tbuckley/cabot-search huggingface dataset:
PTU-175 Value of PET-CT following neo-adjuvant chemotherapy to predict histological outcome in oesophageal adenocarcinoma: Abstract PTU-175 Table 1
Authors: D Nasralla, S Dwerryhouse, D Hall, J Searle, H Barr, I Lyburn
Journal: Gut (2012)

<h3>Introduction</h3> Repeat FDG-PET-CT imaging after neo-adjuvant chemotherapy (NAC) for oesophageal adenocarcinoma is controversial. Some authors claim repeat PET-CT enables clear management decisions to be made in carcinoma of the oesophagus<sup>1 2</sup> but this has been contradicted in a recent systematic review.<sup>3</sup> We reviewed patients with oesophageal adenocarcinoma who underwent pre and post NAC PET-CT to assess if metabolic response of the tumour correlated with operative histology findings. <h3>Methods</h3> 27 patients with oesophageal adenocarcinoma underwent pre-and post-NAC PET-CT scan prior to oesophagectomy. The SUV<sub>max</sub> pre and post NAC and the ratio of the final to initial SUV<sub>max</sub> were calculated and compared with histological T and N stage, tumour area and differentiation. <h3>Results</h3> No new metastatic lesions were discovered on post-NAC PET-CT. There was no significant difference between any of the parameters related to N stage. Initial SUV<sub>max</sub> was greater for tumour stage T3-4 than for T0-2 [11.4 (SEM 1.6) vs 8.3 (1.4), p=0.05] and for poorly differentiated than for moderately differentiated tumours [11.5 (1.5) vs 8.0 (1.2), p=0.05]. Final SUV<sub>max</sub> and the ratio of final to initial SUV<sub>max</sub> were not significantly different for either T-stage or tumour differentiation. A correlation was seen between SUV<sub>max</sub> and tumour area (0.39 vs 0.7). <h3>Conclusion</h3> Initial SUV<sub>max</sub> from PET-CT carried out before NAC is greater for tumours which are poorly differentiated than moderately differentiated, and for stage T3 or T4. The SUV<sub>max</sub> from PET-CT studies carried out after the completion of NAC did not give additional information in this respect. The only area where it did offer potentially valuable information was correlation between tumour area and SUV<sub>max</sub>, although this is unlikely to influence patient management. Post-NAC PET-CT did not predict histological outcome in our patients nor influence their management. <h3>Competing interests</h3> None declared. <h3>References</h3> 1. <b>Lordick F</b>, <i>et al.</i> PET to assess early metabolic response and to guide treatment of adenocarcinoma of the oesophagogastric junction: the MUNICON phase II trial. <i>Lancet Oncol</i> 2007;<b>8</b>:797–805. 2. <b>Bjorn LDM</b>, <i>et al.</i> Neoadjuvant therapy of esophageal squamous cell carcinoma: response evaluation by PET-CT. <i>Ann Surg</i> 233:300–9. 3. <b>Kwee R</b>. Prediction of tumor response to neoadjuvant therapy in patients with esophageal cancer with use of 18 F FDG PET: a systematic review. <i>Radiology</i> 2010;<b>254</b>.
ESTUDIO RANDOMIZADO DE DOS RÉGIMENES DE PREPARACIÓN DE COLON EN PACIENTES DIABÉTICOS
Authors: MA Alvarez, A Seoane, IA Ibañez, A García-Rodriguez, J Flores, A Fernandez-Clotet, F Riu, JM Dedeu, L Barranco, F Bory, V Lorenzo-Zuñiga
Journal: Endoscopy (2014)

Introducción: Estudios previos demuestran que los pacientes diabéticos responden peor a las preparaciones habituales. Un protocolo específico de preparación para pacientes diabéticos puede mejorar la limpieza y aceptabilidad.
Whole-Exome Sequencing (WES) Using Formalin-Fixed Paraffin Embedded (FFPE) Tissue
Authors: K. Ouchi, S. Takahashi, K. Tatsuno, A. Hayashi, S. Yamamoto, H. Ueda, M. Inoue, H. Nakano, H. Aburatani, C. Ishioka
Journal: Annals of Oncology (2013)
Abstract 3704: Clinical efficacy and safety of bevacizumab monotherapy in patients with metastatic melanoma: predictive importance of induced early hypertension in a single-arm Phase II study
Authors: Oddbjorn Straume, Cornelia Schuster, Hanne Puntervoll, Hans P. Eikesdal, Daniel Heinrich, Stephanie B. Geisler, Jurgen Geisler, Anders Molven, Per E. Lønning, Lars Akslen
Journal: Cancer Research (2012)

Abstract Purpose VEGF driven angiogenesis plays a key role in tumor growth. We determined clinical efficacy of bevacizumab monotherapy in unselected patients with metastatic melanoma. Patients and methods Thirty-five patients with metastatic melanoma in progression were enrolled in this phase II, single arm clinical trial. Each patient received bevacizumab monotherapy 10 mg/kg q14 d until intolerable toxicity or disease progression occurred. Clinical efficacy was evaluated by measuring objective response (OR), disease control (DC), and survival. We also evaluated potential predictive value of clinical parameters and BRAF/NRAS mutational status. Results We observed one complete (CR, 3%) and 5 partial (PR, 14%) responses. In addition, 5 patients experienced stable disease &amp;gt; 6 months (SD, 14%), while 24 patients had progressive disease (PD, 69%), corresponding to a total disease control (DC) at 6 months in 11 out of 35 patients (31 %). Median progression free survival (PFS) was 2.14 months and median overall survival (OS) was 9 months (1.12-49). Seven of the 11 patients experiencing DC developed early hypertension (&amp;lt; 2 months) after commencing bevacizumab compared to 3/24 of patients with PD (P= 0.001), and hypertension was associated with improved progression free survival (P= 0.005) and overall survival (P= 0.013). No correlation between BRAF and NRAS mutation status and response was recorded. Conclusion Bevacizumab monotherapy demonstrated promising clinical efficacy in patients with metastatic melanoma with disease control in 31% of the patients. The activity of the drug seemed particularly pronounced in patients developing by hypertension early during. 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 3704. doi:1538-7445.AM2012-3704
Abstract IA-15: Balancing quiescence and proliferation in stem cells and its implications for cancer
Authors: Elaine V. Fuchs
Journal: Cancer Research (2009)

Abstract Even though many adult tissues undergo relatively infrequent turnover, they still require stem cells (SCs) which are then used sparingly to replenish cells during normal homeostasis. Moreover, in response to injury, adult SCs must be mobilized quickly to repair damaged tissue. How SCs balance their ability to rest during periods of quiescence, activate to replenish cells and tissue when needed and replace the SCs used for tissue maintenance and repair are fascinating topics in stem cell biology and tissue morphogenesis. Moreover, increasing evidence suggests that the regulatory circuitry governing this balancing act is at the root of some types of tumors both in mice and in humans. The skin is an excellent model system to understand how undifferentiated SCs self-renew to generate the epidermis and its notable appendages, hair follicles (HFs). In the embryo, skin begins as a single layer of multipotent progenitors, which adhere to each other as well as to an underlying basement membrane rich in extracellular matrix. These progenitors express members of the Lef1/Tcf family of DNA binding proteins thought to act as bipartite transcription factors in association with β-catenin. Excess β-catenin not utilized in intercellular junctions is stabilized when skin progenitors receive Wnt signals from their microenvironment to initiate HF formation. As development proceeds, progenitors respond to additional signals as the skin epithelial tissues mature and differentiate. Postnatally, epidermis retains SCs to undergo homeostasis and maintain the body surface barrier, while HFs undergo cyclical bouts of Wnt signaling that leads to follicle regeneration and hair growth, followed by destruction of the follicle and a resting period to accumulate a new threshold level of signal. The role of Wnt signaling in follicle SC activation and hair regeneration is particularly interesting, as mounting evidence suggests that Wnt signaling may play a general role in governing SC biology and injury repair. Using skin as our paradigm, we have continued to dissect how extrinsic signaling to SCs sets off a cascade of changes in transcription that govern the activation of SCs during tissue development, homeostasis and hair cycling. We've focused our efforts on the roles of three Tcf/Lef1 family members, all expressed initially in the single-layered epithelium, but which then diversify to be differentially expressed in adult skin SCs and rapidly dividing but committed progeny. Our findings point to Wnt-independent as well as Wnt-dependent functions for these transcription factors, which are likely to be important for our understanding of why Wnt signaling is deregulated in a variety of different human cancers and how Wnt circuitry balances quiescence and proliferation in stem cell and progenitor compartments. Citation Information: Cancer Res 2009;69(23 Suppl):IA-15.
Successful endoscopic treatment of Boerhaave syndrome using an over-the-scope clip
Authors: H. Kobara, H. Mori, K. Rafiq, S. Fujihara, N. Nishiyama, K. Kato, M. Oryu, J. Tani, H. Miyoshi, T. Masaki
Journal: Endoscopy (2014)

Boerhaave syndrome, a rare condition involving esophageal perforation and associated with high mortality, has traditionally required surgical repair [1]. In most cases of Boerhaave syndrome, the tear extends several centimeters, because of which it is difficult to completely close with hemoclips. More recently, treatment with self-expandable metal stents has been attempted for Boerhaave syndrome. However this method has a limited success rate and safety concerns have been reported [2]. We have described elsewhere the utility of the over-the-scope clip (OTSC) in patients with perforations and fistulas of the gastrointestinal tract [3] [4] [5]. Here, we present the first patient with Boerhaave syndrome successfully treated nonoperatively with OTSC.
Airway Responsiveness in Transgenic Mice Overexpressing Platelet-activating Factor Receptor
Authors: TAKAHIDE NAGASE, SATOSHI ISHII, HIROFUMI KATAYAMA, YOSHINOSUKE FUKUCHI, YASUYOSHI OUCHI, TAKAO SHIMIZU
Journal: American Journal of Respiratory and Critical Care Medicine (1997)

Platelet-activating factor (PAF) is a potent proinflammatory compound potentially involved in the pathogenesis of inflammatory disorders, including bronchial asthma. To elucidate the pathophysiologic roles of PAF in bronchial asthma, we studied airway responsiveness in transgenic mice overexpressing PAF receptor. In the transgenic mice, PAF-induced airway smooth muscle contraction was demonstrated by physiologic and morphometric analyses, whereas there was no significant response in the littermate control group. The PAF-elicited bronchoconstriction in the transgenic mice was significantly reduced not only by a PAF receptor antagonist (WEB-2086) but also by a thromboxane synthesis inhibitor (indomethacin or ozagrel), an inhibitor of 5-lipoxygenase-activating protein (MK-886), or a cysteinyl leukotriene (LT) antagonist (pranlukast). LTB4 receptor antagonist (ONO-4057), however, had no effect on the PAF-induced responses. The transgenic mice showed a bronchial hyperreactivity to methacholine challenge, which was also inhibited by pretreatment with either thromboxane synthesis inhibitor or cysteinyl LT antagonist. These observations suggest that both thromboxane A2 and cysteinyl LTs (LTC4, LTD4, and LTE4) are involved in the bronchial responses to PAF or cholinergic stimulus in mice. The transgenic mice overexpressing PAF receptor may provide an appropriate model to study various PAF-related lung diseases, including bronchial asthma.
Transrectal endoscopic ultrasound-guided drainage of pelvic abscess with placement of a fully covered self-expandable metal stent
Authors: C. Luigiano, T. Togliani, V. Cennamo, A. Maimone, A. Polifemo, S. Pilati, C. Fabbri
Journal: Endoscopy (2013)

Pelvic abscess developed in an 88-year-old woman (Case 1) following a Hartmann's procedure for a perforated diverticulum and in a 78-year-old woman (Case 2) after diverticulitis ([Fig. 1]). Conservative management was unsuccessful in the first patient due to advanced age and in the second patient due to severe co-morbidities.
Hydatid cyst mimicking cystic neoplasm of the pancreatic tail: an endoscopic ultrasound diagnosis
Authors: Suvadip Chatterjee, Manas Roy, Sudeep Banerjee, Sumit Mukhopadhaya, Saugata Sen, Mohandas Mallath
Journal: Endoscopy (2014)

A 59-year-old woman presented with weight loss and left hypochondrial discomfort that had been present for 2 weeks. Abdominal computed tomography (CT) revealed a 12 cm × 11 cm lobulated nonenhancing cystic lesion with intrinsic heterogeneous hyperdense areas ([Fig. 1]) and peripheral wall calcification ([Fig. 1 b]). A provisional diagnosis of cystic neoplasm of the tail of the pancreas was made and the patient was referred for endoscopic ultrasound (EUS) and fine needle aspiration (FNA).
Abstract 1105: Dysregulated ΔNp63α displaces p73 from the promoter of the tumor suppressor gene maspin in keratinocytes
Authors: Kathryn E. King, Deepti Muraleedharan, Roshini M. Ponnamperuma, Michael Gerdes, Wendy C. Weinberg
Journal: Cancer Research (2010)

Abstract The p53 homologue p63 is critical for normal epidermal development. While overexpression of p63, in particular ΔNp63α, has been reported in many squamous cell cancers including those of the skin, the role of p63 in cancer pathogenesis remains unclear. We have previously shown that elevated levels of ΔNp63α aberrantly maintain keratinocyte proliferation under differentiating conditions. We performed microarray analyses of primary murine epidermal keratinocytes overexpressing adenoviral (Ad)-driven ΔNp63α vs. β-gal to identify target genes impacted by dysregulated ΔNp63α. Our studies revealed a coordinated downregulation of RNA transcripts for multiple protease inhibitors, including two members of the serine protease inhibitor (serpin) family, maspin (serpinB5) and plasminogen activator inhibitor-2, PAI-2 (serpinB2), in addition to the metalloproteinase inhibitor, tissue inhibitor of metalloproteinase-3 (TIMP-3). Downregulation of all three protease inhibitors was confirmed by RT-PCR and examined further by western analysis. TIMP-3 protein was detected in keratinocyte conditioned medium but not in whole cell lysates, supporting a primarily extracellular function for TIMP-3. PAI-2 and maspin were detected in both whole cell lysates and conditioned medium, consistent with both intracellular and extracellular roles for these proteins. Secreted levels of TIMP-3 and PAI-2 declined in Ad-ΔNp63α-cultures compared to Ad-β-gal-cultures, whereas maspin levels remained stable. Intracellular expression of both PAI-2 and maspin was negatively regulated by ΔNp63α. To investigate the mechanism by which ΔNp63α down-regulates maspin, we performed electrophoretic mobility shift assays (EMSAs) using a known p53 consensus DNA binding sequence in the maspin promoter. An endogenous complex was seen by EMSA in normal keratinocytes that was disrupted in the presence of increasing levels of ΔNp63α. Supershift analysis revealed that this endogenous complex was interrupted by the addition of a p73 antibody, but no supershift or block was seen with antibodies to p63 or p53. EMSA analysis of nuclear extracts prepared from p73(-/-) keratinocytes confirmed that p73 is required for this complex formation. The current data suggest additional roles for ΔNp63α in cancer pathogenesis by disrupting p73 transcriptional activity to down-modulate protease inhibitors. 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 1105.
Abstract 5107: Unravelling the complexity of individual cancer genomes
Authors: Francesca Menghi, XingYi Woo, Min Gong, Sigrid L. Rouam, Denis Bertrand, Wah H. Lee, Wendy Wang, Nona Rama, Euan A. Stronach, Krishna Karuturi, Hani Gabra, Roshan Agarwal, Edison T. Liu
Journal: Cancer Research (2012)

Abstract Ovarian cancer affects ∼ 204,000 women each year, and it is one of the leading causes of cancer-related death among women world-wide, as most patients present with advanced stage (III/IV) tumours, and only 40% survive 5 years after diagnosis. Improvement in the clinical management of ovarian patients is likely to derive from a better understanding of the molecular aberrations which initiate and maintain tumour growth as well as from the discovery of novel drug-able targets for the development of personalised targeted therapies. In this study, we comprehensively characterised the cancer genome of a patient diagnosed with grade III serous ovarian carcinoma, using a combination of massive-parallel sequencing technologies, including long distance DNA Paired-End-Tag (DNA-PET) sequencing, RNA-sequencing and exome-capture sequencing. This approach ensures deep coverage (from 50-180X) of critical mutational elements in a cancer genome. By comparing the genomic abnormalities identified in the tumour sample with those found in its normal counterpart (peripheral blood lymphocytes), we were able to compile a catalogue of all of the somatic events which occurred during oncogenesis and to define the overall complexity of this specific cancer genome. Interestingly, chromosomal arm loss appeared to be the predominant feature of this tumour, with more than 30% of the haploid genome being affected by a decrease in copy number. This associated with a prevalence of inter-chromosomal rearrangements, suggesting chromosomal translocations as a preferred consequence of genomic instability. Here we describe some examples of somatic translocation events causing the loss of tumour suppressor genes. Using this genotype as a possible model of ovarian carcinoma evolution, we aim to explain a subset of ovarian cancers displaying a similar chromosomal profile by applying an analysis of copy number variations, and to define common mechanisms of cancer gene loss. 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 5107. doi:1538-7445.AM2012-5107
Undetectable Thyroglobulin in Patients With Differentiated Thyroid Carcinoma and Residual Radioiodine Uptake on a Postablation Whole-Body Scan
Authors: Luca Giovanella, Sergio Suriano, Luca Ceriani, Frederik Anton Verburg
Journal: Clinical Nuclear Medicine (2011)

To assess the impact of laboratory interferences and pitfalls in producing falsely undetectable Tg in differentiated thyroid carcinoma (DTC) patients with residual iodine-avid thyroid tissue on a posttreatment whole-body scan (PT-WBS).From 298 consecutive patients with histologically proven DTC, 47 patients (16%) with undetectable serum Tg but residual ¹³¹I uptake on a PT-WBS were selected. Interferences from antithyroglobulin antibodies (TgAb), heterophile antibodies, and hook-effects were screened; in the remaining samples, serum Tg was measured in 3 different immunoassays.Of 47 patients, 11 (23%) showed interference from either thyroglobulin antibodies (n = 10) or heterophile antibodies (n = 1). Among the 36 remaining patients, 18 showed detectable Tg levels after retesting using a different immunoassay, whereas the remaining 18 patients also showed detectable Tg levels in a third Tg immunoassay. However, only 7 patients showed a detectable Tg in both secondarily used assays. Tg levels remained undetectable in all methods in 9 patients (19%) even after extensive laboratory work-up and despite the presence of ¹³¹I-avid tissue found in PT-WBS.A careful assessment of interferences in Tg measurement significantly reduced the occurrence of undetectable Tg among patients with ¹³¹I uptake in PT-WBS. However, such extensive assessment is difficult in clinical practice and one-fifth of patients still had undetectable Tg in multiple assays despite an intensive laboratory work-up. A benchmark between ¹³¹I imaging and Tg measurement authenticates the interpretation of Tg measurements and, consequently, remains of pivotal value by authenticating the use of serum Tg during further follow-up of DTC patients.
Value of Laparoscopic Microwave Coagulation Therapy for Hepatocellular Carcinoma in Relation to Tumor Size and Location
Authors: T Abe, H Shinzawa, H Wakabayashi, M Aoki, K Sugahara, A Iwaba, H Haga, S Miyano, Y Terui, H Mitsuhashi, H Watanabe, T Matsuo, K Saito, T Saito, H Togashi, T Takahashi
Journal: Endoscopy (2000)

The indications for laparoscopic microwave coagulation therapy (LMCT) for hepatocellular carcinoma (HCC) have not yet been adequately evaluated. This study investigated the value of LMCT in the treatment of HCC.Forty-three patients with liver cirrhosis (including five patients in Child Pugh grade C), with 56 HCC lesions, were enrolled in the study. When dynamic computed tomography (CT) showed a loss in HCC enhancement characteristics and a low concentration area after LMCT, a lesion was judged to have undergone complete necrosis.The rate of complete necrosis for lesions measuring 40 mm or less was significantly higher (P<0.01) than for those measuring 41 mm or more. The rate of complete necrosis for lesions located on the liver surface, excluding those located close to the gallbladder or in contact with the diaphragm, was also significantly higher (P<0.01) than for those situated deep within the liver. The outcome for lesions of 40 mm or less was favorable. Intra-abdominal hemorrhage occurred in two patients, pneumothorax in three, and hepatic infarction in one, all associated with LMCT. However, these patients did not suffer any sequelae of clinical significance.This study suggests that there is a strong indication for LMCT for HCCs measuring 40 mm or less in diameter and those located on the liver surface even if they are as large as 50 mm, but not for those located close to the gallbladder or in contact with the diaphragm. LMCT appears to be applicable in patients with impaired liver function.
Abstract 4853: Reduced expression of DRAM2/TMEM77 in tumor cells interferes with cell death
Authors: Ik-Soon Jang, Soohyun Kim, Jong Soon Choi, Sun-Mi Park, Junsoo Park
Journal: Cancer Research (2010)

Abstract Although the role of autophagy in tumorigenesis remains controversial, recent reports support the notion that inhibition of autophagy promotes tumor formation. Damageregulated autophagy regulator (DRAM) has been identified as an effector molecule that is critical for p53-mediated apoptosis, and we investigated whether there might be other DRAM-like molecules linking autophagy and apoptosis. In this study, we cloned a novel DRAM-homologous protein, DRAM2, and showed that the expression of DRAM2 is down-regulated in ovarian tumors. DRAM2 is mainly localized in the lysosome, and colocalizes with DRAM. While expression of DRAM or DRAM2 individually did not induce cell death, co-expression of DRAM2 with DRAM significantly induced cell death, while the silencing of endogenous DRAM2 attenuated cell death, suggesting that DRAM2 is involved in cell death. Thus, we propose that reduced expression of DRAM2 may contribute to enhanced cell survival in tumor cells. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 4853.