soft Tissue Sarcomas (STS) are rare tumors primarily of mesenchymal origin. The World Health Organization recognizes more than 50 subtypes of STS. Previously reported frequencies of histopathologic types of STS come from a handful of large cancer centers. The incidence of tumor types seen at large cancer treatment centers do not necessarily reflect the histologies seen at community hospitals. We sought to determine the frequency of histopathologic types of adult STS seen at our large community-based hospital. Methods: We performed a search of our tumor registry from the year 1984 through 2004 looking for histologic types of non-GIST STS involving the peripheral nervous system, autonomic nervous system, retroperitoneum, peritoneum, other connective and soft tissue locations. Our tumor registry is certified through the American College of Surgeons. Our pathologist are board certified, highly skilled, and commonly refer pathologic specimens for second opinion if a histologic diagnosis is in doubt. The 10 most common histologies diagnosed are reported. Results: Our hospital diagnosed and treated 250 STS over this 20 year period. The histologic type of sarcoma by number and percent of total cases is as follows: Malignant fibrous histiocytoma 60 (24%), Liposarcoma 51 (20%), Leiomyosarcoma 38(15%), Sarcoma N.O.S. 18(7%), Hemangiosarcoma 15 (6%), Synovial Sarcoma 10 (4%), Rhabdomyosarcoma 9 (4%), Fibrosarcoma 9 (4%), Spindle Cell Sarcoma 7 (3%), and Giant Cell Sarcoma 3 (3%). Conclusions: The frequency of the most common histologic types of soft tissue sarcoma seen at our community hospital is quite consistent with that previously reported in the literature from large referral-based cancer centers. There does not appear to be an influence of selection bias in previous reports of relative frequency of histopathologic types of STS. No significant financial relationships to disclose.
Clodronate compared to ibandronate breast cancer bone metastases patient preference study
Authors: S. Jagdev, H. Berry, A. Newsham, A. Smith, L. Flanagan, T. Perren, D. Dodwell, G. Velikova
Journal: Journal of Clinical Oncology (2007)

1068 Background: The use of bisphosphonates for patients with breast cancer bone metastases confers significant benefits. Prolonged IV bisphosphonate use burdens both patients and services and oral clodronate is often used. Ibandronate is a potent oral third generation bisphosphonate which is effective and well tolerated in patients with metastastic breast cancer. In Phase III studies, the incidence of adverse events for oral ibandronate was similar to placebo. Clodronate requires prolonged fasting and size of tablets and gastric irritation may be problematic, therefore ibandronate may provide advantages. The aim of this study was to investigate patients’ preferences between oral ibandronate and oral clodronate and to assess the reasons for preference. Methods: This randomised, open-label, cross-over study recruited 46 women with breast cancer bone metastases who were starting or established on IV bisphosphonates. Patients were randomised to receive one drug for two months then crossed over to the second for two months. 23 patients received ibandronate then clodronate and 23 received clodronate first. Patients completed questionnaires on pain and symptoms at baseline, at crossover and on completion of the study. Patient preferences were assessed at the end of the study. Results: Data on 41 patients were available for preference assessment in this initial analysis. 5 patients discontinued the study. 26/41 patients preferred ibandronate (63.4%) and 14/41 preferred clodronate (34.5%) (c2=3.10, p=0.078). 1 patient did not state a preference. Significantly more patients receiving ibandronate first preferred ibandronate (13/18), compared with those receiving clodronate first expressing a preference for clodronate (10/23) (c2 =6.44, p= 0.011). Tablet size (p=0.001) and number (p&lt;0.001) scored highly as reasons for preference for ibandronate. The following toxicities were reported on ibandronate and clodronate respectively: nausea (17%, 9.7%), indigestion (9.7%, 4.8%) and pain flare (7.3%, 4.8%). Conclusions: Significantly more patients preferred oral ibandronate compared with oral clodronate, with size and number of tablets being important reasons for preference. No significant financial relationships to disclose.
ACTB-1003: An oral kinase inhibitor targeting cancer mutations (FGFR), angiogenesis (VEGFR2, TEK), and induction of apoptosis (RSK and p70S6K).
Authors: K. Patel, A. Fattaey, A. Burd
Journal: Journal of Clinical Oncology (2010)

e13665 Background: ACTB-1003 is an oral kinase inhibitor targeting cancer mutations (FGFR inhibition), angiogenesis (inhibition of VEGFR2 and Tie-2) and induces apoptosis (targeting RSK and p70S6K, downstream of PI3 kinase). The multi-activity of ACTB- 1003 translates to in vivo efficacy with dose-dependent tumor growth inhibition in a variety of histological cancers including lung, breast and colorectal. Results: ACTB-1003 is an oral kinase inhibitor with multiple modes of action, targeting cancer mutations via FGFR inhibition FGFR1 (IC50=6 nM), angiogenesis through inhibition of VEGFR2 (2 nM), Tie-2 (4 nM), and induces apoptosis likely by targeting RSK (5 nM) and p70S6K (32 nM). ACTB-1003 is highly active with dose-dependent tumor growth inhibition in cell lines with FGFR genetic alterations - OPM2 human multiple myeloma and the murine leukemia Ba/F3-TEL-FGFR1. OPM2 cells harbor the FGFR3 t(4:14) translocation, FGFR3 K650E mutation and PTEN deletion while the Ba/F3-TEL-FGFR1 cells are driven by FGFR1 over-expression. The in vivo mechanism of action studies demonstrated inhibition of RSK and p70S6K kinases coupled to the induction of apoptosis (PARP, TUNEL) in the H460 in vivo tumors. Additionally, ACTB-1003 is shown to inhibit tumor angiogenesis evident by the inhibition of CD31 staining in tumor sections. ACTB-1003 is combinable with 5- FU or paclitaxel without diminishing the activity or increasing the toxicity of these chemotherapy agents in the HCT-116 colon tumor xenograft model. Conclusions: ACTB-1003 is an orally active kinase inhibitor that exhibits potent, low nM activity targeting mutations via FGFR inhibition, inhibition of angiogensis and induction of apoptosis. This creates the potential for additive or synergistic antitumor efficacy that can be achieved not only within each pathway but across multiple pathways with one drug. These results support the clinical testing of ACTB-1003 in the increasing number of tumor types characterized by alterations in FGF receptors. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration ACT Biotech ACT Biotech ACT Biotech
The Disappearance of Sudden Infant Death Syndrome
Authors: Ernest Cutz
Journal: JAMA Pediatrics (2016)

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 Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast 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 Pediatrics journal
Herpesvirus saimiri: Enhancement of Adenovirus-Associated Virus
Authors: Raphael Dolin, Alan S. Rabson
Journal: JNCI Journal of the National Cancer Institute (1973)

Herpesvirus saimiri provided incomplete helper function(s) for adenovirus-associated virus (AAV) in MLC-1 cells, a continuous marmoset lymphoid cell line. AAV fluorescent-stainable antigen was formedl but no infectious AAV was produced. The partial helper function of the oncogenic H. saimiri for AAV appears similar to that provided by human herpesviruses.
Cystine Deprivation Triggers Programmed Necrosis in VHL-Deficient Renal Cell Carcinomas
Authors: Xiaohu Tang, Jianli Wu, Chien-Kuang Ding, Min Lu, Melissa M. Keenan, Chao-Chieh Lin, Chih-An Lin, Charles C. Wang, Daniel George, David S. Hsu, Jen-Tsan Chi
Journal: Cancer Research (2016)

Abstract Oncogenic transformation may reprogram tumor metabolism and render cancer cells addicted to extracellular nutrients. Deprivation of these nutrients may therefore represent a therapeutic opportunity, but predicting which nutrients cancer cells become addicted remains difficult. Here, we performed a nutrigenetic screen to determine the phenotypes of isogenic pairs of clear cell renal cancer cells (ccRCC), with or without VHL, upon the deprivation of individual amino acids. We found that cystine deprivation triggered rapid programmed necrosis in VHL-deficient cell lines and primary ccRCC tumor cells, but not in VHL-restored counterparts. Blocking cystine uptake significantly delayed xenograft growth of ccRCC. Importantly, cystine deprivation triggered similar metabolic changes regardless of VHL status, suggesting that metabolic responses alone are not sufficient to explain the observed distinct fates of VHL-deficient and restored cells. Instead, we found that increased levels of TNFα associated with VHL loss forced VHL-deficient cells to rely on intact RIPK1 to inhibit apoptosis. However, the preexisting elevation in TNFα expression rendered VHL-deficient cells susceptible to necrosis triggered by cystine deprivation. We further determined that reciprocal amplification of the Src–p38 (MAPK14)–Noxa (PMAIP1) signaling and TNFα–RIP1/3 (RIPK1/RIPK3)–MLKL necrosis pathways potentiated cystine-deprived necrosis. Together, our findings reveal that cystine deprivation in VHL-deficient RCCs presents an attractive therapeutic opportunity that may bypass the apoptosis-evading mechanisms characteristic of drug-resistant tumor cells. Cancer Res; 76(7); 1892–903. ©2016 AACR.
Leukocyte Migration Inhibition and Lymphocyte Blastogenesis Responses in Breast Carcinoma Patients to Mouse Mammary Tumor Virus and to Virion gp52 Antigen and Rauscher Murine Leukemia Virus-Kirsten Sarcoma Virus gp69/71 Antigen
Authors: J. L. McCoy, J. H. Dean, G. B. Cannon, L. J. Jerome, T. C. Alford, W. P. Parks, R. V. Gilden, S. T. Oroszlan, R. B. Herberman
Journal: JNCI Journal of the National Cancer Institute (1978)
Clinical Resistance To Ruxolitinib Is More Frequent In Patients Without MPN-Associated Mutations and Is Rarely Due To Mutations In The JAK2 Kinase Drug-Binding Domain
Authors: Annalisa Andreoli, Emmanuelle Verger, Marie Robin, Emmanuel Raffoux, Jean-Marc Zini, Philippe Rousselot, Gérard Socié, Delphine Rea, Nathalie Parquet, Stephane Giraudier, Christine Chomienne, Bruno Cassinat, Jean-Jacques Kiladjian
Journal: Blood (2013)
Urinary TMPRSS2: Use of ERG and PCA3 to predict tumor volume and Gleason grade in an active surveillance cohort—Results from the Canary/EDRN Prostate Active Surveillance Study.
Authors: Daniel W. Lin, Lisa F Newcomb, Elissa C Brown, James D Brooks, Peter Carroll, Ziding Feng, Martin E. Gleave, Ray Lance, Martin G. Sanda, Ian Murchie Thompson, John Wei, Peter Nelson
Journal: Journal of Clinical Oncology (2012)

2 Background: Active surveillance is an increasing alternative for the management of low risk prostate cancer; however, there is a crucial need for better biomarkers to distinguish men with indolent versus aggressive disease. Both PCA3 and TMRPSS2-ERG (T2-ERG) are biomarkers that show promise in that they may be associated with more aggressive disease. This study examines the correlation of these biomarkers with higher volume or grade cancer in an active surveillance cohort. Methods: Post-DRE urine was collected prospectively as part of the multi-institutional Canary/EDRN Prostate Active Surveillance Study (PASS). PCA3 and T2-ERG levels were analyzed in urine collected from 401 men at study entry. Many of the men had undergone previous biopsies after initial prostate cancer diagnosis, and 20% of the urine specimens were associated with a negative serial biopsy. Biomarker scores were correlated to clinical and pathologic variables, including tumor volume - measured by percent of biopsy core involvement - and Gleason score, using non-parametric and univariate analyses. Results: Both PCA3 and T2-ERG scores were significantly associated with higher volume disease. For negative repeat biopsy, 1-10%, 11-34%, &gt;34% positive cores, median (95% CI) PCA3 scores were 27 (24-31), 26 (22-33), 40 (29-51), 47 (26-90), p = 0.003 [Kruskal Wallis test (KW)], and median T2-ERG scores were 5 (2-8), 9 (4-14), 21 (14-40), 23 (4-115), p &lt; 0.0001 (KW). Both PCA3 and T2-ERG scores were also significantly associated with presence of higher grade disease. For negative biopsy, Gleason 5 - 6, and Gleason &gt;7, the median PCA3 scores were 27 (24-31), 31 (27-35), 48 (31-92), p = 0.02 (KW), and median T2-ERG scores were 5 (2-8), 14 (9-18), 29 (13-78), p = 0.001 (KW). The odds ratio for a positive biopsy versus a negative biopsy (ref) on modeling was 1.37 (1.04-1.81), p = 0.02 for PCA3 and 1.30 (1.12-1.51), p = 0.0006 for T2-ERG. Conclusions: Both PCA3 and T2-ERG appear to stratify risk, for men on active surveillance, of having aggressive cancer as defined by tumor volume or Gleason score and may have clinical applicability in selecting men with low volume/low grade disease for active surveillance.
Outcome of Allogeneic Hematopoietic Stem Cell Transplantation in Aplastic Anemia: A Comparison of 3 Conditioning Regimens in 202 Consecutive Cases
Authors: Parvez Ahmed, Qamar Un Nisa Chaudhry, Syed Karman Mahmood, Tariq Mahmood Satti, Mehreen Ali Khan, Nighat Shahbaz, Humayoon Shafique Satti
Journal: Blood (2014)
Exploring a fiscal food policy: the case of diet and ischaemic heart disease Commentary: Alternative nutrition outcomes using a fiscal food policy
Authors: T. Marshall
Journal: BMJ (2000)

# Exploring a fiscal food policy: the case of diet and ischaemic heart disease {#article-title-2} Diet determines cholesterol concentrations, and cholesterol concentrations determine the prevalence of ischaemic heart disease. This paper explores the potential effects of fiscal measures on diet and ischaemic heart disease. There is a clear economic rationale for this approach: the correction of market failure caused by externalities. Externalities are said to occur when some of the costs of consumption are not borne by the consumer. When ischaemic heart disease strikes, there are costs to the community (productivity losses or indirect costs) and to the health service (direct costs). A case can therefore be made for using taxation to compensate for the external costs of an atherogenic diet. #### Summary points Current dietary patterns are partly responsible for the high risk of ischaemic heart disease in Britain, in particular among low income groups; these dietary patterns are reinforced by the material constraints of poverty Pricing of foodstuffs encourages the purchase and consumption of a cholesterol raising diet, particularly among people with tight food budgets By extending value added tax to the main sources of dietary saturated fat, between 900 and 1000 premature deaths a year might be avoided The additional tax revenue could finance compensatory measures to raise income for low income groups Econometric and health policy research should investigate the effects of price changes on diet and health The relation between diet, serum cholesterol concentrations, and ischaemic heart disease is relatively well understood. In individuals, serum cholesterol concentrations—or more specifically, the ratio of low density lipoprotein to high density lipoprotein—are a major determinant of the risk of ischaemic heart disease. Serum cholesterol concentrations are largely determined by the proportion of dietary energy derived from saturated or polyunsaturated fats and by dietary intake of cholesterol. The Keys equation (box), which has recently been corroborated, describes this in a simple mathematical relationship.1 3 #### The Keys equation Change in … Correspondence to: E Kennedy
Adjuvant low-dose interleukin-2 (IL2) plus interferone-alpha (IFN) in operable renal cell cancer (RCC). A phase III, randomized, multicenter, independent trial of the Italian Oncology Group for Clinical Research (GOIRC)
Authors: R. Passalacqua, C. Buzio, S. Buti, R. Labianca, C. Porta, C. Boni, E. Rondini, R. Camisa, R. Sabbatini, F. Artioli, C. Caminiti
Journal: Journal of Clinical Oncology (2007)

LBA5028 Background: For pts with non-metastatic RCC, no standard adjuvant treatment exists. Immunotherapy (IT) using IFN and/or IL2 is effective in metastatic disease setting. Low and chronically repeated doses of IL2 plus IFN induce a persistent stimulation of the immune system with no relevant toxicity. Methods: From July1994 to March 2006, surgically treated RCC pts were randomized to the following arms: A) low-dose IT; B) control arm. IT consisted of a 4-week cycle of s.c. IL2 (5 days/wk, 1 million UI/sqm bid d 1,2 and 1 million UI/sqm × 1 d 3,4,5) + IFN (1,8 million UI/sqm d 3,5 of each week). Cycles were repeated every 4 months for the first 2 years and every 6 months for the remaining 3 years. Each patient received 12 cycles in 5 years. Inclusion criteria were as follows: histological diagnosis of RCC, age &lt;75 yrs, radical or partial nephrectomy within the past 3 months, pT 1 (diameter of T &gt; 2,5 cm), T 2 , T 3 a-b-c; pN0-pN3, M0; good cardiac and renal function and no autoimmune disease. Based on a planned sample size of 320 pts, the trial was designed to have a 80% power to detect a 15% improvement in 5-year survival. Results: A total of 310 pts were randomized: 157 on arm A, 153 on arm B. Pts characteristics were well balanced between the two arms. At a median follow-up of 52 months, 77 pts relapsed: 35 in arm A and 42 in arm B. In the first 5 years of observation, disease free survival (DFS) curves were similar in the two arms, but diverged thereafter. DFS at 5 and 10 years was 0.73 and 0.73 in arm A vs 0.73 and 0.60 in arm B with an estimated Hazard Ratio (HR) of 0.84 (95% CI: 0.54–1.33 p=0.47). Efficacy of IT was more evident in patients with good PS (HR 0.78; 0.47–1.30 p=0.35); age&lt;60 yrs (HR 0.61; 0.31–1.19 p=0.15), and low tumor grade (HR 0.70; 0.38–1.27 p=0.24). As for overall survival, 59 deaths were observed with no differences between the two arms. Toxicity was mild and limited to WHO grade 1 or 2 in the majority of cases. Conclusions: Low-dose adjuvant IL2+IFN is feasible in RCC and seems to reduce the risk of recurrence after 5 years from diagnosis. Follow-up update is still ongoing. No significant financial relationships to disclose.
Efficacy and safety of farletuzumab, a humanized monoclonal antibody to folate receptor alpha, in platinum-sensitive relapsed ovarian cancer subjects: Final data from a multicenter phase II study.
Authors: A. J. White, R. L. Coleman, D. K. Armstrong, D. Glenn, A. Bicher, D. A. Richards, A. Schneeweiss, L. J. Old, C. Schweizer, S. Weil
Journal: Journal of Clinical Oncology (2010)

5001 Background: Farletuzumab (MORAb-003) is a humanized monoclonal antibody to folate receptor alpha, which is overexpressed in most epithelial ovarian cancers (EOC), but largely absent on normal tissue. The phase I study showed signs of activity and did not reach an MTD. Methods: 54 subjects with platinum-sensitive EOC in first relapse received weekly farletuzumab either as single agent (SA) or in combination with carboplatin (AUC 5-6) and taxane (P/T) q 21 days for 6 cycles, followed by farletuzumab maintenance. 28 subjects with asymptomatic CA125 relapse received SA farletuzumab. Subjects could receive P/T plus farletuzumab after SA. 26 subjects with symptomatic relapse entered the combination arm directly and 21 subjects entered after SA. Primary endpoints were normalization of CA125 and Objective Response Rate. Duration of each subject's second response was compared to the duration of their own first response. Results: Farletuzumab was well-tolerated as SA as well as without additive toxicity to P/T. Preliminary data show that of the 44 evaluable subjects who received farletuzumab with P/T, 89% normalized CA-125. In 9/44 (21%) treated subjects, the second remission has been equal to, or longer, than the first remission. There was an unexpectedly high response rate among subjects with a first progression-free interval of <12 months, comparable to that in subjects with a first progression-free interval of >12 months (Table). Conclusions: Preliminary data for this study indicated that farletuzumab with P/T significantly increases objective response rate compared to historic data for P/T alone in platinum-sensitive first-relapsed ovarian cancer subjects and increases the duration of second remission compared to first remission. Combination therapy: Response by length of first progression-free interval First progression-free interval <12 months (n=12) ≥12 months (n=32) CA125 normalization 92% 84% RECIST responder (CR + PR) 64% 71% RECIST patient benefit (CR + PR + SD) 100% 90% Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Morphotek Morphotek Morphotek Morphotek