tbuckley/cabot-search huggingface dataset:
Detection of codon 12 K-Ras mutations using a photopolymerization based signal ampification method
Authors: Ryan Hansen, Hadley Sikes, Christopher Bowman
Journal: Clinical Cancer Research (2007)

A31  The continuing discovery and characterization of genomic biomarkers which may predict the onset of disease have the potential to greatly improve the capabilities of clinical diagnostics and disease prognosis. A specific malignant disorder to which molecular diagnostics can offer vast improvement in is lung cancer, as current detection methods typically lead to detection in the later stages of disease progression, resulting in poor prognosis and survival rates. Coupling knowledge of biomarkers available from non-invasive patient samples with the high-throughput screening capabilities of DNA biochips potentially offers a new tool for early diagnosis, enabling early treatment options for patients and improved outcomes likely. A primary limitation associated with this technology involves the specific detection of low copy number polynucleotide sequences using clinically suitable detection instrumentation, requiring target amplification with PCR-based methods or through signal amplification methods. This research involves developing a novel, rapid, and specific detection method that utilizes a free radical photopolymerization reaction for signal amplification, enabling the sensitive detection of genetic biomarkers while eliminating reliance on expensive detection instrumentation. This approach involves coupling photoinitiators to complementary DNA hybrids on a biosensor surface using an allele-specific primer extension reaction. These molecules catalyze the polymerization of detectable monomers exclusively from DNA hybrids on a biochip surface. Rapid propagation rates characteristic of acrylate monomers enable thick polymer films to be generated on the biosensor surface in a matter of minutes from minute amounts of targeted genetic material, allowing for direct visual detection of polynucleotide sequences upon inspection of the biosensor surface. Such an amplification system has advantages of being rapid, inexpensive, and robust, meeting requirements inherent for use at a doctor9s office or at point of care settings. We are currently using this method for the direct visual detection of single base mutations present in codon 12 of the K-Ras oncogene, known to play a role in the onset of lung, pancreatic, and colorectal cancers.
Tyrosine Kinase Inhibitors Only Partially Inhibit AKT-Dependent Signaling in Cells Expressing Oncogenic KIT, FLT3 or ABL Kinases. A Potential Model for Leukemia Cell Resistance to TKIs.
Authors: Marcus M. Schittenhelm, Kerstin M. Kampa, Sharon Shiraga, Lothar Kanz, Michael C. Heinrich
Journal: Blood (2007)
Abstract P6-09-52: Prognostic factors in breast cancer (BC) associated with the development of brain metastases (BM): A retrospective study of 726 pts
Authors: O Santa Cruz, P Tsoutsou, S Anchisi, K Khanfir, L Negretti, C Girardet, O Ozsoy, M Ozsahin
Journal: Cancer Research (2017)

Abstract This abstract was not presented at the symposium.
Genome Wide Studies in Multiple Myeloma Identify XPO1/CRM-1 As a Critical Target Validated Using the Selective Inhibitor of Nuclear Export (SINE) KPT-276
Authors: Jessica Schmidt, Esteban Braggio, Marta Chesi, Jan Egan, Yuan Xiao Zhu, Chang-Xin Shi, Stephen Palmer, Victoria Garbitt, Dilara McCauley, Sharon Shacham, Michael Kauffman, Leif Bergsagel, Keith Stewart
Journal: Blood (2012)
Abstract P4-06-04: Triple negative breast cancer patient-derived xenografts: Molecular characteristics and sensitivity to emerging therapies
Authors: KW Evans, E Yuca, A Akcakanat, SM Scott, N Paez Arango, X Zheng, K Chen, C Tapia, E Tarco, AK Eterovic, DM Black, LK Jennifer, D Tripathy, GB Mills, F Meric-Bernstam
Journal: Cancer Research (2017)

Abstract Background: Patients with triple negative breast cancer (TNBC) that have significant residual disease following neoadjuvant therapy have a poorer prognosis. The difficulty in developing improved treatment strategies for these patients is compounded by the molecular diversity of this pathology. Thus, preclinical efficacy testing with models representing the molecular heterogeneity of TNBC may not only improve efficacy testing but also has the potential to facilitate biomarker discovery to inform patient selection. Methods: We generated 28 hormone receptor-low/HER2- patient-derived xenografts (PDXs) from 26 patients; the majority from residual disease following neoadjuvant chemotherapy. We characterized the tumors from the patients and the matched PDXs by targeted exome sequencing, RNA sequencing, and Reverse Phase Protein Arrays. We established single agent sensitivity for a set of PDXs to standard TNBC therapies as well as emerging targeted therapies targeting PARP, mTOR, PI3K and MEK1/2. Results: PDXs maintained DNA/RNA profiles similar to the patients' tumors. Our PDX set exhibits a diverse set of potential driver alterations and is comprised of PDXs representative of all TNBC molecular subtypes. The PDXs varied in their sensitivity to standard chemotherapeutics. PI3K, mTOR and MEK inhibition caused tumor growth inhibition in several PDX models but were unable to cause tumor regression as single agent. In contrast, talazoparib caused dramatic regression in 5 out of 12 PDXs tested, including 3 PDXs from patients whose tumors had progressed on neoadjuvant anthracyclines and/or paclitaxel. Four of these talazoparib sensitive PDXs were derived from patients not harboring BRCA1/2 germline alterations; three had somatic alterations in genes linked to DNA damage repair (ATM, BRCA2, PTEN). The comparison of PARP sensitivity with molecular profiles will be presented. Conclusions: TNBC PDXs represent molecular tumor heterogeneity as well as heterogeneity in response to targeted therapeutics. PDXs represent an opportunity for biomarker discovery as well as for rationale combination therapies to enhance the efficacy targeted therapies. Citation Format: Evans KW, Yuca E, Akcakanat A, Scott SM, Paez Arango N, Zheng X, Chen K, Tapia C, Tarco E, Eterovic AK, Black DM, Jennifer LK, Tripathy D, Mills GB, Meric-Bernstam F. Triple negative breast cancer patient-derived xenografts: Molecular characteristics and sensitivity to emerging therapies [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P4-06-04.
Real World Utilization and Practice Patterns of Dose-Adjusted EPOCH for Aggressive B-Cell Lymphomas 2005-2015: Impact of Growth Factor Choice and Resultant Achieved Dose Level
Authors: Sandra Kanan, Ajay K Gopal, Ryan D Cassaday, Andrei R. Shustov, Brian G. Till, Andrew J. Cowan, Mazyar Shadman, Warren Houston, Melinda Tran, Oliver Press, Stephen Smith
Journal: Blood (2016)
Apical Sorting of Adamts13 in Madin-Darby Canine Kidney (MDCK) Cells Requires Cub Domains Via Its Interaction with Detergent-Insoluble Glycosphingolipid- and Cholesterol-Enriched Rafts.
Authors: X. Long Zheng, Julie (Jihui) Ai, Ning Li, David (Dezhi) Shang
Journal: Blood (2004)
Bile acid binding resin prevents fat accumulation through intestinal microbiota in high-fat diet-induced obesity in mice
Authors: Yukie Kusumoto, Junichiro Irie, Kaho Iwabu, Hirotsune Tagawa, Arata Itoh, Mari Kato, Nana Kobayashi, Kumiko Tanaka, Rieko Kikuchi, Masataka Fujita, Yuya Nakajima, Kohkichi Morimoto, Taichi Sugizaki, Satoru Yamada, Toshihide Kawai, Mitsuhiro Watanabe, Yuichi Oike, Hiroshi Itoh
Journal: Metabolism (2017)
Basal cell carcinoma: PD-L1/PD-1 checkpoint expression and tumor regression after PD-1 blockade
Authors: Evan J. Lipson, Mohammed T. Lilo, Aleksandra Ogurtsova, Jessica Esandrio, Haiying Xu, Patricia Brothers, Megan Schollenberger, William H. Sharfman, Janis M. Taube
Journal: Journal for ImmunoTherapy of Cancer (2017)

Monoclonal antibodies that block immune regulatory proteins such as programmed death-1 (PD-1) have demonstrated remarkable efficacy in controlling the growth of multiple tumor types. Unresectable or metastatic basal cell carcinoma, however, has largely gone untested. Because PD-Ligand-1 (PD-L1) expression in other tumor types has been associated with response to anti-PD-1, we investigated the expression of PD-L1 and its association with PD-1 expression in the basal cell carcinoma tumor microenvironment. Among 40 basal cell carcinoma specimens, 9/40 (22%) demonstrated PD-L1 expression on tumor cells, and 33/40 (82%) demonstrated PD-L1 expression on tumor-infiltrating lymphocytes and associated macrophages. PD-L1 was observed in close geographic association to PD-1+ tumor infiltrating lymphocytes. Additionally, we present, here, the first report of an objective anti-tumor response to pembrolizumab (anti-PD-1) in a patient with metastatic PD-L1 (+) basal cell carcinoma, whose disease had previously progressed through hedgehog pathway-directed therapy. The patient remains in a partial response 14&nbsp;months after initiation of therapy. Taken together, our findings provide a rationale for testing anti-PD-1 therapy in patients with advanced basal cell carcinoma, either as initial treatment or after acquired resistance to hedgehog pathway inhibition.
Rapidly Enlarging Thyroid Mass in a Patient With History of Multiple Cancers
Authors: Halis Kaan Akturk, Robert Smallridge, John Casler
Journal: JAMA Oncology (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 Oncology 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 Oncology journal
Inhibition of Protein Kinase C (PKC) delta with Rottlerin Induces Apoptosis in B-CLL Cells, Augments Chemotherapeutic Cytotoxicity and Inhibits Antiapoptotic Survival Signals.
Authors: Ingo Ringshausen, Kathrin Weick, Madlene Oelsner, Christian Peschel, Thomas Decker
Journal: Blood (2004)
A phase I study of vemurafenib and decitabine in metastatic melanoma.
Authors: Sneha Deepak Phadke, Eric Steven Engelman, Roberto Antonio Leon-Ferre, Laith I. Abushahin, Sarah C Mott, Yousef Zakharia, Mohammed M. Milhem
Journal: Journal of Clinical Oncology (2015)

9056 Background: Targeted therapy in metastatic melanoma has shown unprecented response rates. However, this effect is usually short lived, with a median progression free survival of 5.3 months with the use of vemurafenib. This phase I study explored the novel combination of vemurafenib and decitabine. Methods: Patients with BRAF V600E mutated metastatic melanoma were eligible for participation. Dosing of decitabine was modified for each cohort, which is detailed in the Table. The primary objective was safety while the secondary objective was response rate. Results: There were 4 patients were enrolled in cohort 1, 3 in cohort 2, 4 in cohort 3, and 3 in cohort 4. Seven patients had previously been exposed to vemurafenib. The most common adverse events included hyperbilirubinemia, hypophosphatemia, leukopenia, arthralgia, and rash. Most were grade 1-2. Ten patients required a dose reduction of vemurafenib. Maximum tolerated dose of decitabine was not reached, and there were no dose limiting toxicities. Six patients (43%) had a response to therapy with three (21%) achieving a complete response (CR). Five patients (36%) achieved stable disease while 3 (21%) had progressive disease. Two of the 3 patients with partial response had previously progressed on single agent vemurafenib. Of the 6 patients that had a response, 3 were in cohort 1. Conclusions: This study demonstrated that the combination of vemurafenib and decitabine in BRAF V600E mutated metastatic melanoma is safe and resulted in an overall response rate of 43%. In comparison to the BRIM-3 trial, this trial had a significantly higher rate of patients achieving CR with the combined treatment (21% vs < 1%, p < 0.01). As half the patients that responded were enrolled in cohort 1, a similar phase I trial is planned which explores the effect of decitabine given at a low dose for a longer duration to ensure maximal depletion of DNA methyltransferase, the enzyme to which decitabine binds. Table. Clinical trial information: NCT01876641. Cohort Dose of decitabine Duration of decitabine treatment Dose of vemurafenib 1 0.1 mg/kg SQ three times weekly 2 weeks 960 mg BID continuous 2 0.2 mg/kg SQ three times weekly 2 weeks 960 mg BID continuous 3 0.3 mg/kg SQ three times weekly 1 week 960 mg BID continuous 4 0.3 mg/kg SQ three times weekly 2 weeks 960 mg BID continuous
The LTB4 Receptor Is Involved Not Only in the Downstream Pathway of rh-GCSF Mobilization but in the LTB4 Mobilization Pathway in C57BL/6 Mice.
Authors: Yeung-Chul Mun, Seung-Eun Lee, Kyoung-Eun Lee, Eun-Sun Yoo, Sang Min Lee, Jee Hyun Kong, Jee-Young Ahn, Yun-Kyung Bae, Soon-Nam Lee, Jae-Hong Kim, Chu-Myong Seong
Journal: Blood (2006)
Outcomes of treatment cessation in select metastatic renal cell carcinoma (mRCC) patients.
Authors: Kriti Mittal, Lisa Derosa, Laurence Albiges, Laura S. Wood, Paul Elson, Timothy D. Gilligan, Jorge A. Garcia, Robert Dreicer, Bernard J. Escudier, Brian I. Rini
Journal: Journal of Clinical Oncology (2014)

4521 Background: Tyrosine kinase inhibitors (TKIs) demonstrate efficacy in mRCC, but may cause significant adverse effects (AEs). We have previously evaluated outcomes in patients (pts) receiving prolonged treatment breaks on TKIs and expand and update this experience herein. Methods: mRCC pts on targeted therapy who discontinued treatment for ≥3 months were analyzed retrospectively. Treatment break was defined as a period of drug cessation for reasons other than progressive disease. Pts could receive treatment breaks with multiple lines of therapy (defined sequentially as treatment A, B, C etc.) A number of patients continue on treatment/observation, hence durations were estimated using the Kaplan-Meier method. Results: Baseline characteristics (n=112) were: 75% male; median age at diagnosis 56; 95% clear cell. 19% pts had received prior systemic therapy. 48% pts were favorable, 48% intermediate and 4% poor risk by Heng criteria. Table 1 depicts outcomes with sequential lines of therapy. Overall, pts received a median of 2 treatments. Treatment A primarily included sunitinib (55%), sorafenib (13%), or bevacizumab in combination with temsirolimus (10%)/ interferon (9%). Common reasons for breaks in treatment A were toxicity/AEs (57%) & physician choice (26%). 40 (36%) pts remain on treatment break from the first treatment (A). 25 (22%) pts have undergone 2 treatment breaks. 68 (61%) pts restarted treatment (B); 33 (49%) of these were rechallenged with previously used therapy & 35 (51%) received alternative TKIs. Overall, 30 patients have died; median survival is 71.7 months (range 1.3- 93+ months). Achievement of CR prior to the initial treatment break (n=15) was associated with a longer surveillance period (p=.0004). Conclusions: A treatment break is feasible in selected pts, especially after achievement of CR with TKIs. This strategy may be associated with acceptable overall disease control and reduced toxicity. Treatment Number of pts starting treatment Median duration of therapy in months (95% CI) Number of pts on treatment break Median duration of break in months (95% CI) A 112 13.5 (11-16.4) 112 16.8 (12.5-26.4) B 68 16.1 ( 11.4-20) 24 9.5 (4.6-10.3) C 43 14.8 ( 12-17.2) 10 7.1 D 15 13.8 (5.7-18.6) 3 15.9
Half of NHS doctors trained in other EU countries are considering quitting UK, warns GMC
Authors: Adrian O’Dowd
Journal: BMJ (2017)

Around half of NHS doctors who were trained in other countries in Europe are considering leaving the UK because of concerns over the effect Brexit will have on their working life and right to stay in the country, MPs have been told.

There was a general feeling of worry about what Brexit could mean for those NHS doctors who trained elsewhere in the European Economic Area, said Charlie Massey, chief executive and registrar of the General Medical Council. Massey, giving evidence at a session of the parliamentary health committee’s inquiry into the implications of Brexit, held on 28 February, said that the UK’s departure from the European Union was causing unrest despite …
Nilotinib 300 Mg Twice Daily as First Line Treatment of Ph-Positive Chronic Myeloid Leukemia In Chronic Phase: Updated Results of the ICORG 0802 Phase 2 Study with Analysis of the GeneXpert System Versus IS BCR-ABL RQ PCR.
Authors: Eibhlin Conneally, Ronan T Swords, Francis J. Giles, Mary Frances McMullin, Philipp le Coutre, Stephen Langabeer, Marzena Wieczorkowska, Cliona McDowell, Brian Moulton, Karine Egan, Michael O'Dwyer
Journal: Blood (2010)
Pre-Transplant Weight Loss Influences Outcome of Patients with Myelodysplastic Syndrome Undergoing Allogeneic Stem Cell Transplantation
Authors: Aleksandar Radujkovic, Natalia Becker, Axel Benner, Sascha Dietrich, Olaf Penack, Uwe Platzbecker, Friedrich Stölzel, Martin Bornhäuser, Ute Hegenbart, Anthony D Ho, Peter Dreger, Thomas Luft
Journal: Blood (2014)
The Akt/Mcl-1 Pathway Plays a Prominent Role in Mediating Pro-Survival Signals Derived from the B-Cell Receptor in Chronic Lymphocytic Leukemia B-Cells.
Authors: Pablo G. Longo, Luca Laurenti, Stefania Gobessi, Simona Sica, Giuseppe Leone, Dimitar G. Efremov
Journal: Blood (2007)
In Vitro Analysis of Defibrotide’s (DF) Uptake by the Human Cell, as Well as DF’s Spesificity for the Viral Envelope Proteins of HIV-! HIV-3, and of Spesific HIV, with Conformatory Data Regarding the Dose Dependency of DF’s Pharmacological Paleiotropism.
Authors: Arsinur D. Oral, Mark Wagner
Journal: Blood (2005)
Abstract IA16: Spherical nucleic acids as a powerful new platform for cancer immunotherapy
Authors: Chad A. Mirkin
Journal: Cancer Research (2017)

Abstract Spherical nucleic acids (SNAs) are nanoparticle-oligonucleotide conjugates characterized by a dense, spherical shell of radially oriented oligonucleotides. SNAs enter cells without the need for auxiliary transfection reagents, are more resistant to nuclease degradation than their linear counterparts, and show minimal toxicity and off-target immunogenicity. These emergent properties of the SNA platform enable the design of powerful immunotherapy agents against cancer cells. The SNA platform allows simultaneous delivery of Toll-like receptor (TLR) agonist oligonucleotides and cancer-associated antigen peptides to antigen-presenting cells (APCs). The oligonucleotides on the surface of the SNAs activate of the innate immune system through TLRs to mature the APCs, which in turn activates effector immune cells to target cell displaying the cancer-associated peptide. Compared to mixtures of free peptides and oligonucleotides, SNAs exhibit up to 80-fold increase in potency, 400-fold higher cellular response to antigens and improve median survival in mice with lymphomas through antigen-specific targeting of cancer cells. The enhancement of the immune properties arises from a combination of increase in cellular uptake, polyvalent binding of SNAs to TLRs and the co-delivery of the TLR agonist oligonucleotides and peptide to the same cell. Additionally, the SNA architecture enables the control of oligonucleotide to peptide ratio, subcellular release location of the peptide and release kinetics. Combined with their high serum stability, at-scale synthesis and minimal toxicity profile, SNAs hold great promise for the development of cancer vaccines. Citation Format: Chad A. Mirkin. Spherical nucleic acids as a powerful new platform for cancer immunotherapy. [abstract]. In: Proceedings of the AACR Special Conference on Engineering and Physical Sciences in Oncology; 2016 Jun 25-28; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2017;77(2 Suppl):Abstract nr IA16.
A Pharmacokinetic Study of the Plasma-Derived Factor IX AlphaNine® and Its Comparison with the Recombinant Factor IX BeneFIX®, in Previously Treated Patients with Severe Hereditary Hemophilia B.
Authors: Vicente R. Cortina, T. Lissichkov, K. Zavilska, M. Matysiak, L. Gercheva, José A. Aznar
Journal: Blood (2007)
Circulating Endothelial Progenitor Cells (EPCs): Variability between Normal Individuals as Measured by a New Standardized, Functional 5-Day In Vitro Colony Assay.
Authors: C. S. Russell, S. M. Faulkes, C. G. Pereira, T. E. Thomas, A. C. Eaves, E. M. Clarke
Journal: Blood (2004)
We Are Not Afraid
Authors: Fatima Z. Syed
Journal: Annals of Internal Medicine (2017)

Ad Libitum7 March 2017We Are Not AfraidFatima Z. Syed, MD, MScFatima Z. Syed, MD, MScFrom Thomas Jefferson University Hospital, Philadelphia, Pennsylvania.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M16-2632 Audio Reading - “We Are Not Afraid” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "We Are Not Afraid," by F.Z. Syed. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail I went to an elementary school named in honor of Dr. Martin Luther King Jr. Every January, we would commemorate the life of Dr. King in a school-wide assembly. We would hold our little hands together and sing.We are not afraid,We are not afraid,We are not afraid, TODAYOh, deep in my heart,We shall overcome,We shall overcome,We shall overcome, some day.Oh, deep in my heart,I do believeWe shall overcome, some day.On Wednesday, November 9th, 2016, the person I thought would become president did not. Like much of the country, I was surprised. However, I remembered the advice ... Author, Article, and Disclosure InformationAffiliations: From Thomas Jefferson University Hospital, Philadelphia, Pennsylvania.Current Author Address: Fatima Z. Syed, MD, MSc, Thomas Jefferson University Hospital, 1025 Walnut Street, Philadelphia, PA 19107; e-mail, [email protected]com. PreviousarticleNextarticle Advertisement Audio Reading - “We Are Not Afraid” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "We Are Not Afraid," by F.Z. Syed. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics 7 March 2017Volume 166, Issue 5Page: 375KeywordsHeart ePublished: 7 March 2017 Issue Published: 7 March 2017 Copyright & PermissionsCopyright © 2017 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Development of a Mouse Model of DS Megakaryoblastic Leukemia and Identification of the Hsa21 Gene DYRK1A as a Prominent Contributor to DS-AMKL
Authors: Sebastien Malinge, Gina Kirsammer, Meghan Bliss-Moreau, Timothy M Chlon, Lauren Diebold, Stella T Chou, Mitchell Weiss, Sandeep Gurbuxani, John Crispino
Journal: Blood (2010)