tbuckley/cabot-search huggingface dataset:
Case 25-1986
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, Betty U. McNeely, Howard L. Weiner, Suzanne de la Monte
Journal: New England Journal of Medicine (1986)

Presentation of CaseA 24-year-old woman was admitted to the hospital because of progressive deterioration in her mental status.The patient was born legally blind in the left eye because of a central chorioretinal lesion that was believed typical of congenital toxoplasmosis. At the age of 15 years chorioretinitis developed in the right eye and was treated with adrenocorticosteroids and later with sulfadoxine and pyrimethamine. She soon became legally blind in both eyes. Thereafter she functioned well until three months before admission, when her family noticed that she became withdrawn and lost interest in activities, and they suspected that she . . .
PROGNOSTIC UTILITY OF CORONARY ATHEROSCLEROSIS IN THE ABSENCE OF STENOSIS: A PROSPECTIVE MULTICENTER INTERNATIONAL STUDY OF 6,656 PATIENTS UNDERGOING CORONARY COMPUTED TOMOGRAPHIC ANGIOGRAPHY
Authors: Iksung Cho, Joshua Schulman-Marcus, Stephen Achenbach, Daniel Berman, Matthew Budoff, Tracy Callister, Hyuk-Jae Chang, Mouz Al-Mallah, Filippo Cademartiri, Kavitha Chinnaiyan, Augustin DeLago, Todd Villines, Martin Hadamitzky, Joerg Hausleiter, Jonathon Leipsic, Leslee Shaw, Philipp Kaufmann, Ricardo Cury, Gudrun Feuchtner, Yong-Jin Kim, Erica Maffei, Gilbert Raff, Gianluca Pontone, Daniele Andreini, James Min
Journal: Journal of the American College of Cardiology (2015)
Abstract 4952: Persistent expression of Nqo1 by p62-mediated Nrf2 activation facilitates p53-dependent mitotic catastrophe
Authors: Chi Bao Bui
Journal: Cancer Research (2012)

Abstract Prolonged mitosis due to aberrant chromosome segregation permits cells to enter the G1 phase without cytokinesis and subsequently triggers the p53-dependent cell death program, known as mitotic catastrophe. Cells which fail to go through mitotic catastrophe create aneuploidy, posing a risk of oncogenesis. In the present report, we show that p62-mediated non-canonical activation of Nrf2 leads to the persistent expression of Nqo1, which plays a critical role for p53 stabilization during mitotic catastrophe. With prolonged exposure to nocodazole, a microtubule-depolymerizing agent, p62-deficient HCT116 cells exhibited an accumulation of a polyploid population with a limited appearance of apoptoic cells, which was attributable to the attenuated stabilization of p53. Combinatorial gene manipulation analysis verified that the regulatory cascade with a hierarchy of p62-Keap1-Nrf2-Nqo1 is required for p53 stabilization for mitotic catastrophe. This is consistent with the role of Nqo1 as a gatekeeper for proteasomal degradation of p53. Thus, we demonstrate for the first time the functional connection between the non-canonical Nrf2 pathway and p53-dependent cell death program upon prolonged mitosis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4952. doi:1538-7445.AM2012-4952
Key gp120 Glycans Pose Roadblocks to the Rapid Development of VRC01-Class Antibodies in an HIV-1-Infected Chinese Donor
Authors: Leopold Kong, Bin Ju, Yajing Chen, Linling He, Li Ren, Jiandong Liu, Kunxue Hong, Bin Su, Zheng Wang, Gabriel Ozorowski, Xiaolin Ji, Yuanzi Hua, Yanli Chen, Marc C. Deller, Yanling Hao, Yi Feng, Fernando Garces, Richard Wilson, Kaifan Dai, Sijy O’Dell, Krisha McKee, John R. Mascola, Andrew B. Ward, Richard T. Wyatt, Yuxing Li, Ian A. Wilson, Jiang Zhu, Yiming Shao
Journal: Immunity (2016)
Molecular differences between the triple negative tumors of African-American women and white women.
Authors: M Lund, JW Eley, RM O'Regan, SS Gabram, HI Saavedra, JM Liff, OW Brawley, PL Porter
Journal: Cancer Research (2009)

Abstract Abstract #2087 Purpose. We recently reported associations between triple negative tumors (TNTs) and several key cell-cycle proteins. TNTs have also been associated with: 1) younger age and African-American (AA) race, 2) a relative lack of therapeutic targets, and 3) higher recurrence and poorer survival relative to other tumor subtypes. Furthermore, AA women diagnosed with TNTs experience worse outcomes than white women. TNTs are a mixed group of tumors that includes both basal and non-basal types. Markers that could help differentiate tumors with the poorest outcome would be of great use in determing how to effectively treat women with TNT. This study examines whether there are racial differences in key cell-cycle and apoptotic proteins among women with TNTs and could help to identify potential molecular mechanisms underlying racial disparities in these aggressive tumors.&amp;#x2028; Methods. Invasive TNTs from a population-based cohort of 136 Atlanta women (56 AA and 79 white) aged 20–54, diagnosed between 1990 and 1992, were centrally reviewed and immuno-histochemically analyzed for ER, PR, HER2, Bcl2, Cyclins D1 and E, pRb, p16, p21, p27, p53, p130, Ki67, and apoptotic index (AI). Weighted frequency distributions, Chi-square tests, and logistic regression were used to assess racial differences. Age and stage-adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated.&amp;#x2028; Results. Among the 136 women diagnosed with TNTs, AA women were significantly more likely than white women to present at a later stage, with larger tumors, and increased grade, mitotic activity, tumor necrosis, and apoptotic index. AA women were also significantly younger, poorer, and obese. Cell cycle protein differences between AA and white women diagnosed with TNTs included higher expression of Cyclin E [OR = 4.0 (95% CI=1.9, 8.5)], pRB [OR = 2.8 (95% CI=1.6, 4.9)], p16 [OR = 2.2 (95% CI=1.3,3.8)], p21 [OR = 2.0 (95% CI=1.1, 3.5)], AI [OR = 2.1 (95% CI=1.3, 3.9)], and lower expression of p130 [OR = 0.6 (95% CI=0.3, 1.0)].&amp;#x2028; Conclusions. Exclusively among triple negative tumors, we identified racial differences in expression levels of several key cell-cycle and apoptotic related proteins. Combined with other poor prognostic factors, these differences may account for racial disparities in outcome. Future etiologic studies and clinical trials dedicated to TNTs should consider underlying molecular differences. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 2087.
Asymmetric Pulmonary Hypermetabolism on 18F-FDG PET/CT Caused by Pulmonary Embolism
Authors: Evert Caekebeke, Christophe M Deroose, Peter Verhamme, Johan Coolen, Olivier Gheysens
Journal: Clinical Nuclear Medicine (2015)

We present a case of diffuse and moderately increased 18F-FDG uptake in the entire left lung on 18F-FDG PET without any morphological parenchymal abnormalities in a patient with recent history of esophageal adenocarcinoma treated by minimal invasive surgery and adjuvant chemotherapy. Contrast-enhanced CT revealed a large embolism in the left pulmonary artery with near total occlusion. In the absence of parenchymal lesions, the increased 18F-FDG uptake is most likely an inflammatory response to a recent ischemic insult. This case illustrates that asymmetric lung hypermetabolism in the absence of parenchymal disease can be caused by a central pulmonary embolism.
Abstract 927: Combined targeting c-Src and c-Met pathways to impair prostate cancer cell growth and invasion.
Authors: Yao Dai, Kyung-Mi Bae, Dietmar W. Siemann
Journal: Cancer Research (2013)

Abstract Overexpression of tyrosine kinases c-Src and c-Met has been shown to be highly associated with prostate cancer progression and poor clinical outcomes, therefore small molecule Src or Met inhibitors are being extensively evaluated in clinical trials for advanced prostate cancer. However clinical data suggest that single treatment with any of these inhibitors only yield limited effects in patients. One possibility is that redundant signaling pathways in tumor cells exist that allows tumor cell uninterrupted upon blockade of purely one pathway. We hypothesize that c-Src and c-Met are two compensatory pathways that may cooperate to promote prostate cancer progression, hence here we studied treatment effects of combining inhibitors targeting c-Src (dasatinib, saracatinib) and c-Met (ASLAN002, also named BMS-777607) on multiple functional behaviors associated with tumor growth and metastasis in c-Src and c-Met expressing prostate cancer cells (PC-3, DU145). Combination of Src inhibitors and ASLAN002 was found to inhibit cell proliferation and colony formation more strongly than either single agent, as assessed by MTT and clonogenicity, respectively. In a wound-healing assay, compared to either treatment alone, the combinatorial treatment exhibited greater suppression on cell motility induced by hepatocyte growth factor, the only known ligand of c-Met. Similarly, using a Matrigel-based Transwell assay, Src inhibitors plus ASLAN002 resulted in significant reduction of cell invasion in the presence or absence of HGF. Western blot analysis demonstrated that co-targeting Met and Src kinases lead to not only inhibition on c-Met and c-Src autophosphorylation but also greater blockade of multiple downstream kinases such as focal adhesion kinase (FAK), Akt and extracellular signal-regulated kinase (ERK). These data indicate that combined application of small molecule Src and Met inhibitors cause significant impairment on various phenotypes associated with prostate cancer progression in vitro including proliferation, survival, migration and invasion, suggesting that this combination intervention modality may serve as a potential anti-metastatic strategy that could be further tested in metastatic prostate cancer models in vivo. Citation Format: Yao Dai, Kyung-Mi Bae, Dietmar W. Siemann. Combined targeting c-Src and c-Met pathways to impair prostate cancer cell growth and invasion. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 927. doi:10.1158/1538-7445.AM2013-927
P4-17-11: Central Nervous System Involvement and Clinical Outcome, Review of 135 Patients, 9-Year Follow Up.
Authors: J Watanabe, A Ogiya, Y Tadokoro, K Tanaka, K Takahashi, T Uematsu, K Mitsuya
Journal: Cancer Research (2011)

Abstract Background: Breast cancer infiltrates into central nervous system (CNS) with the incidence of 10–20%. It is commonly accepted CNS screening does not contribute to maintain patients’ survival in metastatic breast cancer (MBC). We review our MBC cases with CNS involvement with the aim of searching prognostic factors and evaluating benefits derived from early detection of CNS lesion. Patients and Methods: From October 2002 to January 2011, 473 MBC patients treated at our hospital were reviewed and assessed. CNS lesion was found in 133 of 473 (28.5%) mostly by magnetic resonance imaging. Receptor statuses in patients with CNS disease were as follows; Estrogen receptor-positive 52.4%, HER2−positive 41.1% and triple-negative 12.7%. Asymptomatic patient at the diagnosis of CNS metastasis, in other words, CNS screening performed case, was 57.8%. Liver metastasis prior to CNS involvement was observed in 51.2% of patients. Results: Within our 9-year follow-up, 122 patients received irradiation or operation, and 118 died. While major cause of death was lung or liver failure, 23.7% was considered as CNS death. Median overall survival from the diagnosis of primary breast cancer, survival from the MBC development and survival from CNS involvement were 1951, 1027 and 321 days respectively. Patients having HER2−disease showed superior survival after detection of CNS disease than HER2−negative patients. (median 514.0 vs 220.0 days, p=0.001) Asymptomatic patients, excluding underwent best supportive care (BSC), could not receive any survival benefit from early detection of CNS lesion. Liver metastasis prior to CNS involvement did not affect patients’ survival. Nineteen patients (14.1%), 17 of them were asymptomatic, received stereotactic irradiation as an initial treatment for CNS lesion, and showed superior survival after CNS event than patients received whole brain irradiation, surgery or BSC (median 670.0 vs 287.0 days, p=0.01). Conclusion: Our review disclosed superior survival of HER2−disease with CNS metastasis. Early detection of CNS metastasis is only beneficial to patients when stereotactic irradiation will be suited for. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P4-17-11.
P500 MINIMAL HEPATIC ENCEPHALOPATHY IS INDEPENDENTLY ASSOCIATED WITH POOR SURVIVAL AND INCREASED RATE OF HOSPITALIZATION: A PROSPECTIVE STUDY OF 170 PATIENTS
Authors: K. Patidar, L. Thacker, M. White, N. Noble, R.K. Sterling, R. Stravitz, A. Sanyal, I. Bouneva, M. Siddiqui, V. Luketic, M. Fuchs, D. Heuman, H. Gilles, J. Wade, J.S. Bajaj
Journal: Journal of Hepatology (2014)
P446Myocardial ischemic tolerance and expression of selected genes in spontaneously hypertensive rats adapted to chronic continuous hypoxia
Authors: D Kolar, I Brabcova, J Zurmanova, P Mandikova, P Zajickova, M Kalous, M Pravenec, O Novakova, F Kolar, J Neckar
Journal: Cardiovascular Research (2014)

Purpose: Spontaneously hypertensive rats (SHR) are more susceptible to acute myocardial ischemia/ reperfusion injury than normotensive Brown Norway (BN) strain. It has been shown that the adaptation to chronic hypoxia improves ischemic tolerance in normotensive rats and the cardioprotective phenotype can be related to mitochondrial metabolism and signalling. Here we aimed at investigating effects of continuous normobaric hypoxia (CNH) on myocardial ischemic tolerance of SHR and conplastic strain SHR-mtBN (with mitochondrial genome from BN). We also analyzed the expression levels of selected genes of energy metabolism, antioxidant systems and signalling pathways. Methods: Rats were kept 21 days at CNH (inspired O2 fraction 0.1). Myocardial infarct size was determined after 20 min of ischemia and 2 h of reperfusion in open-chest rats (tetrazolium staining). In a separate group of animals, the total mRNA was isolated from left ventricles and gene expression was assessed by RT-PCR. Results: CNH reduced infarct size from 71 ± 4% of the area at risk in normoxic SHR to 49 ± 6% in hypoxic SHR. As compared to SHR, CNH induced more pronounced infarct size-limiting effect in SHR-mtBN. In both strains, CNH increased the mRNA expression of monoaminooxidase and β1-adrenoceptor, and decreased the expression of mitochondrial creatine kinase, superoxide dismutase, thioredoxin 2, thioredoxin-reductase 2 and peroxiredoxin 5. However, the expression of catalase, peroxiredoxin 3, mitochondrial hexokinase 2 and hypoxia-inducible factor 1α was markedly elevated in hypoxic SHR-mtBN as compared to hypoxic SHR. Conclusions: We demonstrate that CNH protects SHR hearts against acute ischemia/reperfusion injury with a possible involvement of mitochondrial genes. This work was supported by the Czech Science Foundation grant No. 13-10267S
Lesion Induced by Blood Pressure Cuff in Epidermolysis Bullosa
Authors: Ba D. Nguyen, Michael C. Roarke
Journal: Clinical Nuclear Medicine (2011)

Epidermolysis bullosa encompasses a group of inherited cutaneous disorders with characteristic blisters easily induced by minor mechanical injury from pressure or friction of the skin. The authors present a case of recessive dystrophic epidermolysis bullosa with positive PET finding from non-neoplastic skin lesion of the upper extremity caused by blood pressure cuff.
Dominant-negative C/ebpα and polycomb group protein Bmi1 extend short-lived hematopoietic stem/progenitor cell life span and induce lethal dyserythropoiesis
Authors: Ting Zhou, Lei Wang, Kang-Yong Zhu, Mei Dong, Peng-Fei Xu, Yi Chen, Sai-Juan Chen, Zhu Chen, Min Deng, Ting Xi Liu
Journal: Blood (2011)
Preserved Value of Bone Scintigraphy for the Detection of Skeletal Metastases in Prostate Cancer Patients with Low Prostate-Specific Antigen Levels
Authors: MELTEM CAGLAR, MURAT TUNCEL
Journal: Clinical Nuclear Medicine (2002)

From Hacettepe University Medical Faculty, Department of Nuclear Medicine, Ankara, Turkey Received for publication September 20, 2001. Revision accepted December 17, 2001. Correspondence: Meltem Caglar, Hacettepe University Medical Faculty, Department of Nuclear Medicine, Sihhiye-06100, Ankara, Turkey. E-mail: [email protected]
Gene Therapy OK'd for Pediatric Brain Tumors
Authors: S. Jenks
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Gene Therapy OK'd for Pediatric Brain Tumors Get access Susan Jenks Susan Jenks Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 13, 7 July 1993, Page 1026, https://doi.org/10.1093/jnci/85.13.1026 Published: 07 July 1993
P3-11-02: Changing Paradigms for Breast Cancer Chemoprevention?
Authors: RT Chlebowski
Journal: Cancer Research (2011)

Abstract The SERMs tamoxifen and raloxifene are approved for breast cancer risk reduction but their acceptance in clinical practice has been poor largely related to rare but potentially life threatening side effects which requires identification of populations at higher breast cancer risk and careful risk benefit discussion (Visvanathan 2009). Recent findings from randomized placebo-controlled clinical trials suggest potential alternative approaches. In the MAP.3 placebo-controlled trial including 4,650 postmenopausal women, exemestane decreased breast cancer incidence by 65% (P=0.002) (Goss 2011) with no significant difference between groups for fractures, CVD events, other cancers or treatment-related deaths. While the median Gail 5-yr risk score of participants was 2.3, eligibility factors included age alone (≥ 60 years) regardless of calculated breast cancer risk and accounted for 49% of entries. With extended follow-up from the Women's Health Initiative (WHI) randomized, placebo-controlled trial evaluating estrogen alone in 10,739 postmenopausal women with prior hysterectomy, a statistically significant decrease in breast cancer incidence of 23% was seen with estrogen use (P=0.02) (LaCroix 2011). Younger postmenopausal women (age 50–59 years at entry) randomized to estrogen alone had lower risk of myocardial infarction (HR 0.54, 95% CI 0.34−0.86) and death (HR 0.73, 95% CI 0.53−1.00). These findings contrast to those in the WHI trial evaluating combined estrogen plus progestin in 16,608 postmenopausal women with an intact uterus where breast cancers were increased 25% (P=0.004) as was breast cancer mortality (increased by 96%, P=0.049) (Chlebowski 2010). The apparently paradoxical findings that in postmenopausal women estrogen addition, as conjugated equine estrogen, lowers breast cancer incidence and estrogen reduction, by aromatase inhibitor use, also lowers breast cancer incidence are consistent with preclinical studies indicating condition dependent change in estrogen influence on mammary cancers (Jordan 2011). Major eligibility for the WHI trials included anticipated 3-yr survival regardless of breast cancer or CVD risk. The findings from the MAP.3 and WHI trials highlight the complex relationships between estrogen and breast cancer and suggest potential strategies for chronic disease risk reduction in select populations of postmenopausal women which may not require formal breast cancer risk assessment. Visvanathan K, Chlebowski RT, et al. J Clin Oncol 2009;27:3235–3258. Goss PE, Ingle JN, Ales-Martinez J, Cheung A, Chlebowski RT, et al. The NCIC CTG MAP.3 Trial. N Engl J Med 10.1056/NEJMos 1103507. Chlebowski RT, Anderson GL, et al. JAMA 2010;304(15):1684–1692. LaCroix AZ, Chlebowski, RT, et al. JAMA 2011;305(13):1305–14. Jordan VC, Ford LG. Cancer Prev Res. 4:633–7 (2011). Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P3-11-02.
β-Amyloid and the Pathogenesis of Alzheimer's Disease
Authors: Jeffrey S. Flier, Lisa H. Underhill, Bruce A. Yankner, M.-Marsel Mesulam
Journal: New England Journal of Medicine (1991)

SIXTY to 80 percent of cases of dementia among persons over the age of 65 are caused by Alzheimer's disease. Most of the remainder are caused by cerebrovascular disease with multiple infarcts, and a smaller proportion are due to tumors, infections (e.g., infection with the human immunodeficiency virus), metabolic disorders, depression ("pseudodementia"), and the less common neurodegenerative diseases, including Pick's disease, progressive supranuclear palsy, and Huntington's disease.1 2 3 Alzheimer's disease has been estimated to afflict 5 to 11 percent of the population over the age of 65 and as much as 47 percent of the population over the age of 85. . . .
Assessing Therapy Response of Secreting Pineal Germ Cell Tumor on Simultaneous 18F-Choline PET/MRI
Authors: Emmanouil Panagiotidis, Ananth Shankar, Asim Afaq, Jamshed Bomanji
Journal: Clinical Nuclear Medicine (2013)

An 18-year-old man presented with 6 weeks' history of diplopia, early morning headaches, and blurred vision; on ophthalmologic examination, Parinaud syndrome was revealed. Brain MRI scan showed a calcified pineal mass. Brain simultaneous PET/MRI with 18F-choline showed an avid enhancing mass occupying the pineal region with restricted diffusion. A second examination after chemotherapy demonstrated reduction in both size and radiotracer activity of the mass. Our study emphasizes the potential of simultaneous 18F-choline PET/MRI being a useful tool for contribution in the diagnosis and treatment assessment in a convenient way with minimal radiation exposure and reduced throughput patient time.
Soundings: Feeding frenzy
Authors: George Dunea
Journal: BMJ (2001)

“A meeting without food,” to mutilate an old Italian proverb, “is like life without love”—“come la vita senza l'amore.” For how can we absorb and assimilate so much science without the benefit of at least an elegant opening reception with some facilitative high energy precursors?

On the old continent of Europe such scientific meetings are often held in picturesque places replete with history, tradition, and ancient ruins. The opening ceremony begins with speeches of varying brevity and languages, by congress and scientific society presidents, the all too usual speakers, and officials not too important or busy to attend.

But where is the food? And where is the wine? For a meal without wine (“pranzo senza vino”) is indeed like life without love. But wait, first a classical concert. Respectfully, and with varying degrees of rapture, the guests listen to classical pieces by Corelli, Albinoni, and Monteverdi; and show their appreciation by applauding after every movement of Mozart's Serenade in G.

At last it is time to go to the banqueting hall. The doors open. Is it the Vandal cohorts of Genseric that are approaching? Is it a crowd that has fasted for weeks in anticipation of the event? Could this be the end of Ramadan? But no, for the Saracens were turned back in 732, and we are in the land of the once victorious Charles Martel, the Hammer.

Repudiating the prudent heart diet, the crowd rushes to the buffet, pushing all obstacles aside. Five pairs of hands converge on one single shrimp, and food is snatched out of the hands of waitresses. Some people pick up whole trays, others full bottles of wine. A man steps on a young woman's toes; a blonde matron projects herself unstoppably towards the hors d'oeuvres, leaving behind a trail of bruised smaller men. Within minutes entire tables of neatly arranged tarts and sandwiches are devastated, the food vanishing as in the wake of an army of locusts.

Soon nothing is left but empty plates, empty bottles, and trash. Is this the work of the Exterminating Angel? Remember Luis Bunuel's 1962 movie, where high society guests, mysteriously and inexplicably shut up in their elegant banqueting hall, end up behaving like beasts, fighting over chairs and drinks and scrambling for scraps of food? For like it or not, when the chips are down, the veneer of human civilization is still pretty thin.