tbuckley/cabot-search huggingface dataset:
Abstract P4-01-15: Impact of Preoperative MRI on the Surgical Treatment of Breast Cancer: A SEER-Medicare Analysis
Authors: CM Thorsen, JE Weiss, K Kerlikowske, EM Ozanne, DS Buist, RA Hubbard, AN Tosteson, LM Henderson, BA Virnig, ME Goodrich, TL Onega
Journal: Cancer Research (2012)

Abstract Background: Preoperative magnetic resonance imaging (MRI) use has increased for women with invasive breast cancer and ductal carcinoma in situ (DCIS). Prior studies have disputed whether preoperative MRI is associated with increased rates of mastectomy. We evaluated the rates of mastectomy versus breast conserving surgery (BCS) and their association with preoperative MRI in older women. Methods: We identified women in SEER-Medicare 66 years or older diagnosed with DCIS or invasive breast cancer between 2002 and 2007 treated within 6 months of diagnosis with mastectomy or breast conserving surgery (BCS) with or without radiotherapy (RT). Preoperative MRI was defined as MRI occurring before a woman's first surgery after her initial diagnosis. We looked for surgical treatment (BCS or mastectomy) and radiotherapy, age at diagnosis, year of diagnosis and cancer type, overall and separately by receipt of MRI. We examined the association of surgical treatment with MRI using multivariable logistic regression adjusting for age at diagnosis, year of diagnosis, cancer type and radiotherapy. Results: Among the 70,758 women identified, 5,126 (7.2%) had a preoperative MRI. The overall use of MRI increased from 1.2% in 2002 to 18.0% in 2007 (p &amp;lt; 0.0001). Women with MRI were more likely to undergo mastectomy than those without MRI (331 per 1000 vs. 314 per 1000; respectively, p &amp;lt; 0.0001) and more likely to undergo BCS RT (432 per 1000 vs. 354 per 1000; respectively, p &amp;lt; 0.0001). Conclusion: The use of preoperative MRI has increased in recent years and is significantly associated with increased rates of BCS RT and mastectomy. Limitations of this study include that it is an observational analysis and that selection bias may exist for MRI and aggressive treatment that is not related to what is observed on MRI. Further studies are needed to understand how patient characteristics and information obtained from MRI influence treatment choices. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P4-01-15.
Abstract 4308: Dynamic regulation of CD24 and the invasive, CD44posCD24neg phenotype in breast cancer cell lines
Authors: Matthew J. Meyer, Jodie M. Fleming, Mustapha A. Ali, Mitchell W. Pesesky, Erika Ginsburg, Barbara K. Vonderhaar
Journal: Cancer Research (2010)

Abstract Introduction The invasive, mesenchymal phenotype of CD44posCD24neg breast cancer cells has made them a promising target for eliminating the metastatic capacity of primary tumors. It has been previously demonstrated that CD44neg/lowCD24pos breast cancer cells lack the ability to give rise to their invasive CD44posCD24neg counterpart. Here we demonstrate that noninvasive, epithelial-like CD44posCD24pos cells readily give rise to invasive, mesenchymal CD44posCD24neg progeny in vivo and in vitro. This interconversion was found to be dependent upon Activin/Nodal signaling. Methods Breast cancer cell lines were sorted into CD44posCD24pos and CD44posCD24neg populations to evaluate their progeny for the expression of CD44, CD24, and markers of a mesenchymal phenotype. The FACS sorted populations were injected into immunocompromised mice to evaluate their tumorigenicity and invasiveness of the resulting xenografts. Results CD24 expression was dynamically regulated in vitro in all evaluated breast cancer cell lines. Furthermore, a single noninvasive, epithelial-like CD44posCD24pos cell had the ability to give rise to invasive, mesenchymal CD44posCD24neg progeny. Importantly, this interconversion occurred in vivo as CD44posCD24pos cells gave rise to xenografts with locally invasive borders as seen in xenografts initiated with CD44posCD24neg cells. Lastly, the ability of CD44posCD24pos cells to give rise to mesenchymal progeny, and vice versa, was blocked upon ablation of Activin/Nodal signaling. Conclusions Our data demonstrate that the invasive, mesenchymal CD44posCD24neg phenotype is under dynamic control in breast cancer cell lines both in vivo and in vitro. Furthermore, our observations suggest that targeted therapy against CD44posCD24neg tumor cells may have limited success in preventing primary tumor metastasis unless Activin/Nodal signaling is arrested. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4308.
Growth of Marrow Registries Increases Patients' Odds
Authors: Tom Reynolds
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Growth of Marrow Registries Increases Patients' Odds Get access Tom Reynolds Tom Reynolds Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 14, 17 July 1991, Pages 988–990, https://doi.org/10.1093/jnci/83.14.988 Published: 17 July 1991
Somatostatin Receptor Scintigraphy
Authors: J W Thomason, R S Martin, M E Fincher
Journal: Clinical Nuclear Medicine (2000)

Vasoactive intestinal peptide–secreting tumors (VIPomas) are extremely rare and difficult to diagnose. The authors describe a patient who was found to have a VIPoma after 3 years of symptoms. Somatostatin receptor scintigraphy using indium-labeled octreotide localized her tumor and prompted a surgical resection. This is the preferred imaging study for the earliest, most accurate, and cost-effective identification of VIPomas and their metastases.
Case 34-2013
Authors: MingMing Ning, R. Gilberto Gonzalez
Journal: New England Journal of Medicine (2013)

A 69-year-old man was admitted to this hospital because of dizziness and vomiting, which had begun abruptly 9 hours earlier, on awakening. Examination revealed nystagmus and a wide-based gait. CT revealed no intracranial hemorrhage. A diagnostic procedure was performed.
Abdominal Aortic Aneurysm Demonstrated on Renal Scintigraphy
Authors: Sorot Phisitkul, Susan Brian, Ariwan Rakvit, Leigh A. Jenkins, W. Todd Bohannon, Jennifer Harris, James Tsikouris, Michael B. Silva, Gary E. Meyerrose
Journal: Clinical Nuclear Medicine (2003)

A 74-year-old hypertensive woman presented with abdominal discomfort and a pulsatile abdominal mass. Anterior abdominal angiography during cardiac blood pool, and renal scintigraphic imaging demonstrated a large abdominal aortic aneurysm. 1,2 Before endovascular repair with an aortoiliac endograft, the abdominal aneurysm measured 7.5 × 7.0 cm on abdominal computed tomography. This study demonstrates that a suspected abdominal aortic aneurysm can be confirmed using the addition of anterior abdominal imaging with normal posterior imaging at the time of renal scintigraphy. 3–5
Abstract 4881: Influence of polyphenols on selenoprotein expression in human colon cancer cells.
Authors: Sarah E. Galinn, Lindsay C. Rosenthal, Steven M. Barsotti, Petra A. Tsuji
Journal: Cancer Research (2013)

Abstract Selenium, an essential micronutrient, is recognized as a cancer protective agent that functions through low-molecular weight selenocompounds, and, importantly, through selenoproteins. Previous studies suggest that the 15 kDa selenoprotein (Sep15), a gene polymorphic in humans, has an important role in colon cancer in vivo, and that reduction of Sep15 in human HCT116 colon cancer cells reverses their cancer phenotype. Our diet contains a wide array of nutrients, and it is conceivable that these share molecular targets with selenium and regulate selenoprotein expression. The selenoproteins Thioredoxin Reductase 1 (TR1) and Glutathione Peroxidase (GPx) 2 are regulated by the transcription factor Nrf2, whereas GPx1 is not. Some dietary compounds, e.g., Sulforaphane, are known Nrf2-inducers, impacting expression of TR1 and GPx2. However, the effect of Sulforaphane and many polyphenols on other selenoproteins, or, how other polyphenols influence TR1 and GPx2 remains to be elucidated. Using HCT116 cells, we are investigating the effects of polyphenols and Sulforaphane on selenoprotein expression. Cells with wild type or down-regulated expression of Sep15 were exposed to 5 μM Sulforaphane or 20 μM 5,7-Dimethoxyflavone (5,7-DMF) for 48 hours. Subsequently, mRNA was isolated and examined with real-time RT-PCR. Our preliminary results suggest that, Sulforaphane exposure resulted in a slight increase of TR1 mRNA in both control and shSep15 cells, but not GPx2. Interestingly, 5,7-DMF exposure resulted in increased GPx1 (P&amp;lt;0.01) and GPx2 (P&amp;gt;0.05) mRNA in control cells. Surprisingly, GPx2 mRNA appeared significantly down-regulated (P&amp;lt;0.01) in shSep15 cells compared to DMSO treated cells, whereas GPx1 mRNA appeared unaffected. Western blotting and activity measurements are currently underway to support these results. Citation Format: Sarah E. Galinn, Lindsay C. Rosenthal, Steven M. Barsotti, Petra A. Tsuji. Influence of polyphenols on selenoprotein expression in human colon cancer cells. [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 4881. doi:10.1158/1538-7445.AM2013-4881
Abstract 1597: C646, a selective small molecule inhibitor of p300, radiosensitizes cancer cells through enhancement of mitotic catastrophe.
Authors: Takahiro Oike, Mayumi Komachi, Hideaki Ogiwara, Jun Yokota, Takashi Nakano, Takashi Kohno
Journal: Cancer Research (2013)

Abstract Background: The histone acetyltransferases (HATs) including p300, CBP and TIP60 are transcriptional co-activators implicated in many gene regulatory pathways and protein acetylation events. We have previously shown that siRNA-mediated ablation of p300 and CBP sensitized cancer cells to ionizing radiation (IR) (Ogiwara, Oncogene 2011), and that garcinol, curcumin and anacardic acid, natural compounds with multi-HATs inhibitory activity, had radiosensitizing effect in cancer cells (Oike, Int J Radiat Oncol Biol Phys 2012). However, radiosensitization by selective small molecule inhibitors targeting activity of a specific HAT, that can have much potential for clinical use, have not been well investigated. C646 is a selective small molecule inhibitor of p300 identified by structure-based and active site-directed in silico screening (Bowers, Chem Biol 2010). In this study, we investigated the in vitro effect of C646 on radiosensitization and cell death in human cancer cells. Materials and Methods: The radiosensitizing effect in A549 (lung adenocarcinoma), H460 (lung squamous cell carcinoma) and H157 (lung large cell carcinoma) cells were assessed by colony formation assay, while that in MRC-5 (fibroblast) cells lacking in colony-forming ability was examined by ATP assay. Cell cycle distribution in A549 cells was analyzed using flow cytometry. The effect on mitotic catastrophe, apoptosis and senescence in A549 cells was evaluated by DAPI, annexin V and senescence-associated β-galactosidase staining, respectively. C646 was used at concentrations less than IC50. Results: C646 radiosensitized A549, H460 and H157 cancer cells with dose enhancement ratio at 10% surviving fraction of 1.4, 1.2 and 1.2, respectively. Meanwhile, C646 unaffected the radiosensitivity of MRC-5 cells. Cell cycle analysis showed that the hyperploid cell population (&amp;gt; 4N DNA cells) increased in C646-treated A549 cells after IR. Analyses of mode of cell death revealed that C646 enhanced mitotic catastrophe, but not apoptosis nor senescence, induced by IR in A549 cells. Conclusion: These data indicate that C646 is a radiosensitizer which enhances mitotic catastrophe induced by IR. Citation Format: Takahiro Oike, Mayumi Komachi, Hideaki Ogiwara, Jun Yokota, Takashi Nakano, Takashi Kohno. C646, a selective small molecule inhibitor of p300, radiosensitizes cancer cells through enhancement of mitotic catastrophe. [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 1597. doi:10.1158/1538-7445.AM2013-1597
Further Observations on the Swiss Type of Agammaglobulinemia (Alymphocytosis)
Authors: Fred S. Rosen, Samuel P. Gotoff, John M. Craig, Joshua Ritchie, Charles A. Janeway
Journal: New England Journal of Medicine (1966)

A SEVERE, lethal form of agammaglobulinemia associated with alymphocytosis and aplasia of the thymus gland has been described in western Europe,1 2 3 4 Great Britain5 and the United States.6 7 8 Because investigators in Switzerland1 2 3 were the first to recognize and define this syndrome it is often called the Swiss type of agammaglobulinemia. Afflicted infants fail to thrive, and intractable diarrhea, generalized moniliasis and recurrent pulmonary infection develop. Gamma-globulin therapy is of no avail in preventing death from infection, which occurs by the end of the second year of life. A few attempts to restore immunologic competence and to populate the lymphoid tissue by . . .
Abstract 649: Dynamic magnetic resonance imaging of the effects of vascular targeting agents on intracerebral metastases
Authors: Leslie L. Muldoon, Seymur Gahramanov, Deborah J. Marshall, Edward A. Neuwelt
Journal: Cancer Research (2010)

Abstract Objective: Agents that target tumor vasculature are gaining use as therapeutics for brain tumors. We used dynamic magnetic resonance imaging (MRI) to evaluate the vascular effects of the monoclonal antibodies bevacizumab, targeting vascular endothelial growth factor (VEGF), and intetumumab (CNTO 95), targeting αV integrins, in a rat model of lung cancer brain metastasis. Methods: Female nude rats received intracerebral implantation of human LX-1 small cell lung carcinoma cells. At 10 days after tumor implantation, rats were untreated or treated with intetumumab (30 mg/kg IV) or bevacizumab (45 mg/kg IV) (n = 4-5 per group). MRI at 12T was performed prior to treatment and at 1, 3, and 7 days after treatment, using dynamic contrast enhanced (DCE) MRI with gadolinium-based contrast agent (GBCA), and dynamic susceptibility contrast (DSC) MRI with the blood pool iron oxide nanoparticle ferumoxytol. Tumor relative cerebral blood volume (rCBV) and permeability markers were assessed. Results: Intetumumab increased brain tumor vascular permeability at 3 and 7 days after treatment on DCE-MRI, as determined by the ratio of maximum GBCA signal intensity to normal brain, a measure of the interstitial space volume fraction (ve), and time to peak enhancement, a surrogate for Ktrans, the rate constant for passive leakage across the blood-brain barrier. Intetumumab also increased tumor rCBV on DSC-MRI as compared to untreated controls. Tumors uniformly grew during the week assessment period. In contrast, bevacizumab decreased tumor permeability and rCBV, and slowed the increase in the volume of enhancing tumor on both T1-weighted and T2-weighted images, compared with controls. Conclusions: The vascular targeting agents intetumumab and bevacizumab had diametrically opposite effects on dynamic MRI of tumor vasculature in a rat brain metastasis model. The αV integrin inhibitory antibody intetumumab appeared to increase tumor vascular permeability and blood volume, suggesting it may enhance chemotherapy efficacy by improving chemotherapy delivery to intracerebral tumors. Conversely, the effects of bevacizumab on tumor vasculature suggest it would actually decrease chemotherapy delivery, thereby minimizing chemotherapy efficacy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 649.
PROLONGED TPEAK-END AND TPEAK-END/QT RATIO AS A PREDICTOR OF MALIGNANT VENTRICULAR ARRHYTHMIAS IN THE ACUTE PHASE OF ST ELEVATION MYOCARDIAL INFARCTION: A PROSPECTIVE CASE CONTROL STUDY
Authors: Maneesh K Rai, Jayaprakash Shenthar, Surender Deora, Manjunath C. Nanjappa
Journal: Journal of the American College of Cardiology (2015)
CYTOMEGALOVIRUS CONTRIBUTES TO GLIOBLASTOMA IN THE CONTEXT OF TUMOR SUPPRESSOR MUTATIONS
Authors: E. A. Chiocca, R. L. Price, T. Hollon, C. Alvarez-Breackenridge, S. Fernandez, M. Oglesbee, C. Cook, S. Lawler, C.-H. Kwon
Journal: Neuro-Oncology (2014)

BACKGROUND: There have been several reports that have linked human cytomegalovirus (CMV) to gliomas. Although clinical trials of immunotherapy against CMV antigens found in gliomas have commenced in multiple institutions, the data linking these tumors to this virus remains controversial. METHODS: To study the controversial role of cytomegalovirus (CMV) in glioblastoma, we assessed the effects of murine CMV (MCMV) perinatal infection in a GFAP-cre; Nf1loxP/+ ; Trp53-/+ genetic mouse model of glioma (Mut3 mice). RESULTS: Early on after infection, MCMV antigen was predominantly localized in CD45+ lymphocytes in the brain with active viral replication and local areas of inflammation, but by 7 weeks there was a generalized loss of MCMV in brain, confirmed by bioluminescent imaging. MCMV-infected Mut3 mice exhibited a shorter survival time from their gliomas, when compared to control Mut3 mice, perinatally infected with mock or with a different neurotropic virus. Animal survival was also significantly shortened when orthotopic gliomas were implanted in mice perinatally infected with MCMV vs. controls. MCMV infection increased phosphorylated STAT3 (P-STAT3) levels in neural stem cells (NSCs) harvested from Mut3 mice SVZ and in vivo there was increased P-STAT3 in NSCs in MCMV-infected compared to control mice. Of relevance, human CMV (HCMV) also increased P-STAT3 and proliferation of patient-derived glioblastoma neurospheres, while a STAT3 inhibitor reversed this effect in vitro and in vivo. CONCLUSIONS: These findings thus associate CMV infection to a STAT3-dependent modulatory role in glioma formation/progression in the context of tumor suppressor mutations in mice and possibly in humans. SECONDARY CATEGORY: Neuropathology & Tumor Biomarkers.
Abstract 482: High CD44/CD24 expressive cells presented cancer stem cell characteristics and undergo mitochondrial resetting and metabolic shift in nasopharyngeal carcinoma
Authors: Yao-An Shen, Yau-Huei Wei, Yann-Jang Chen
Journal: Cancer Research (2011)

Abstract Cancer stem cells (CSCs) are a rare subset cancer cells with self-renewal property and cause many difficulties in clinical treatment. CSCs have been found in different tumors by specific surface markers. However, the surface marker of CSC remains unknown in various cancer types, including in nasopharyngeal carcinoma (NPC). Here, we took advantage of CSC's properties, such as chemoresistance, radioresistance, and the ability to form tumor spheres, to isolate CSCs from NPC cell lines. Combining these three isolation methods, and surface marker screening, we identified that NPC CSCs had high level of CD44 and CD24 surface antigen expression. We then validated the CD44/CD24 high positive as NPC CSC surface marker. In cell proliferation assay by MTT test, tumorigenity assay in soft agar and in vivo xenotransplantation, and radioresistant assay, CD44/CD24 high positive cells expressed significant CSC properties compared with CD44/CD24 double negative and parental NPC cells. We further found that CSCs underwent mitochondria resetting, including the distribution, quantity, and quality of mitochondria. Metabolic shift that largely relied on glycolysis also occured in CSCs. They predominately ultilized glycolysis instead of mitochondrial respiration to meet energy demand. Inhibiting glycolysis or treating antioxidants suppresses the viability and malignant traits of CSCs which provides therapeutic implication in NPC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 482. doi:10.1158/1538-7445.AM2011-482
Abstract 714: Survivin expression in patients with resected pancreatic adenocarcinoma
Authors: Saad A. Khan, Donghua Yang, Fang Zhu, Cara Dubyk, Mohamed Tejani, Steven J. Cohen, John P. Hoffman, Barbara A. Burtness
Journal: Cancer Research (2012)

Abstract Introduction: Pancreatic cancer remains highly refractory to treatment and biomarkers of treatment responsiveness are urgently needed. Survivin is an inhibitor of apoptosis and one such potential marker. Undetectable in most normal differentiated and non-proliferating tissues, it is highly expressed in cancer. We measured pancreatic cancer survivin expression and examined its association with differential treatment response. Methods: We constructed 4 pancreatic cancer tissue microarrays with 1mm duplicate cores using tumor samples from 88 resected pancreatic cancer patients at our center. They were then followed with 60 patients receiving chemotherapy or radiation, both as adjuvant therapy and also for palliative treatment upon recurrence. We measured survivin expression using highly quantitative automated immunofluorescence via AQUA R(HistoRx, Branford CT). Scores were individually reported for the nuclear, cytoplasmic and total cellular compartments, and validated by the pathologist. Results: Median survivin AQUA scores were: nuclear 5838 (range 2126-13728), cytoplasm 4177 (2173-9914) and total 4543 (2120-10344). Survivin expression was significantly higher in nodal specimens compared to primary tumor in nucleus (p=0.02), cytoplasm (p=0.006) and in total (p=0.0095). Higher cytoplasmic survivin correlated with higher grade (p=0.03), and primary tumor location in head compared to body or tail (p=0.03). There was a trend toward higher nuclear survivin in younger (p=0.08) and female patients (p=0.08). Disease-free survival (DFS) was significantly longer in patients with high compared to low nuclear survivin (p=0.048), using median as the cut-off. This effect was greater for patients treated with gemcitabine (p=0.0481) than those treated with 5-FU (p=0.0698) or radiation therapy (p=0.094). Overall survival for all patients was not different in the higher than median group compared to lower group patients (p=0.300). There was a trend toward longer overall survival (OS) for patients whose tumors had high nuclear survivin in those treated with fluorouracil (p=0.0856), gemcitabine (p=0.0868) or radiation therapy (p=0.0862). Discussion: Survivin expression is higher in nodal metastases than primary resected pancreatic cancer tumors and is associated with particular clinical and pathologic characteristics. High nuclear survivin expression is associated with longer DFS in patients with resected pancreatic cancer. This effect is most pronounced in patients treated with gemcitabine. Further examination of survivin in a larger series of pancreatic cancers is warranted. 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 714. doi:1538-7445.AM2012-714