tbuckley/cabot-search huggingface dataset:
Immediate Sequential Bilateral Pediatric Vitreoretinal Surgery
Authors: Yoshihiro Yonekawa, Wei-Chi Wu, Shunji Kusaka, Joshua Robinson, Daishi Tsujioka, Kai B. Kang, Michael J. Shapiro, Tapas R. Padhi, Lubhani Jain, Jonathan E. Sears, Ajay E. Kuriyan, Audina M. Berrocal, Polly A. Quiram, Amanda E. Gerber, R.V. Paul Chan, Karyn E. Jonas, Sui Chien Wong, C.K. Patel, Ashkan M. Abbey, Rand Spencer, Michael P. Blair, Emmanuel Y. Chang, Thanos D. Papakostas, Demetrios G. Vavvas, Robert A. Sisk, Philip J. Ferrone, Robert H. Henderson, Karl R. Olsen, M. Elizabeth Hartnett, Felix Y. Chau, Shizuo Mukai, Timothy G. Murray, Benjamin J. Thomas, P. Anthony Meza, Kimberly A. Drenser, Michael T. Trese, Antonio Capone
Journal: Ophthalmology (2016)
Toxicity of fluorouracil in patients with advanced colorectal cancer: effect of administration schedule and prognostic factors. Meta-Analysis Group In Cancer.
Authors: E Lévy, P Piedbois, M Buyse, J P Pignon, P Rougier, L Ryan, R Hansen, B Zee, B Weinerman, J Pater, C Leichman, J Macdonald, J Benedetti, J Lokich, J Fryer, G Brufman, R Isacson, A Laplanche, E Quinaux, P Thirion
Journal: Journal of Clinical Oncology (1998)

PURPOSE Fluorouracil (5-FU) continuous infusion is superior to 5-FU bolus in patients with advanced colorectal cancer, but the survival difference between the two treatments is small and, therefore, the difference in toxicity profile is crucial in choosing a treatment for individual patients. MATERIALS AND METHODS We conducted a meta-analysis of all randomized trials that compared 5-FU bolus with 5-FU CI, based on individual data from 1,219 patients, to compare the toxicity of the two schedules of 5-FU administration and to identify predictive factors for toxicity. The toxicities considered were World Health Organization (WHO) grade 3 to 4 anemia, thrombopenia, leukopenia, neutropenia, nausea/vomiting, diarrhea, mucositis, and hand-foot syndrome. RESULTS Hematologic toxicity, mainly neutropenia, was more frequent with 5-FU bolus than with 5-FU CI (31% and 4%, respectively; P &lt; .0001). Hand-foot syndrome was less frequent with 5-FU bolus than with 5-FU CI (13% and 34%, respectively; P &lt; .0001). There was no difference between the two treatment groups in terms of other nonhematologic toxicities. Independent prognostic factors were age, sex, and performance status for nonhematologic toxicities, performance status, and treatment for hematologic toxicities, and age, sex, and treatment for hand-foot syndrome. CONCLUSION Based on a large data set, this study confirmed and quantified the toxicity profile of the two schedules of administration of 5-FU and allowed the identification of clinical predictors of toxicity.
Abstract IA06: Regulation of BRCA1- and BRCA2-dependent DNA repair.
Authors: Daniel Durocher
Journal: Clinical Cancer Research (2016)

Abstract High-grade serous epithelial ovarian cancers are strongly associated with defective homologous recombination (HR), a DNA repair pathway involved in the mending of DNA double-strand breaks (DSB) and in which the BRCA1, PALB2 and BRCA2 tumor suppressors play key roles. In late December last year, the first poly(ADP-ribose) polymerase (PARP) inhibitor, lynparza or olaparib as it is widely known was approved in Europe and in the US for the treatment of ovarian cancer in tumors with deleterious mutations in the BRCA1 and BRCA2 genes. The approval of olaparib marks a milestone in the development of targeted cancer therapies, as it is the first approved drug that is based on the concept of synthetic lethality. In my presentation, I will report the identification of a system that licenses the assembly of a BRCA1-PALB2-BRCA2 complex in the S and G2 phases of the cell cycle. This system plays a major role in restricting the activation of DNA repair by HR to these cell cycle phases and I will discuss the implication of this newly discovered regulatory pathway to our understanding of genome maintenance and PARP inhibitor therapy. Citation Format: Daniel Durocher. Regulation of BRCA1- and BRCA2-dependent DNA repair. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr IA06.
Phase II study of neoadjuvant docetaxel and androgen suppression (AS) plus radiation therapy (RT) for high-risk localized prostate cancer (HRLCaP)
Authors: M. R. McKenzie, K. N. Chi, A. Neville, S. Ellard, B. Baerg, D. Ruether, E. Winquist, R. Segal, H. Lukka
Journal: Journal of Clinical Oncology (2006)

4631 Background: Docetaxel increases survival in hormone-refractory prostate cancer and is active in hormone-sensitive disease. In HRLCaP, improvement upon AS plus RT is required, as many patients eventually develop metastases. This trial’s objective was to assess the tolerability of neoadjuvant docetaxel plus AS and RT in men with HRLCaP. Methods: Fifty-four men with newly diagnosed previously untreated HRLCaP were accrued to a Phase II single-arm, 2-stage, open-label study involving 7 Canadian centres. All were to receive 3 years of AS (LHRH-agonist + antiandrogen for 4 weeks). Chemotherapy started week 5. Twenty-four men received docetaxel 35 mg m 2 iv weekly × 6 q8 weeks for 2 cycles, RT starting week 25. After protocol revision, 30 men received docetaxel 75 mg m 2 iv q3 weekly for 4 cycles, RT starting week 21. The primary endpoint was unacceptable toxicity (UT), defined as ≥Grade 3 non-hematologic toxicity (except nausea/vomiting, tearing, short-term fatigue, and easily-controlled diarrhea), grade 4 thrombocytopenia, grade 4 neutropenia lasting &gt;7 days, febrile neutropenia, or toxicity-related RT change (delay&gt;2 weeks, &gt;25% dose reduction). Results: Median age was 68 (49–79) years. Median iPSA was 19.15 (2.8–138) μg/L. Gleason Score and T-stage were ≥8 and ≥T3a in 70.4% and 42.6%, respectively. All patients have completed RT. Adverse events were as expected for docetaxel. UT occurred in 8 patients (14.8%), including 5 with qweekly docetaxel (Grade 3 acute RT-related genitourinary toxicity - 3, Grade 3 docetaxel hypersensitivity - 1, Grade 3 fatigue &gt;2 weeks - 1) and 3 with q3 weekly docetaxel (Grade 3 acute RT-related genitourinary toxicity - 1, febrile neutropenia - 1, Grade 4 neutropenia &gt;7 days - 1). The following table summarizes PSA response to neoadjuvant treatment. Conclusions: Neoadjuvant AS and docetaxel plus RT in men with HRLCaP appeared well tolerated. Patients will be followed for other outcomes. This approach will be tested in a phase 3 trial. [Table: see text] No significant financial relationships to disclose.
Risk of Premature Cardiovascular Disease vs the Number of Premature Cardiovascular Events
Authors: Allan D. Sniderman, George Thanassoulis, Ken Williams, Michael Pencina
Journal: JAMA Cardiology (2016)

Discussion | In women with signs and symptoms of ischemia and nonobstructive CAD, those with prior infarct had a 2.84-fold increased risk of death for up to 8.5 years of follow-up.Ischemia on stress testing was not associated with an increase in risk of mortality in this population of women.Our results may not be generalizable to nonangiographic populations of women or to men.A second limitation is that our classification of women is based on a mixture of stress testing results with different sensitivity and specificity for ischemia and/or infarct.Our findings underscore the need for heightened recognition of an adverse event profile in these women.
Screening for Abdominal Aortic Aneurysm: Recommendation Statement
Journal: Annals of Internal Medicine (2005)

This statement summarizes the U.S. Preventive Services Task Force (USPSTF) recommendations on screening for abdominal aortic aneurysm and the supporting scientific evidence and updates the 1996 recommendations on this topic. The complete information on which this statement is based, including evidence tables and references, is available in the accompanying article in this issue and in the evidence synthesis on this topic, which is available on the USPSTF Web site (www.preventiveservices.ahrq.gov). *For a list of the members of the U.S. Preventive Services Task Force, see the Appendix.
Abstract P1-05-02: The N-terminus of Twist1 is responsible for interacting with transcriptional repressors to promote EMT and metastasis of breast cancer cells
Authors: X Yu, T He, J Xu
Journal: Cancer Research (2016)

Abstract Twist1, a basic helix-loop-helix transcription factor, plays a key role to mediate epithelial-mesenchymal transition (EMT) and promote breast cancer metastasis. However, knowledge about Twist1 structure-function relationships to cancer-related phenotypes is limited. Therefore, we studied the requirement of Twist1 N-terminus in Twist1-dependent breast cancer metastasis. We showed that the amino-terminus of Twist1 was the dominant negative mutant of Twist1. Overexpression of Twist1 N-terminus exhibited different cell morphology and motility in vitro. Inoculation of Twist1 N-terminus overexpression cells into SCID mice showed delayed tumor formation and reduced lung metastasis. Furthermore, Twist1 N-terminus overexpression induced expression change of EMT markers, including E-cadherin, β-catenin, vimentin and Twist1 both in vivo and in vitro. Co-immunoprecipitation and mass spectrometry revealed that Twist1 N-terminus interacted with several members of the Mi2/nucleosome remodeling and deacetylase (Mi2/NuRD) complex, HDAC2, 3 and 7, MTA1 and 2, RbAp46/48, and many corepressors including NCoR1 and 2, which released them from the proximal region of E-cadherin promoter for transcriptional activation. These data suggest that Twist1 N-terminus is required for Twist1-mediated transcriptional programs and breast cancer metastasis. Citation Format: Yu X, He T, Xu J. The N-terminus of Twist1 is responsible for interacting with transcriptional repressors to promote EMT and metastasis of breast cancer cells. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P1-05-02.
Prognostic Significance of Beta-2 Microglobulin in Patients with Diffuse Large B Cell Lymphoma in Rituximab Era
Authors: Seyoung Seo, Dok Hyun Yoon, Changhoon Yoo, Yumun Jeong, Ji Hyun Park, Shin Kim, Jooryung Huh, Cheolwon Suh
Journal: Blood (2014)
Immunological Studies With Nucleoproteins From Tissue-Culture Cells. II. Nucleoproteins From HeLa and H.Ep #1 Cells2
Authors: Vittorio Defendi, John S. Colter
Journal: JNCI Journal of the National Cancer Institute (1959)

Antiserums prepared in the rabbit against the nucleoprotein fractions deoxyribonucleoprotein (DNP) and ribonucleoprotein (RNP), which were isolated from HeLa and H.Ep #1 cells, were tested for their effect on 29 tissue-culture cell lines. In the presence of complement, the antiserums produced destruction of homologous and many heterologous cell lines. At higher dilutions the antiserums were shown to cause agglutination of cells without any marked cytopathology. DNP and RNP were found to have similar spectra of activity. However, quantitative studies of the rate of cell destruction by the antiserums revealed an initial lag period in the DNP antiserums—a lag not generally seen with the RNP antiserums. Cytotoxic indexes were calculated for a number of antiserum-cell pairs and showed that the toxicity of any particular serum was higher for the homologous line than for susceptible heterologous lines. Vulnerability of the cells to the toxic action of the antiserums was not related to the stated species, organ, malignancy, or nonmalignancy of the tissue of origin. The tissue-culture cell lines examined could be divided into two broad groups: (1) those sensitive to HeLa and H.Ep #1 antiserums, with epitheliallike characteristics, and (2) those sensitive to MCN antiserums, with fibroblast-like morphology. No cell line was affected by both groups of antiserums, though two lines were shown to be unaffected by either. Many of the cell lines in group 1, but none in group 2, have been shown to be capable of supporting the growth of poliomyelitis virus.
Abstract B45: Characterization of human fallopian tube epithelial stem-like cells.
Authors: Dah-Ching Ding, Tang-Yuan Chu
Journal: Clinical Cancer Research (2016)

Abstract Purpose: Recent studies have suggested a large part of ovarian high grade serous carcinomas arise from the fallopian tube epithelium (FTE). The purpose of this study was to derive the stem-like cells of fallopian tube epithelium (FTESC). Results: Immunohistochemistry of human fallopian tube revealed expression of Pax8 in secretory cells, Tubb4 in ciliated cells and Epcam in all the epithelial cells, whereas Lgr5 was expressed in a small subset of cells in the epithelial layer. The presumed FTESC were cultured from the fallopian tube fimbria epithelium exhibiting a cuboidal cell morphology and could be maintained at a constant proliferation rate up to P9. When cultured on matrigel, these cells formed spheroids with Pax8, Tubb4 and Lgr5 expression. Flowcytometry revealed decreasing expression of EpCAM, CD73, CD133 and CD105, and increasing of Pax 8 secretory cell marker (87% in P6, 78% in P3) with the advance of passage. Adding of estrogen to the culture resulted in an enlargement of cell body (4 nM) and differentiation toward ciliated cells (400 nM). When these FTESC were cultured on the mouse embryonic fibroblast feeder, or mixe-cultured with fallopian tube stromal cells and HUVECs, they formed tubal-like structures mimicking the fallopian tube. Conclusion: We successfully derived a presumed FTESC with self-renewal and differentiation capability. These cells may provide new insight to investigate how FTE regenerate, respond to hormone and ROS injury and subjected to cancer initiation. Citation Format: Dah-Ching Ding, Tang-Yuan Chu. Characterization of human fallopian tube epithelial stem-like cells. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr B45.
Eye on the B-ALL: B-cell receptor repertoires reveal persistence of numerous B-lymphoblastic leukemia subclones from diagnosis to relapse
Authors: R J M Bashford-Rogers, K A Nicolaou, J Bartram, N J Goulden, L Loizou, L Koumas, J Chi, M Hubank, P Kellam, P A Costeas, G S Vassiliou
Journal: Leukemia (2016)

The strongest predictor of relapse in B-cell acute lymphoblastic leukemia (B-ALL) is the level of persistence of tumor cells after initial therapy. The high mutation rate of the B-cell receptor (BCR) locus allows high-resolution tracking of the architecture, evolution and clonal dynamics of B-ALL. Using longitudinal BCR repertoire sequencing, we find that the BCR undergoes an unexpectedly high level of clonal diversification in B-ALL cells through both somatic hypermutation and secondary rearrangements, which can be used for tracking the subclonal composition of the disease and detect minimal residual disease with unprecedented sensitivity. We go on to investigate clonal dynamics of B-ALL using BCR phylogenetic analyses of paired diagnosis-relapse samples and find that large numbers of small leukemic subclones present at diagnosis re-emerge at relapse alongside a dominant clone. Our findings suggest that in all informative relapsed patients, the survival of large numbers of clonogenic cells beyond initial chemotherapy is a surrogate for inherent partial chemoresistance or inadequate therapy, providing an increased opportunity for subsequent emergence of fully resistant clones. These results frame early cytoreduction as an important determinant of long-term outcome.
Reply to Yu-Wen Hu's Letter to the Editor re: William C. Jackson, Matthew J. Schipper, Skyler B. Johnson, et al. Duration of Androgen Deprivation Therapy Influences Outcomes for Patients Receiving Radiation Therapy Following Radical Prostatectomy. Eur Urol 2016;69:50–7
Authors: William C. Jackson, Matthew J. Schipper, Felix Y. Feng
Journal: European Urology (2016)
A Review of the Cancer Control Problem&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/xref&gt;
Authors: John R. Heller, M. D.
Journal: JNCI Journal of the National Cancer Institute (1952)

Journal Article A Review of the Cancer Control Problem Get access John R. Heller, M. D. John R. Heller, M. D. National Cancer Institute2Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 13, Issue 3, December 1952, Pages 577–589, https://doi.org/10.1093/jnci/13.3.577 Published: 01 December 1952
First-in-human application of the novel hepatitis B and hepatitis D virus entry inhibitor myrcludex B
Authors: Antje Blank, Christoph Markert, Nicolas Hohmann, Alexandra Carls, Gerd Mikus, Thorsten Lehr, Alexander Alexandrov, Mathias Haag, Matthias Schwab, Stephan Urban, Walter E. Haefeli
Journal: Journal of Hepatology (2016)
Seroreactivity to an Envelope Protein of Human T-Cell Leukemia/Lymphoma Virus in Patients With CD3− (Natural Killer) Lymphoproliferative Disease of Granular Lymphocytes
Authors: Thomas P. Loughran, Kenneth G. Hadlock, Qing Yang, Raisa Perzova, Renato Zambello, Gianpietro Semenzato, Steven K.H. Foung, Bernard J. Poiesz
Journal: Blood (1997)
Abstract A14: Loss of LKB1 gene alone causes malignant transformation of astrocytes
Authors: David Braun, Douglas Feinstein, Herbert Engelhard
Journal: Cancer Research (2015)

Abstract Liver Kinase B1 (LKB1) is a master kinase regulating activation of multiple downstream kinases, and plays roles in cell polarity, metabolism, proliferation, and inflammatory activation. The role LKB1 plays in the malignant transformation of normal astrocytes has not previously been reported. We hypothesized that LKB1 deficiency would influence the growth and differentiation of astrocytes. To test this, we prepared primary cortical astrocytes from homozygous LKB1 f/f mice. When the cells reached confluency, they were infected with AAV-CMV-Cre-GFP virus (knocking out the LKB1 gene), or with AAV-CMV-GFP as control. After 7 additional days, the control cells continued to have the typical appearance of astrocytes, while the LKB1 knockout cells began to form spheroids, with a 5-fold increase in proliferation by MTS assay. The LKB1 knockout astrocytes also showed loss of contact inhibition, increased migrative capability (by scratch assay), and loss of GFAP staining. Our data show that LKB1 deficiency alone induces a transformed phenotype in astrocytes, providing a new model for glioma and indicating its pathogenesis. Citation Format: David Braun, Douglas Feinstein, Herbert Engelhard. Loss of LKB1 gene alone causes malignant transformation of astrocytes. [abstract]. In: Proceedings of the AACR Special Conference: Advances in Brain Cancer Research; May 27-30, 2015; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2015;75(23 Suppl):Abstract nr A14.
Race and myeloma survival.
Authors: H J Cohen
Journal: Journal of Clinical Oncology (1996)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1996.14.12.3175 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 8955663 Race and myeloma survival. H J CohenxH J CohenSearch for articles by this author https://doi.org/10.1200/JCO.1996.14.12.3175 PDF "Race and myeloma survival.." Journal of Clinical Oncology, 14(12), p. 3175© 1996 by American Society of Clinical Oncology
Primary Culture of Rat Mammary Epithelial Cells. II. Cytotoxic Effect and Metabolism of 7,12-Dimethylbenz[&lt;italic&gt;a&lt;/italic&gt;]anthracene and &lt;italic&gt;N&lt;/italic&gt;-Nitroso-&lt;italic&gt;N&lt;/italic&gt;-methylurea&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: James Richards, S. Nandi
 5
Journal: JNCI Journal of the National Cancer Institute (1978)

To determine the cytotoxicity of 7,12-dimethylbenz[a]anthracene (DMBA) and N-nitroso-N-methylurea (NMU) on primary cultures of rat mammary cells, cultures were exposed to various concentrations of these carcinogens. Cytotoxicity was evident after exposure for 24 hours to as little as 0.1 microgram DMBA/ml. Cytotoxicity was evident after exposure for 2 hours with NMU at concentrations between 80 and 160 microgram/ml. Primary cultures of rat mammary cells were also examined for their ability to metabolize [3H]DMBA into water-soluble products. During a 48-hour period, mammary cells could convert 2.2% [3H]DMBA to water-soluble metabolites. The cells retained (for at least 4 days) small quantities of [3H]DMBA that were insoluble in organic solvents.
Brief Communication: Therapy of Advanced Colorectal Cancer With a Combination of 5-Flourouracil, Methyl-l,3-cis(2-chlorethyl)-1-nitrosourea, and Vincristine2
Authors: C. G. Moertel, A. J. Schutt, R. G. Hahn, R. J. Reitemeier
Journal: JNCI Journal of the National Cancer Institute (1975)

In a randomized, controlled study of 80 patients with advanced colorectal carcinoma, the combination of 5-fluorouracil (5-FU), methyl-1, 3-cis(2-chlorethyl)-1-nitrosourea, and vincristine produced an overall degree to toxicity comparable to that of 5-FU used alone. At 10 weeks, a positive objective response rate of 43.5% was observed with the three-drug combination compared to 19.5% with 5-FU alone (P less than 0.5).
Abstract IA28: Preclinical strategies to target resistance in colorectal cancer: Opportunities and challenges
Authors: Livio Trusolino, Francesco Sassi
Journal: Cancer Research (2016)

Abstract More than ten years after completion of the Human Genome Project, genetic alterations with causative roles in cancer have been identified. Inhibitors that target druggable mutant gene products have been developed. Finally, a number of these drugs have entered the clinic and are now used in patients. Some fundamental issues need to be addressed before the informative potential of genome-wide molecular surveys is translated into clinical benefit. First, given the heavy mutational load accrued during neoplastic progression, driver alterations are difficult to distinguish from passenger events. Second, next-generation approaches are likely to identify previously neglected small subsets of very rare variants, which requires population-scale studies for statistically solid genotype/response correlations. Third, not always does the presence of an oncogenic driver predict response. Therefore, treatment paradigm may not be decided on the sole basis of the mutational status of a single gene with potential cancer-causing function, but rather on the basis of the heterogeneous context in which that mutation is found (precision medicine). All these challenges also apply to metastatic colorectal cancer (mCRC). Less than 20% of mCRC patients respond to anti-EGFR antibodies, the gold standard targeted therapy, which calls for the identification of novel predictive biomarkers and suggests that uncharacterized drivers other than EGFR can sustain the growth of different CRC subsets. The categorization of tumor subpopulations featuring specific driver lesions, the validation of such lesions as targets, and the need for discrimination between “actionable” opportunities and those with weak clinical transferability require reliable preclinical models. The scope of our research is to refine genetic, mechanistic and therapeutic annotation of mCRC subsets using predictive in vivo models as a means to systematically increase the success rate of rationally based clinical trials that emanate from preclinical findings. Citation Format: Livio Trusolino, Francesco Sassi. Preclinical strategies to target resistance in colorectal cancer: Opportunities and challenges. [abstract]. In: Proceedings of the Fourth AACR International Conference on Frontiers in Basic Cancer Research; 2015 Oct 23-26; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2016;76(3 Suppl):Abstract nr IA28.