tbuckley/cabot-search huggingface dataset:
Comparison of upper tract urothelial carcinoma and urothelial carcinoma of the bladder to reveal key differences in mutational profile and load.
Authors: Sumanta K. Pal, Siraj Mahamed Ali, Julia Andrea Elvin, Garrett Michael Frampton, Jo-Anne Vergilio, James Suh, Vijay Gunuganti, Badar Mian, Hugh A.G. Fisher, Tipu Nazeer, Vincent A. Miller, Philip J. Stephens, Jeffrey S. Ross
Journal: Journal of Clinical Oncology (2016)

4522 Background: Upper tract urothelial carcinoma (UTUC) is generally thought to have a more aggressive clinical phenotype as compared to urothelial carcinoma of the bladder (UCB). We interrogated genomic differences between these entities. Methods: DNA was extracted from 40 microns of FFPE sections from 295 and 195 consecutive patients with UCB and UTUC, respectively. Comprehensive genomic profiling (CGP) was performed on hybridization-captured, adaptor ligation based libraries to a mean coverage depth of 627X for up to 315 cancer-related genes plus 37 introns from 14 genes frequently rearranged in cancer. The CGP assay included base substitutions (SUB), INDELs, copy number alterations (CNA) and fusions/rearrangements. Genomic alterations (GAs) linked to drugs on the market or under evaluation in mechanism driven clinical trials were considered clinically relevant GAs (CRGAs). A 2-sided Z-test for comparison of population proportions was used to juxtapose the frequency of GAs and CRGAs in UTUC and UCB. Results: There were 70% male and 30% female patients with a mean age of 66 years. Although both UCB and UTUC harbored a similar number of GAs/sample (6.4 for both), CRGAs were slightly more common with UCB (2.6 vs 2.0). The most frequent GA was in TP53, and this was more common in UCB (56% vs 46%, P = 0.03). In contrast, the next most frequent GA (CDKN2A) was more common in UTUC (43% vs 34%, P = 0.047). Amongst CRGAs, differences in FGFR3 alteration approached statistical significance, with a higher frequency in UTUC (28% vs 21%, P = 0.08). A borderline increase in frequency of ERBB2 alterations in UCB was also seen (17% vs 11%, P = 0.07). Mutational load was higher in UCB as compared to UTUC (6.6 GAs/MB vs 5.5 GAs/MB). Conclusions: These results highlight key differences in the frequency of GAs present in UTUC and UCB. In addition to explaining the clinical phenotype of these disease, they may inform ongoing and future trials of targeted therapy in this population.
Pictilisib PI3Kinase inhibitor (a phosphatidylinositol 3-kinase [PI3K] inhibitor) plus paclitaxel for the treatment of hormone receptor-positive, HER2-negative, locally recurrent, or metastatic breast cancer: interim analysis of the multicentre, placebo-controlled, phase II randomised PEGGY study
Authors: P. Vuylsteke, M. Huizing, K. Petrakova, R. Roylance, R. Laing, S. Chan, F. Abell, S. Gendreau, I. Rooney, D. Apt, J. Zhou, S. Singel, L. Fehrenbacher
Journal: Annals of Oncology (2016)
Comment on Koivusalo et al. Gestational Diabetes Mellitus Can Be Prevented by Lifestyle Intervention: The Finnish Gestational Diabetes Prevention Study (RADIEL): A Randomized Controlled Trial. Diabetes Care 2016;39:24–30
Authors: Wei Bao
Journal: Diabetes Care (2016)

I read with great interest the recent article in Diabetes Care by Koivusalo et al. (1). In a randomized controlled trial, namely the Finnish Gestational Diabetes Prevention Study (RADIEL), Koivusalo et al. report that lifestyle intervention reduced the incidence of gestational diabetes mellitus (GDM) by 39% in pregnant women with a history of GDM and/or prepregnancy obesity (1). The authors highlighted that this significant reduction in GDM incidence was achieved through a moderate lifestyle intervention including only three visits to the study nurse and one group visit to the dietitian during pregnancy, which was much less intensive than previous trials for the prevention of type 2 diabetes among individuals with impaired glucose …
Long-term survival in patients with metastatic melanoma who received ipilimumab in four phase II trials.
Authors: Celeste Lebbé, Jeffrey S. Weber, Michele Maio, Bart Neyns, Kaan Harmankaya, Omid Hamid, Steven O'Day, Kevin M. Chin, Diane Opatt McDowell, Lori Cykowski, Brent McHenry, Jedd D. Wolchok
Journal: Journal of Clinical Oncology (2013)

9053 Background: Ipilimumab (Ipi) has shown improved overall survival (OS) in two phase III trials of patients (pts) with metastatic melanoma (MM), with survival follow-up of &gt;4 years in one trial. The present analyses provide survival follow-up of &gt;5 years in four phase II trials of Ipi in MM. Methods: Pts with MM were enrolled in one of four phase II trials: (1) CA184-004, a biomarker study with Ipi at 3 or 10 mg/kg in treatment-naive (TN) and previously treated (PT) pts; (2) CA184-007, with Ipi at 10 mg/kg +/- prophylactic budesonide in TN and PT pts; (3) CA184-008, a single-arm study with Ipi at 10 mg/kg in PT pts; and (4) CA184-022, a dose-ranging study of Ipi at 0.3, 3, or 10 mg/kg in PT pts (crossover from lower dose groups to 10 mg/kg was allowed upon disease progression). Ipi was administered q3 wk x4 (induction), followed by maintenance (q12 wk from week 24) in eligible pts. Some pts were retreated with Ipi at 10 mg/kg upon disease progression. Along with survival data collected through March 2012 for studies 007, 008, and 022, we report updated 5-year OS data for study 004 collected through September 2012. Results: Five-year OS rates for TN and PT pts are reported in studies 007, 008, and 022, with combined analyses for TN and PT pts within each dose group in study 004 (Table). The results show that survival rates reach a plateau beginning at year 3. Conclusions: In pts who received Ipi at 3 or 10 mg/kg in phase II studies, regardless of prior treatment, a proportion (12.3–49.5%) remained alive 5 years after the start of treatment. These results demonstrate long-term survival with Ipi therapy in MM. An ongoing phase III trial will compare OS for Ipi at 3 vs 10 mg/kg in pts with MM. Clinical trial information: NCT00162123. [Table: see text]
Abstract 3997: The impact of PD-L1 expression in patients with metastatic GEP-NETs
Authors: Seung T. Kim, Won Lee
Journal: Cancer Research (2016)

Abstract Programmed death-ligand 1 (PD-L1), which is expressed on many cancer cells, interacts with PD1 expressed on the surface of T cells, inhibiting the T cells and blocking the antitumor immune response. Expression of PD-L1 in gastroenteropancreatic neuroendocrine tumors (GEP-NETs) has not been studied. We investigated the impact of PD-L1 expression in 32 patients with metastatic GEP-NET. The expression of PD-L1 was evaluated using an anti-PD-L1 immunohistochemistry (IHC) antibody optimized for staining of formalin-fixed paraffin-embedded (FFPE) tissue samples. The correlation between PD-L1 and clinicopathological data including survival and response to systemic treatments was analyzed. Primary sites were 24 foregut-derived GEP-NETs, including stomach (n = 1), duodenum (n = 2), biliary tract (n = 7), and pancreas (n = 14), and 8 hindgut-derived GEP-NETs of the distal colon and rectum. Among the 32 patients with metastatic GEP-NET analyzed in this study, 7 (21.9%) had expression of PD-L1 in tumor tissues. Expression of PD-L1 was significantly associated with high-grade WHO classification (grade 3) (p = 0.008) but not with gender, primary site, and number of metastatic sites (p&amp;gt;0.05). The status of PD-L1 expression was statistically associated with progression-free survival (PFS) for first-line systemic treatment (p = 0.047). Moreover, the status of PD-L1 expression could significantly predict overall survival (p = 0.037). The expression of PD-L1 was associated with higher WHO tumor grade (grade 3) in metastatic GEP-NETs. PD-L1 expression had both predictive and prognostic value for survival of patients with metastatic GEP-NETs. Citation Format: Seung T. Kim, Won Lee. The impact of PD-L1 expression in patients with metastatic GEP-NETs. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3997.
Videofluoroscopy and oropharyngeal manometry for evaluation of swallowing in elderly patients
Authors: Alfonso Reginelli, Marilina D'Amora, Lucia Del vecchio, Luigi Monaco, Maria Rosaria Barillari, Natale Di Martino, Umberto Barillari, Gaetano Motta, Salvatore Cappabianca, Roberto Grassi
Journal: International Journal of Surgery (2016)
Abstract 2447: PIN1 protects GLI1 from ubiquitination and promotes Hedgehog-driven medulloblastoma tumorigenesis
Authors: Jean-Francois M. Rual, Tao Xu, Honglai Zhang, Sung-Soo Park, Sriram Venneti, Rork Kuick, Kimberly Ha, Lowell Michael, Mariarita Santi, Chiyoko Uchida, Takafumi Uchida, Ashok Srinivasan, Andrzej Dlugosz, Sandra Camelo-Piragua
Journal: Cancer Research (2016)

Abstract Medulloblastoma is the most common malignant brain tumor of childhood. Therapeutic approaches to medulloblastoma have led to significant improvements, but are achieved at a high cost to quality of life. Aberrant upregulation of the hedgehog (Hh) pathway drives cerebellar tumorigenesis in ∼30% of medulloblastoma patients. Hh pathway inhibitors such as the SMO antagonist Vismodegib are currently being tested in Hh-activated medulloblastoma and the preliminary results are encouraging. However, resistance to SMO inhibition can be acquired, leading to relapse. Alternative therapeutic approaches are needed. We aim to uncover novel Hh signal modulators that are essential in medulloblastoma to maintain tumorigenic potential. Using our proteomic platform for systematic protein interaction mapping, we discovered a novel interaction between GLI1, a key transcription factor for the mediation of Hh signals, and PIN1, a peptidylprolyl cis/trans isomerase that regulates the post-phosphorylation conformation of its substrates. Our results support a molecular model in which PIN1 protects GLI1 from proteasomal degradation, thus contributing to the positive regulation of Hh signals. Most importantly, our in vivo functional analyses of PIN1 in mouse models of Hh-driven medulloblastoma demonstrate that the loss-of-PIN1 impairs tumor development and increases survival by 3 fold, from 57 to 158 days (P &amp;lt; 0.0001), establishing PIN1 as a key factor in Hh-driven medulloblastoma tumorigenesis. Finally, in human medulloblastoma tumor samples, the GLI1 and PIN1 proteins are correlated in their expression, supporting the relevance of the GLI1/PIN1 interaction in this disease context. In summary, the discovery of the GLI1/PIN1 interaction uncovers PIN1 as a novel therapeutic target in medulloblastoma tumorigenesis. If our hypothesis is validated, i.e., PIN1 inhibitors can improve survival in mouse models of Hh-driven medulloblastoma, our project will strongly justify testing the clinical relevance of PIN1 blockade in medulloblastoma patients. Citation Format: Jean-Francois M. Rual, Tao Xu, Honglai Zhang, Sung-Soo Park, Sriram Venneti, Rork Kuick, Kimberly Ha, Lowell Michael, Mariarita Santi, Chiyoko Uchida, Takafumi Uchida, Ashok Srinivasan, Andrzej Dlugosz, Sandra Camelo-Piragua. PIN1 protects GLI1 from ubiquitination and promotes Hedgehog-driven medulloblastoma tumorigenesis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2447.
A phase II study of intermittent sorafenib with bevacizumab (B) in B-naive and prior B-exposed epithelial ovarian cancer (EOC) patients.
Authors: Jung-min Lee, Christina M. Annunziata, John L. Hays, Peter L. Choyke, Liang Cao, Minshu Yu, Nilofer Saba Azad, Nicole D. Houston, Lori M. Minasian, Nicolas Gordon, Helen X. Chen, John Joseph Wright, Elise C. Kohn
Journal: Journal of Clinical Oncology (2014)

5553 Background: We targeted the VEGF pathway at multiple points combining the VEGFR2/Raf inhibitor sorafenib (S) with bevacizumab (B), an anti-VEGF antibody. Our goals were to define efficacy and explore correlative endpoints for a B+S regimen in B-naïve (B-) or prior B-treated (B+) EOC pts. Methods: Eligible pts had recurrent EOC, ECOG PS 0-1, good end organ function, were B- or B+ (progression ≤ 6 mo from last B dose). The primary endpoint was objective response rate (CR+PR). A Simon 2-stage optimal design targeted a 40%, and 20% RR in B- and B+ pts, respectively. All pts received S 200mg bid days 1-5/wk and B 5mg/kg q2wk in 4 wk cycles. Pts were evaluated every 2 cycles using RECISTv1.0, underwent functional imaging, research biopsies, and serial FACT-O quality of life (QoL) studies. Pretreatment plasma cytokine concentrations of IL-6, IL-8, VEGF, and sVEGFR-2 were evaluated. Results: 54 EOC pts were enrolled (B- 41; B+ 13; median 49 yrs [27-79]). Median prior treatments exceeded 5. 48 pts (B- 35; B+ 13) were evaluable; 6 were not because of intercurrent illness (5), and withdrawal (1), absent progression prior to the first reassessment. Clinical benefit (CR+PR+SD≥4mo) occurred in 30/35 (86%) B- pts, PR occurred in 9/35 pts (26%; median duration 14mo; 5-22mo), and SD ≥4mo in 21/35 pts (median 6mo; 4-18mo). 7/13 (54%) B+ pts had SD with a median response of 6mo (4-23+mo). Therapy-related gr3/4 events included hypertension (33%), DVT or PE (9%), and renal hemorrhage, perforation, anal fissure, and HFS, 2% each. HFS resulted in S reduction to 200mg qd in 76% of pts at a median of 2 cycles (1-7). Pts experienced improvement in QoL scores. Pretreatment low IL8 (n=52 ITT) was predictive of PFS >4mo (p<0.0001; ROC AUC 0.8). Under analysis and to be presented are: pretreatment v. day 3 DCE-MRI and 18FDG-PET scan analysis, and RPPA tumor biopsy proteomics changes pretreatment to wk6. Conclusions: S+B yields promising clinical benefit in heavily pretreated B- EOC pts, with manageable toxicity, although did not meet the primary response endpoint. Extensive prospectively planned biomarker and functional imaging studies may yield information to focus therapy to those EOC patients who may best respond. Clinical trial information: NCT00436215.
Final results of 2-dose fractionation of <sup>177</sup>Lu-J591 for progressive metastatic castration-resistant prostate cancer (mCRPC).
Authors: Scott T. Tagawa, Jaspreet Batra, Shankar Vallabhajosula, Yuliya Jhanwar, Paul J. Christos, Lauren Emmerich, Beerinder S. Karir, Irene Karpenko, Linda Lam, Victor RA Febles, Ana M. Molina, Himisha Beltran, Stanley J. Goldsmith, Neil Harrison Bander, David M. Nanus
Journal: Journal of Clinical Oncology (2016)

5022 Background: Phase 1 and 2 studies of single dose 177Lu-J591 are published. We hypothesized dose fractionation may improve safety and efficacy. Methods: Patients with progressive mCRPC; no selection for PSMA expression. Initially, 6 cohorts of 3-6 pts got 2 doses of 177Lu-J591 2 wks apart (20 mCi/m2, escalating to 45 mCi/m2 x2). Subsequently, pts enrolled in 2 expansion cohorts at the recommended phase 2 doses (RP2D). Planar 177Lu-J591 imaging was semi-quantitatively scored. Endpoints: PSA changes and survival (OS); CTC count (CellSearch) changes in expansion cohorts. Results: 49 pts, median age 74.1 yrs (range 55-95), PSA 44.9 (1.9-766.5); 83.7% with bone, 61.2% LN, 40.8% visceral mets. 8.2% CALGB (Halabi) low, 34.7% intermediate, 57.1% high risk group. RP2D’s of fractionated 177Lu-J591 were 40 mCi/m2 x2 or 45 mCi/m2 x2 with option for GCSF. PSA changes and OS in Table. Accurate targeting of 177Lu-J591 was seen in 79.6%. Pts with lower PSMA expression by imaging were less likely to respond (p=0.07). Of 25 with CTC counts, 14 declined, 8 stably favorable, 3 increased. RP2D associated with more PSA declines (p=0.036) and longer OS (p=0.004), even after controlling for CALGB prognostic grouping (adjusted HR 0.42 [95% CI 0.21, 0.84] p=0.01). Predictable, reversible myelosuppression was seen. 36 (73.5%) pts had grade 3/4 heme toxicities; 19 (57.6%) had Gr 4 heme tox in RP2D cohorts with 45.4% receiving prophylactic platelet transfusions (median 1, range 1-4) and 6 GCSF (without fever). 14 (28.6%) had infusion reactions (without pre-meds), with 1 pt having Gr 2 and withdrawing prior to 2nddose. 5 (10.2%) had transient Gr 1/2 AST/ALT. Conclusions: Fractionated 177Lu−J591 is well tolerated with predictable, reversible myelosuppression and PSA and CTC declines. With dose-fractionation, the cumulative dose MTD is 14−28% higher than single dose MTD with similar toxicity. Prior dose-response is confirmed. Clinical trial information: NCT00538668.Group N Any PSA decline > 30% PSA decline > 50% PSA decline Median OS mo [95% CI] Total 49 55.1% 32.7% 16.3% 22.9 [16.2, 29.7] Low dose 16 37.5% 12.5% 6.3% 14.6 [9.9, 19.4] RP2D 33 66.7% 42.4% 21.2% 27.7 [15.8, 39.6] 40 x2 cohort 16 50.0% 25.0% 12.5% 19.6 [9.1, 302] 45 x2 cohort 17 87.5% 58.8% 29.4% 48.3 [16.0, 80.6]
Abstract 907: Brain microenvironment induced PTEN loss by microRNAs promotes brain metastasis
Authors: Lin Zhang, Siyaun Zhang, Jun Yao, Frank J. Lowery Lowery, Qingling Zhang, Wen-Chien Huang, Ping Li, Min Li, Xiao Wang, Chenyu Zhang, Hai Wang, Kenneth Ellis, Mujeeburahiman Cheerathodi, Joseph McCarty, Diane Palmieri, Patricia Steeg, Jodi S Saunus, Sunil Lakhani, Suyun Huang, Aysegul Sahin, Kenneth Aldape, Dihua Yu
Journal: Cancer Research (2016)

Abstract Metastasis is the number one cause of cancer-related mortality. Major neoplastic diseases such as melanoma, lung, breast, and colon cancers have high incidences of brain metastases. One-year survival after diagnosis of brain metastasis is less than 20%. Cancer cells dynamically interacts with specific organ microenvironments to establish metastasis as depicted by the “seed and soil” hypothesis. Yet it is unclear when and how disseminated tumor cells acquire the essential traits from the brain microenvironment that primes their subsequent metastatic outgrowth. Here we found that primary tumor cells with normal PTEN expression lose PTEN after dissemination to the brain, but not to other organs. Metastatic brain tumor cells that have experienced PTEN loss have PTEN levels restored once they leave the brain. This brain microenvironment-dependent, reversible PTEN mRNA and protein down-regulation is epigenetically regulated by microRNAs (miRNAs) from astrocyte-derived exosomes. Furthermore, this adaptive PTEN loss in brain metastatic tumor cells leads to an increased secretion of cytokine chemokine (C-C motif) ligand 2 (CCL2), which recruits Iba1+ myeloid cells that reciprocally enhance outgrowth of brain metastatic tumor cells via enhanced proliferation and reduced apoptosis. Our findings signify the dynamic and reciprocal cross-talk between tumor cells and other brain stromal cells. Disseminated tumor cells acquire the essential traits from the microenvironment of brain that prime their outgrowth. Importantly, our finding provides new opportunities for effective anti-metastasis therapies: inhibiting CCL2 might be an effective therapeutic intervention of life-threatening brain metastases. Citation Format: Lin Zhang, Siyaun Zhang, Jun Yao, Frank J. Lowery Lowery, Qingling Zhang, Wen-Chien Huang, Ping Li, Min Li, Xiao Wang, Chenyu Zhang, Hai Wang, Kenneth Ellis, Mujeeburahiman Cheerathodi, Joseph McCarty, Diane Palmieri, Patricia Steeg, Jodi S Saunus, Sunil Lakhani, Suyun Huang, Aysegul Sahin, Kenneth Aldape, Dihua Yu. Brain microenvironment induced PTEN loss by microRNAs promotes brain metastasis. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 907.
Comparison of eight commonly used regimens as first-line treatment of metastatic non-small lung cancer.
Authors: Ahmed Ashour Badawy, Waleed O. Arafat, Sejong Bae, Abbas Omar, Gehan Abd Elatti Khedr, Stefan C. Grant
Journal: Journal of Clinical Oncology (2016)

e20661 Background: Despite the wide availability of many chemotherapeutic regimens for the treatment of advanced non-small cell lung cancer (NSCLC), by design most clinical trials compare a treatment to a single standard regimen, making the choice between various treatment regimens challenging. Methods: We undertook a retrospective comparison of common treatment regimens given to patients with stage IV NSCLC between 2002 and 2012 at the University of Alabama at Birmingham to explore outcomes by first line treatment regimen. Statistical analysis was performed using SPSS 22 software and calculated by log-rank testing Results: 409 patients received systemic treatment between 2002 and 2012. The commonly used regimens with numbers of patients sufficient for analysis are summarized in table, with median overall survival and median progression free survival and histological subtype for each regimen. In the first line setting tyrosine kinase inhibitors (TKI) for EGFR driven mutations were associated with best overall survival, with 19.11 months median survival. This was followed by paclitaxel/carboplatin/bevacizumab with median survival 18.3, followed by pemetrexed containing regimens. This difference in overall survival is statistically significant (p = 0.012). Conclusions: As well documented, patients with targetable EGFR mutations do best with TKIs. Of the patients without EGFR mutations, the longest survival was observed in those patients receiving frontline carboplatin/paclitaxel/bevacizumab mainly in non-squama histology. Pemetrexed and gemcitabine containing regimens also were associated with long survivals in patients with adenocarcinoma and squamous cell histology tumors, respectively. Regimens Overall Survival months Progression Free Survival months Histological percentage Adenocarcinoma SCC Other Tyrosine kinase inhibitor 19.11 8.03 57.1 11.9 31 paclitaxel+ Carboplatin+ bevacizumab 18.03 7.11 67.9 10.7 21.4 paclitaxel+ carboplatin 11.31 4.50 40.6 23.6 35.8 Docetaxel + platinum 9.97 4.13 33.3 16.7 50 Carboplatin+ Gemcitabine 11.64 4.44 28.6 22.9 48.6 Carboplatin+ pemetrexed 15.31 6.08 88 0 1 pemetrexed single agent 16.92 5.77 59.3 25.9 14.8 Gemcitabine single agent 15.15 4.95 0 100 0
Genetic risk of extranodal natural killer T-cell lymphoma: a genome-wide association study
Authors: Zheng Li, Yi Xia, Li-Na Feng, Jie-Rong Chen, Hong-Min Li, Jing Cui, Qing-Qing Cai, Kar Seng Sim, Maarja-Liisa Nairismägi, Yurike Laurensia, Wee Yang Meah, Wen-Sheng Liu, Yun-Miao Guo, Li-Zhen Chen, Qi-Sheng Feng, Chi Pui Pang, Li Jia Chen, Soo Hong Chew, Richard P Ebstein, Jia Nee Foo, Jianjun Liu, Jeslin Ha, Lay Poh Khoo, Suk Teng Chin, Yi-Xin Zeng, Tin Aung, Balram Chowbay, Colin Phipps Diong, Fen Zhang, Yan-Hui Liu, Tiffany Tang, Miriam Tao, Richard Quek, Farid Mohamad, Soo Yong Tan, Bin Tean Teh, Siok Bian Ng, Wee Joo Chng, Choon Kiat Ong, Yukinori Okada, Soumya Raychaudhuri, Soon Thye Lim, Wen Tan, Rou-Jun Peng, Chiea Chuen Khor, Jin-Xin Bei
Journal: The Lancet Oncology (2016)
Disorganized Steroidogenesis in Adrenocortical Carcinoma, a Case Study
Authors: Toyoyoshi Uchida, Koshiro Nishimoto, Yuki Fukumura, Miki Asahina, Hiromasa Goto, Yui Kawano, Fumitaka Shimizu, Akira Tsujimura, Tsugio Seki, Kuniaki Mukai, Yasuaki Kabe, Makoto Suematsu, Celso E. Gomez-Sanchez, Takashi Yao, Shigeo Horie, Hirotaka Watada
Journal: Endocrine Pathology (2016)