tbuckley/cabot-search huggingface dataset:
Regorafenib for previously treated metastatic colorectal cancer (mCRC): results from 683 Italian patients treated in the open-label phase IIIB CONSIGN study
Authors: F. Ciardiello, L. Salvatore, S. Cascinu, A. Sobrero, M. Banzi, C. Barone, A. Spallanzani, T.L. Latiano, A. Amatu, V. Zagonel, M. Biglietto, F. Di Costanzo, M. Di Bartolomeo, A. Santoro, A. Russo, M. Moscovici, E. Van Cutsem, A. Zaniboni
Journal: Annals of Oncology (2015)
TR4: Inhibitor of notch activation.
Authors: A. A. Epenetos, C. Kousparou, S. Stylianou, M. Deonarain
Journal: Journal of Clinical Oncology (2011)

e13509 Background: We report on the development of a new class of therapeutic proteins that interfere with intracellular targets in both cancer cells and cancer stem cells (CSC). Methods: We used a delivery platform based on drosophila transcription factor antennapedia (ANTP) which allows for intracellular and intranuclear delivery as well as enabling the transport of agents across the blood-brain barrier. The following example exemplifies this approach: we have engineered a fusion protein, consisting of antennapedia (ANTP) and the truncated version of mastermind-like (MAML) that behaves in a dominant negative (DN) fashion and inhibits the notch transactivation complex. This fusion protein, (ANTP/DN‐MAML) or TR4, has been tested for its ability to target tumor cells in vitro and in vivo. Results: TR4 has been: shown that it has a killing effect at clinically meaningful IC50; shown that it acts specifically on the notch pathway; and shown to be stable when stored and freeze/thawed. Conclusions: The results described here demonstrate the features of this approach with the principal benefit being the delivery of therapies with improved tissue and cellular penetration which may lead to improved efficacy of existing therapies and open up new treatment pathways.
Plastic CD34 and CD38 expression in adult B–cell precursor acute lymphoblastic leukemia explains ambiguity of leukemia-initiating stem cell populations
Authors: F Lang, B Wojcik, S Bothur, C Knecht, J H F Falkenburg, T Schroeder, H Serve, O G Ottmann, M A Rieger
Journal: Leukemia (2016)

Plastic CD34 and CD38 expression in adult B–cell precursor acute lymphoblastic leukemia explains ambiguity of leukemia-initiating stem cell populations
Nitrite Levels Are Associated To Fetal Hemoglobin Concentration In Patients With Sickle Cell Anemia: Implications In Inflammatory Process
Authors: Thassila Nogueira Pitanga, Bruno A. V. Cerqueira, Wendell Vilas Boas, Sanzio S. Santana, João O. Reis, Marilda Souza Goncalves
Journal: Blood (2013)
Utility of preoperative ferumoxtran-10 enhanced MRI to evaluate retroperitoneal lymph node metastasis in advanced cervical cancer: Results of ACRIN 6671/GOG 0233.
Authors: M. Atri, Z. Zhang, H. Marques, J. Gorelick, M. Harisinghani, A. Sohaib, D. Koh, S. Raman, M. S. Gee, H. Choi, L. M. Landrum, R. S. Mannel, L. T. Chuang, J. Q. Yu, C. K. McCourt, M. Gold
Journal: Journal of Clinical Oncology (2011)

5035 Background: Ferumoxtran-10 MRI has been evaluated for lymph node (LN) metastasis. Objective of the study was to determine utility of ferumoxtran-10 MRI in detection of LN metastasis in advanced cervical cancer. Methods: This is an NCI funded phase II multicenter clinical trial conducted by ACRIN/GOG. Patients with locally advanced cervical cancer undergoing pelvic and abdominal lymphadenectomy prior to chemoradiation were accrued. Preoperative MRI including T2W, T1W, and T2*GRE were obtained following IV administration of ferumoxtran -10 that was provided by AMAG Pharmaceutical Inc. Results of a blinded review by 7 imagers were correlated with pathology findings. Readers reviewed ferumoxtran-10 insensitive sequences (standard MRI) followed by all sequences including ferumoxtran-10 sensitive (T2*GRE) sequence. Correlation was made per region for 8 regions, left and right (para-aortic, common iliac, external iliac, and obturator) LNs. Ferumoxtran-10 MRI was considered positive when there was a defect in LN on T2*GRE. Standard MRI was considered positive when LN short axis was > 8mm. Results: Thirty three women (mean age 49 ± 11) were included. Mean cervical tumor size was 5.4±1.5cm. Prevalence of LN metastasis was 36% (12/33) in abdomen and 67% (22/33) in pelvis. Median size of largest focus of cancer was 18mm (range 2-50, Q1 11mm). Average sensitivity/specificity for seven readers on ferumoxtran-10 MRI were 0.60 (95% CI:0.49-0.70)/0.75 (95% CI: 0.67-0.82) in abdomen, and 0.81 (95% CI:0.73-0.86)/0.45 (95% CI: 0.32-0.58) in pelvis. Corresponding numbers for standard MRI were 0.54 (95% CI:0.43-0.64)/0.83 (95% CI: 0.75-0.88) and 0.74 (95% CI:0.67-0.80)/0.71 (95% CI: 0.58-0.82). Use of ferumoxtran-10 showed no significant difference in the diagnostic accuracy of MRI with the exception of specificities in pelvis (p=0.006). Performances of the seven readers were comparable (p>0.32). Conclusions: In this cohort, ferumoxtran -10 MRI showed modest accuracy that was not significantly different from standard MRI. ACRIN/GOG receive funding from the National Cancer Institute through grants U01 CA079778 and U01 CA080098/ CA 27469 and CA 37517.
Abstract 3910: Acetylation of ΔNp63α by Tip60 affects its stability
Authors: Andrew J. Stacy, Zachary J. Smith, Jin Zhang, Madhavi Kadakia
Journal: Cancer Research (2015)

Abstract p63, a member of the transcription factor p53 family, exists as six different isoforms due to the usage of alternative promoter sites and splicing. ΔNp63α is the most abundant and predominant isoform and is identified to being involved in epithelial morphogenesis. ΔNp63α expression is up-regulated in non-melanoma skin cancers. We have identified ΔNp63α as a potential target for acetylation by the Tat Interacting Protein 60 kDa (TIP60) histone acetyltransferase (HAT) by mass spectometry. Co-expression of ΔNp63α with Tip60 leads to stabilization of ΔNp63α protein levels. The change in protein levels are not due to an increase in transcription or translation, and is likely the result of stabilization by post-translational modification as confirmed by half-life studies in presence of cycloheximide and measurement of transcript levels by quantitative reverse transcriptase PCR. This was further supported by our observations that ΔNp63α and Tip60 interact using immunoprecipitation studies. ΔNp63α levels are not affected by Tip60 HAT mutant, but increased with Tip60 double sumoylation mutant which retains its acetyltransferase ability. These results identify a possible biologically important interaction between ΔNp63α and Tip60, warranting further investigation. Citation Format: Andrew J. Stacy, Zachary J. Smith, Jin Zhang, Madhavi Kadakia. Acetylation of ΔNp63α by Tip60 affects its stability. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3910. doi:10.1158/1538-7445.AM2015-3910
Subacute Thrombotic Events Associated with Drug Eluting Cardiac Stents May Be Localized Hypersensitivity Reactions to Polymers.
Authors: Charles Bennett, Jonathan Nebeker, Renu Virmani, June McKoy, Jenny Hoffman, Dennis Raisch, Dennis West, Matthew Samore, Paul Yarnold, Charles Davidson, Steven Belknap, Marc Feldman
Journal: Blood (2004)
Bcl2 Accelerates Onset but Not Progression of MYC-Induced T-Cell Leukemia in Transgenic Zebrafish.
Authors: Hui Feng, David M. Langenau, Jennifer A. Kilgore, Andre Quinkertz, Cicely A. Jette, Donna S. Neuberg, Jose A. Campos-Ortega, John P. Kanki, Thomas Look
Journal: Blood (2006)
Imatinib Mesylate Versus Allogeneic HSCT for Patients with Chronic Myelogenous Leukemia In Accelerated Phase: A Single Center Experience In China After a 9-Year Follow-up
Authors: Qian Jiang, Lan-Ping Xu, Dai-Hong Liu, Kaiyan Liu, Shan-Shan Chen, Bin Jiang, Hao Jiang, Huan Chen, Yu-Hong Chen, Wei Han, Xiao-hui Zhang, Yu Wang, Ya-Zhen Qin, Yan-Rong Liu, Yue-yun Lai, Xiao Jun Huang
Journal: Blood (2010)
Biochemical recurrence in 3,671 patients following robot-assisted radical prostatectomy.
Authors: C. Rogers, J. D. Sammon, M. Diaz, S. Sukumar, C. Hwang, J. Peabody, M. Menon
Journal: Journal of Clinical Oncology (2011)

e15048 Background: Long-term oncologic outcomes for patients undergoing robot-assisted radical prostatectomy (RARP) for prostate cancer (PCa) are limited. We evaluated oncologic outcomes in patients undergoing RARP at a high-volume tertiary center, with a focus on long-term biochemical recurrence free survival (BCRFS). Methods: A total of 4,047 consecutive patients underwent RARP from September 2001 to December 2008; 3,671 patients comprised the study cohort (excluding for: loss to follow-up, incomplete data, positive lymph nodes, neo-adjuvant and adjuvant treatment). Biochemical recurrence (BCR) was defined as a serum prostate-specific antigen ≥ 0.2 ng/ml with a confirmatory value. BCRFS, metastasis free survival (MFS) and cancer specific survival (CSS) were estimated using the Kaplan-Meier method. A Cox proportional hazards regression model was used to determine variables predictive of BCR. Event time distributions for the time to failure were compared using the log rank test. Results: Mean preoperative PSA was 6.1 ng/ml. Biopsy Gleason score was ≥ 7 in 44.4% of patients, pathologic Gleason grade was ≥ 7 in 64.5% of patients, and pathologic stage was ≥ pT3 in 30.3% of patients. BCR was noted in 324 (8.8%) patients; mean follow up was 33.8 months (median follow up – 27.3 months). Nine patients died of PCa (0.3%) and 18 patients developed metastatic disease (0.5%). Actuarial 3 and 5-year BCRFS was 91.3% and 87.0%. Actuarial 3 and 5-year CSS was 99.8% and 99.6%. Conclusions: In a large contemporary cohort of patients treated in the PSA era, robot-assisted radical prostatectomy appears to confer effective intermediate and long-term biochemical control. To our knowledge, this is the largest report of oncologic outcomes in a RARP series to date. Despite a cohort in which a majority of patients possessed Gleason 7 or greater disease, and 30% had extraprostatic extension or seminal vesicle invasion, 8.8% experienced a BCR, with a 5-year actuarial BCRFS of 87%, 0.5% experienced metastasis and 0.3% experienced a cancer specific death.
ZEB1-induced tumourigenesis requires senescence inhibition via activation of DKK1/mutant p53/Mdm2/CtBP and repression of macroH2A1
Authors: Oriol de Barrios, Balázs Győrffy, María Jesús Fernández-Aceñero, Ester Sánchez-Tilló, Lidia Sánchez-Moral, Laura Siles, Anna Esteve-Arenys, Gaël Roué, José I Casal, Douglas S Darling, Antoni Castells, Antonio Postigo
Journal: Gut (2016)

<h3>Objective</h3> Understand the role of ZEB1 in the tumour initiation and progression beyond inducing an epithelial-to-mesenchymal transition. <h3>Design</h3> Expression of the transcription factor ZEB1 associates with a worse prognosis in most cancers, including colorectal carcinomas (CRCs). The study uses survival analysis, in vivo mouse transgenic and xenograft models, gene expression arrays, immunostaining and gene and protein regulation assays. <h3>Results</h3> The poorer survival determined by <i>ZEB1</i> in CRCs depended on simultaneous high levels of the Wnt antagonist <i>DKK1</i>, whose expression was transcriptionally activated by ZEB1. In cancer cells with mutant <i>TP53</i>, ZEB1 blocked the formation of senescence-associated heterochromatin foci at the onset of senescence by triggering a new regulatory cascade that involves the subsequent activation of DKK1, mutant p53, Mdm2 and CtBP to ultimately repress macroH2A1 (<i>H2AFY</i>). In a transgenic mouse model of colon cancer, partial downregulation of <i>Zeb1</i> was sufficient to induce <i>H2afy</i> and to trigger in vivo tumour senescence, thus resulting in reduced tumour load and improved survival. The capacity of ZEB1 to induce tumourigenesis in a xenograft mouse model requires the repression of <i>H2AFY</i> by ZEB1. Lastly, the worst survival effect of <i>ZEB1</i> in patients with CRC ultimately depends on low expression of <i>H2AFY</i> and of senescence-associated genes. <h3>Conclusions</h3> The tumourigenic capacity of ZEB1 depends on its inhibition of cancer cell senescence through the activation of a herein identified new molecular pathway. These results set ZEB1 as a potential target in therapeutic strategies aimed at inducing senescence.
Abstract 5107: Divergent behaviors and underlying mechanisms of cell migration and invasion in non-metastatic T24 and its metastatic derivative T24T bladder cancer cell lines
Authors: Honglei Jin, Jingxia Li, Chuanshu Huang
Journal: Cancer Research (2015)

Abstract Previous studies on cancer cell invasion were primarily focused on its migration because these two events were often considered biologically equivalent. Here we found that T24T cells exhibited higher invasion but lower migration abilities than T24 cells. Expression of Rho-GDPases was much lower and expression of SOD2 was much higher in T24T cells than in T24 cells. Indeed, knockdown of SOD2 in T24T cells can reverse the cell migration but without affecting cell invasion. We also found that SOD2 inhibited the JNK/C-Jun cascade, and the inhibition of c-Jun activation by ectopic expression of TAM67 impaired Rho-GDPases expression and cell migration in T24T shSOD2 cells. Further, we found that Sp1 can upregulate SOD2 transcription in T24T cells. Importantly, matrix metalloproteinase-2 (MMP-2) was overexpressed in T24T and participated in increasing its invasion, and MMP-2 overexpression was mediated by increasing nuclear transport of nucleolin, which enhanced mmp-2 mRNA stability. Taken together, our study unravels an inverse relationship between cell migration and invasion in human bladder cancer T24T cells and suggests a novel mechanism underlying the divergent roles of SOD2 and MMP-2 in regulating metastatic behaviors of human bladder T24T in cell migration and invasion. Citation Format: Honglei Jin, Jingxia Li, Chuanshu Huang. Divergent behaviors and underlying mechanisms of cell migration and invasion in non-metastatic T24 and its metastatic derivative T24T bladder cancer cell lines. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5107. doi:10.1158/1538-7445.AM2015-5107
A single-center experience of EMA/CO chemotherapy for high-risk gestational trophoblastic neoplasia: Induction low-dose cisplatin and etoposide chemotherapy improves outcome.
Authors: C. Alifrangis, R. Agarwal, D. Short, P. Savage, M. Seckl
Journal: Journal of Clinical Oncology (2011)

5024 Background: Patients with Gestational Trophoblastic Neoplasia (GTN) classified as high risk, or who fail low risk single agent chemotherapy usually receive etoposide, methotrexate and actinomycin D alternating weekly with cyclophosphamide and vincristine (EMA/CO). At our institute overall survival (OS) after EMA/CO was 87% between 1979-1995. Here we compare a more recent patient cohort (1994-2010) to determine whether survival rates have improved. Methods: The Charing Cross GTD database was screened for patients who received EMA/CO chemotherapy between Jan 1994 and 2010. Patient characteristics and outcomes were recorded. Pathology was centrally reviewed and patients with PSTT or non-gestational tumours were excluded. The introduction in 1994 and use of low-dose etoposide 100mg/m2 and cisplatin 20mg/m2 (EP) on days 1 and 2 repeated weekly as induction chemotherapy for 1-2 weeks before commencing EMA/CO was noted. Results: EMA/CO was given to 442 patients. This was first line therapy for 170 with high risk disease, and second line for 278 failing single agent chemotherapy. OS (median follow-up 4.29 years) was 98% (9 deaths / 442 pts; 95% CI : 96.6-99.3%)in the modern, compared to 87% (95% CI : 81.9 - 90.5%) in our previous cohort. This was not explained by an increase in low-risk patients receiving EMA/CO. EP-induction chemotherapy was given to 21% (35/170) of high risk patients who were significantly more likely to have a high disease burden (FIGO score >8 and > 6 metastases (p<0.01)). Strikingly, this correlated with a reduction in early deaths from 4% (95% CI : 1.9-6.9) in the early pre-EP cohort to 0.2% (95% CI : 0-0.65%) in the current cohort. Of the remaining 8 patients, 7 died due to drug resistance, and one of pulmonary embolism post surgery. Conclusions: Overall survival following EMA/CO for GTN has improved significantly from 87% to 98% in our recent patient cohort. This is partly due to the introduction of low-dose EP-induction chemotherapy for patients with advanced disease. Low dose EP induction chemotherapy should be routinely considered for patients with a FIGO score >8 and metastasis score >6 to minimise the risk of early deaths.
698. Eliminating TLR9+ Prostate Cancer Stem Cells In Vivo Using NF-kB/RELA- or STAT3-Targeting CpG-siRNA Conjugates
Authors: Dayson F. Moreira, Qifang Zhang, Dewan M. Hossain, Sergey Nechaev, Haiqing Li, Claudia M. Kowolik, Massimo D'Apuzzo, Stephen Forman, Jeremy Jones, Sumanta K. Pal, Marcin Kortylewski
Journal: Molecular Therapy (2015)

Treatment of hormone-refractory and frequently reoccurring prostate cancers is a major clinical challenge. Here, we demonstrate that Toll-like Receptor 9 (TLR9) is commonly upregulated in late-stage prostate cancers and provides a potential therapeutic target. As a sensor of immunogenic cell death, TLR9 bridges intra-prostatic inflammation to cancer stem cell phenotype. Our limited dilution/serial transplantation experiments in vivo demonstrate that TLR9 is essential for prostate cancer cells' potential to propagate and self-renew. In addition, low expression or silencing of TLR9 limits the clonogenic potential and mesenchymal stem cell-like properties of prostate cancer cells. Genome-wide transcriptional analysis of cancer cells isolated from xenotransplanted prostate tumors revealed a unique TLR9-dependent gene expression signature. Further analysis of the TLR9 downstream signaling indicated that tumorigenic transcription factors NF-kB/RELA and STAT3 cooperate to orchestrate expression of stem cell-related genes. Both RELA and STAT3 bound and co-regulated promoters of NKX3.1 and KLF4 prostate cancer stem cell-related genes. We further demonstrated the feasibility of targeting prostate cancer-propagating potential in vivo by TLR9-targeted siRNA delivery using CpG-siRNA conjugates. Local administration of CpG-RELAsiRNA or CpG-STAT3siRNA but not control conjugates, inhibited tumor growth and cancer cell clonogenic potential in two xenotransplanted prostate cancer models. Selective elimination of tumor-propagating cells using TLR9-targeted blockade of NF-?B/RELA and STAT3 signaling has potential for clinical translation to benefit patients with late-stage prostate cancers.
Abstract 4594: Serum microRNA signatures predict recurrence and survival in Caucasian patients with early stage non-small cell lung cancer
Authors: Liren Zhang, Jack A. Roth, Jie Lian, Yuanqing Ye, Jian Gu, Xifeng Wu
Journal: Cancer Research (2015)

Abstract Early stage non-small cell lung cancer (NSCLC) patients can be curatively treated by surgery alone or with adjuvant chemotherapy. However, about half of patients develop recurrence and eventually die of this disease. The purpose of this study is to identify circulating microRNAs (miRNA) as minimally invasive biomarkers for the prognosis of early stage NSCLC that may allow personalized clinical management of early stage NSCLC patients. Using a large series of 171 stage I and II NSCLC Caucasian patients, we screened and validated serum miRNA signatures predictive of recurrence and survival in these patients. We identified six miRNA expression ratios that were associated with recurrence and three miRNA expression ratios that were associated with overall survival. In Receiver Operating Characteristic (ROC) curve analysis, the area under the curve (AUC) for clinical variable-only model was 0.714 for recurrence and 0.678 for survival; however, the AUC increased to 0.878 for recurrence and 0.796 for survival when the miRNA ratio signatures were added to the recurrence and survival models respectively. The patients in the high risk group as defined by the 6 miRNA ratio signature exhibited an approximately 5-fold increased risk of develop recurrence compared with low risk patients. In survival analysis, the death rate increased over 4-fold in the high risk group compared with the low risk group. Our results suggest that the miRNA ratio signatures could serve as prognostic biomarkers for early stage NSCLC. Citation Format: Liren Zhang, Jack A. Roth, Jie Lian, Yuanqing Ye, Jian Gu, Xifeng Wu. Serum microRNA signatures predict recurrence and survival in Caucasian patients with early stage non-small cell lung cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4594. doi:10.1158/1538-7445.AM2015-4594
Phase II Study of the Cyclin-Dependent Kinase (CDK) Inhibitor Dinaciclib (SCH 727965) In Patients with Advanced Acute Leukemias
Authors: Ivana Gojo, Alison Walker, Maureen Cooper, Eric J Feldman, Swaminathan Padmanabhan, Maria R Baer, Jennifer Poon, Karen Small, Da Zhang, Mariola Sadowska, Rajat Bannerji
Journal: Blood (2010)
Activity of Allosteric, Switch-Pocket, ABL/FLT3 Kinase Inhibitor DCC2036 Against Cultured and Primary AML Progenitors with FLT-ITD or FLT3 Kinase Domain Mutations
Authors: Warren Fiskus, Catherine C. Smith, Jacqueline Smith, Scott C. Wise, Elisabeth Lasater, Lauren E. Damon, Sara Salerno, Allan Fleming, Ruben Reyes, Siddhartha Ganguly, Mark S. Berger, Tom J. Rutkoski, Joseph McGuirk, Neil Shah, Kapil N. Bhalla
Journal: Blood (2011)
Long-term survival among Hodgkin lymphoma (HL) patients with gastrointestinal (GI) cancers: A population-based study.
Authors: P. Youn, H. Li, M. T. Milano, M. Stovall, L. S. Constine, L. B. Travis
Journal: Journal of Clinical Oncology (2011)

8037 Background: The markedly increased risk of GI cancers after HL is well-established, with GI tumors accounting for the 3rd largest absolute risk of second cancers. However, no large, population-based studies have described overall survival (OS) and cause-specific survival (CSS) of HL survivors who developed GI cancers (HL-GI). Methods: For 209 HL-GI patients (105 colon, 35 stomach, 30 pancreas, 21 rectum, 18 esophagus) and 484,165 patients with first primary GI cancers (GI-1), actuarial OS and CSS were compared, accounting for age, gender, race, SES, GI cancer stage, radiation (RT) for HL, and other variables. Radiation doses to ascending, transverse, and descending colon with standard para-aortic and inverted-Y RT fields were estimated using water and anthropomorphic phantoms. Results: Survival of HL-GI group was inferior compared to GI-1 for most sites (Table). For localized stomach cancer, OS was more than three times worse among HL survivors. Whereas survival of HL patients who developed localized colon cancer (CC) was similar to that of GI-1 group, OS of HL patients with regional or distant CC was reduced 50%. HL survivors with regional or distant CC (transverse segment) had especially high risks of mortality (hazard ratios: 2.7 and 2.6; P=0.001 and 0.002 for OS and CSS respectively). Despite similarities in GI cancer stage between most HL-GI and GI-1 sites, transverse colon cancer was diagnosed at significantly more advanced stages in HL-GI vs. GI-1 (P=0.024). Dosimetry modeling of abdominal RT showed that transverse colon received 81% of total dose (vs. 4-43% to other segments). Conclusions: HL patients who develop GI cancer have significantly reduced survival compared to patients with a first primary cancer in GI sites. Further research is needed to explain the inferior survival of HL patients and to define selection criteria for screening colonoscopies in HL survivors. OS hazard ratios (HR) from Cox model. Localized Regional/distant GI cancer site HR (P value) HR (P value) Colon 1.3 (0.40) 1.5 (0.01) Stomach 3.5 (0.006) 1.0 (0.8) Pancreas Sample size too small for analysis 1.1 (0.6) Rectum 1.7 (0.19) 2.1 (0.06) Esophagus 4.3 (0.012) 0.8 (0.46)