18 results on '"Masato Yozu"'
Search Results
2. Untutored learning curve for endoscopic submucosal dissection in New Zealand.
- Author
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Fox, Tara, Masato Yozu, Sze-Lin Peng, Schauer, Cameron, and Sekra, Anurag
- Published
- 2024
- Full Text
- View/download PDF
3. Non‐conventional dysplasia is frequently associated with low‐grade tubuloglandular and mucinous adenocarcinomas in inflammatory bowel disease
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Fahire Goknur Akarca, Masato Yozu, Lindsay Alpert, Bence P Kővári, Lei Zhao, Marcela Salomao, Xiaoyan Liao, Maria Westerhoff, Gregory Y Lauwers, and Won‐Tak Choi
- Subjects
Histology ,General Medicine ,Pathology and Forensic Medicine - Published
- 2023
4. Non‐conventional dysplasias of the tubular gut: a review and illustration of their histomorphological spectrum
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Rish K. Pai, Tetsuo Ushiku, Kun Jiang, Won-Tak Choi, Ian Brown, Yukihiro Nakanishi, Baek Hyun Kim, Paula Chaves, Gregory Y. Lauwers, Ryoji Kushima, Till Clauditz, Kyoung Mee Kim, Bence Kővári, Daniela Pereira, Masato Yozu, Gregory Miller, John R. Goldblum, Amitabh Srivastava, Masoumeh Ghayouri, and Marian Priyanthi Kumarasinghe
- Subjects
Gastritis, Atrophic ,0301 basic medicine ,medicine.medical_specialty ,Histology ,Colon ,Duodenum ,Gastrointestinal Diseases ,Atrophic gastritis ,Inflammatory bowel disease ,Gastroenterology ,Endoscopy, Gastrointestinal ,Pathology and Forensic Medicine ,Diagnosis, Differential ,Barrett Esophagus ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,Gastrointestinal tract ,business.industry ,General Medicine ,Inflammatory Bowel Diseases ,medicine.disease ,Gastrointestinal Microbiome ,Gastrointestinal Tract ,030104 developmental biology ,medicine.anatomical_structure ,Dysplasia ,030220 oncology & carcinogenesis ,Practice Guidelines as Topic ,business ,Precancerous Conditions - Abstract
The increasing use of gastrointestinal endoscopic procedures has led to the recognition by histopathologists of non-conventional (or special-type) dysplasias of the gastrointestinal tract. These lesions can be recognised in association with prevalent underlying gastrointestinal conditions, such as Barrett oesophagus, chronic atrophic gastritis, and inflammatory bowel disease. The diagnosis of these special types can be challenging, and their biological behaviours are not fully characterised. The aim of this review is to provide a global view of non-conventional dysplastic lesions observed in the various segments of the tubular gastrointestinal tract and describe their salient features. Furthermore, as the clinical implications of these various subtypes have not been broadly tested in practice and are not represented in most management guidelines, we offer guidance on the best management practices for these lesions.
- Published
- 2021
5. Gastrointestinal stromal tumour (GIST) arising in Meckel’s diverticulum
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Ak Muhd Izzan Zulfiqah, Linda Leys, and Masato Yozu
- Subjects
Pathology and Forensic Medicine - Published
- 2022
6. Australasian Gastrointestinal Pathology Society (AGPS) consensus guidelines for universal defective mismatch repair testing in colorectal carcinoma
- Author
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Ian Brown, Anthony J. Gill, Christophe Rosty, M. Priyanthi Kumarasinghe, and Masato Yozu
- Subjects
0301 basic medicine ,congenital, hereditary, and neonatal diseases and abnormalities ,medicine.medical_specialty ,Cost effectiveness ,MLH1 ,DNA Mismatch Repair ,Pathology and Forensic Medicine ,03 medical and health sciences ,0302 clinical medicine ,Neoplastic Syndromes, Hereditary ,Humans ,Medicine ,Intensive care medicine ,neoplasms ,Early Detection of Cancer ,Brain Neoplasms ,business.industry ,Endometrial cancer ,Australia ,nutritional and metabolic diseases ,Microsatellite instability ,Gastrointestinal pathology ,Mismatch Repair Protein ,medicine.disease ,digestive system diseases ,Lynch syndrome ,030104 developmental biology ,030220 oncology & carcinogenesis ,Mutation ,Microsatellite Instability ,DNA mismatch repair ,Colorectal Neoplasms ,business ,New Zealand - Abstract
Lynch syndrome is the most common hereditary form of colorectal carcinoma caused by a constitutional pathogenic mutation in a DNA mismatch repair gene. Identifying Lynch syndrome is essential to initiate intensive surveillance program for the patient and affected relatives. On behalf of the Australasian Gastrointestinal Pathology Society (AGPS), we present in this manuscript consensus guidelines for Lynch syndrome screening in patients with colorectal carcinoma. The goal of this consensus document is to provide recommendations to pathologists for diagnosis of Lynch syndrome with discussion of the benefits and limitations of each test. Universal screening for defective mismatch repair is recommended, in agreement with the recent endorsement of universal testing by the National Health and Medical Research Council in Australia and the New Zealand Ministry of Health. The value of evaluating defective mismatch repair is acknowledged not only for Lynch syndrome screening but also for therapeutic decision information in patient management. AGPS advocates appropriate government funding for the molecular tests necessary for Lynch syndrome screening (BRAF mutation, MLH1 methylation testing).
- Published
- 2019
7. Histologic and Outcome Study Supports Reclassifying Appendiceal Goblet Cell Carcinoids as Goblet Cell Adenocarcinomas, and Grading and Staging Similarly to Colonic Adenocarcinomas
- Author
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Michelle Yang, Gregory Y. Lauwers, Namrata Setia, David P. Ryan, Masato Yozu, Melanie Johncilla, Robert D. Odze, James C. Cusack, Leona A. Doyle, Joseph Misdraji, and Amitabh Srivastava
- Subjects
Adult ,Male ,0301 basic medicine ,Pathology ,medicine.medical_specialty ,Biopsy ,Carcinoid Tumor ,Adenocarcinoma ,Pathology and Forensic Medicine ,03 medical and health sciences ,0302 clinical medicine ,Predictive Value of Tests ,Terminology as Topic ,Humans ,Medicine ,Stage (cooking) ,Grading (tumors) ,Goblet cell carcinoid ,Aged ,Neoplasm Staging ,Aged, 80 and over ,Neoplasm Grading ,Goblet cell ,medicine.diagnostic_test ,business.industry ,Mucin ,Middle Aged ,medicine.disease ,030104 developmental biology ,medicine.anatomical_structure ,Appendiceal Neoplasms ,030220 oncology & carcinogenesis ,Colonic Neoplasms ,Female ,Surgery ,Goblet Cells ,Anatomy ,business - Abstract
Goblet cell carcinoid tumors are amphicrine tumors whose biological behavior ranges from indolent to highly aggressive, depending on tumor grade. Current grading systems for these tumors are based on identifying an adenocarcinoma arising in the setting of a goblet cell carcinoid tumor, which distinguishes this tumor from other gastrointestinal tract adenocarcinomas. Because goblet cell tumors are predominantly tumors of mucin secreting cells, we propose that they be classified as goblet cell adenocarcinomas, and graded using a methodology that has parallels in colorectal adenocarcinoma grading. We graded a large series of goblet cell adenocarcinomas by assessing the proportion of the tumor that demonstrates tubular or clustered growth. Histologic grade correlated with overall survival independent of stage, with median overall survival of 204, 86, and 29 months for low-grade, intermediate-grade, and high-grade goblet cell adenocarcinomas, respectively. Tumor stage also correlated with overall survival. We also graded the tumors according to previously proposed grading systems, and found that these systems are valid, in that they segregate patients according to prognosis.
- Published
- 2018
8. Mutational landscape of goblet cell carcinoids and adenocarcinoma ex goblet cell carcinoids of the appendix is distinct from typical carcinoids and colorectal adenocarcinomas
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Gregory Y. Lauwers, Melanie Johncilla, Joseph Misdraji, Neal I. Lindeman, Robert D. Odze, Masato Yozu, Mikhail Lisovsky, Amitabh Srivastava, and Matthew D. Stachler
- Subjects
Adult ,Male ,0301 basic medicine ,Pathology ,medicine.medical_specialty ,ARID1A ,Carcinoid Tumor ,Adenocarcinoma ,Biology ,medicine.disease_cause ,Pathology and Forensic Medicine ,CDH1 ,03 medical and health sciences ,0302 clinical medicine ,medicine ,Humans ,neoplasms ,Exome sequencing ,Goblet cell carcinoid ,Aged ,Goblet cell ,Middle Aged ,medicine.disease ,digestive system diseases ,Gene Expression Regulation, Neoplastic ,030104 developmental biology ,medicine.anatomical_structure ,Appendiceal Neoplasms ,030220 oncology & carcinogenesis ,Mutation ,biology.protein ,Female ,CDKN1B ,KRAS ,Colorectal Neoplasms - Abstract
There is limited data on the spectrum of molecular alterations in goblet cell carcinoids and adenocarcinoma ex goblet cell carcinoids of the appendix. We used next generation sequencing to determine mutations of potential pathogenetic and therapeutic significance in this rare group of tumors. Adequate DNA was successfully extracted in 34/46 cases and the final group included 18 goblet cell carcinoids and 16 adenocarcinoma ex goblet cell carcinoids. Illumina TruSeq™ was used for sequencing exons of a custom 282 gene panel using an Illumina HiSeq 2000. All cases had a minimum coverage depth of at least 50 reads. After filtering through the Exome Sequencing Project, the number of mutations per case ranged from 0–9 (mean:3). The mutational burden in adenocarcinoma ex goblet cell carcinoids was significantly higher than goblet cell carcinoids (mean 5 vs. 3; p
- Published
- 2018
9. Gastric pyloric gland adenoma: a multicentre clinicopathological study of 67 cases
- Author
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Ian Brown, Namrata Setia, Tetsuo Ushiku, Gregory Y. Lauwers, Amitabh Srivastava, Masato Yozu, Won-Tak Choi, Joseph Misdraji, Rish K. Pai, Ryan M. Gill, Masashi Fukayama, and Melanie Johncilla
- Subjects
Adenoma ,Adult ,Male ,0301 basic medicine ,medicine.medical_specialty ,Histology ,Autoimmune Gastritis ,Adenocarcinoma ,Gastroenterology ,Pathology and Forensic Medicine ,Familial adenomatous polyposis ,Young Adult ,03 medical and health sciences ,0302 clinical medicine ,Immunophenotyping ,Stomach Neoplasms ,Internal medicine ,Biomarkers, Tumor ,medicine ,Genetic predisposition ,Humans ,Aged ,Aged, 80 and over ,business.industry ,General Medicine ,Middle Aged ,medicine.disease ,Cell Transformation, Neoplastic ,030104 developmental biology ,Gastric Mucosa ,Dysplasia ,030220 oncology & carcinogenesis ,Disease Progression ,Immunohistochemistry ,Female ,Neoplasm Recurrence, Local ,business - Abstract
AIMS There is limited information regarding the clinicopathological and immunohistochemical characteristics of gastric pyloric gland adenomas (PGAs). METHODS AND RESULTS Sixty-seven cases of gastric PGA from 57 patients were analysed. PGAs occurred with similar frequency in men and women (47.4 and 52.6%, respectively), with a mean age of 66 years. Most presented in the gastric body/fundus (67.2%). Fifteen cases (22.4%) developed against a background of autoimmune gastritis (AIG), whereas normal mucosa was seen in 35.8%. Only 16.4% (11 cases) developed in patients with a genetic predisposition, most commonly familial adenomatous polyposis. Low-grade lesions had a mean size of 1.5 cm, while PGAs with high-grade dysplasia (HGD) or adenocarcinoma had a mean size of 3.5 cm (P < 0.001) and more commonly showed tubulovillous architecture (50.0 versus 25.6% in low-grade dysplasia; P = 0.040). Most PGAs (61.2%) co-expressed mucin (MUC)5AC and MUC6 (mixed type), which was associated significantly with HGD or adenocarcinoma (P = 0.013). AIG was also associated with HGD (P = 0.027), but genetic predisposition did not correlate with the grade of dysplasia (P = 0.793). The recurrence rate of PGA was similar for high- (11.8%) and low-grade lesions (7.4%) (P = 0.624). CONCLUSIONS The risk of HGD increases with the size of PGA, tubulovillous architecture and the presence of AIG as well as mixed immunophenotype. As the overall local recurrence rate is less than 10%, PGAs may be treated conservatively, but they should be excised completely if possible, particularly if they are large or show high-grade features.
- Published
- 2018
10. Nonconventional dysplasia in patients with inflammatory bowel disease and colorectal carcinoma: a multicenter clinicopathologic study
- Author
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Gregory Y. Lauwers, Masato Yozu, Won-Tak Choi, Joseph Misdraji, Priyanthi Kumarasinghe, Gregory Miller, Noam Harpaz, and Angela R. Shih
- Subjects
0301 basic medicine ,Adult ,Male ,Pathology ,medicine.medical_specialty ,Colorectal cancer ,Mixed type ,Gastroenterology ,Inflammatory bowel disease ,Pathology and Forensic Medicine ,Lesion ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,In patient ,Aged ,Retrospective Studies ,Aged, 80 and over ,business.industry ,Not Otherwise Specified ,Retrospective cohort study ,Middle Aged ,medicine.disease ,Inflammatory Bowel Diseases ,digestive system diseases ,030104 developmental biology ,Dysplasia ,030220 oncology & carcinogenesis ,Female ,medicine.symptom ,business ,Colorectal Neoplasms - Abstract
Several types of nonconventional dysplasia have been recently described in inflammatory bowel disease (IBD). However, strict morphologic criteria are lacking, and their clinicopathologic features (including potential association with conventional dysplasia and/or colorectal cancer [CRC]) are poorly understood. A total of 106 dysplastic or serrated lesions in 58 IBD patients with CRC were retrospectively identified from five institutions. Thirty-six cases of nonconventional dysplasia were identified in 26 (45%) of the 58 patients and occurred with similar frequency in men and women (58% and 42%, respectively), with a mean age of 54 years (range: 24–73) and a long history of IBD (mean: 17 years, range: 2–43). Six morphologic patterns were recognized. Hypermucinous dysplasia (n = 15; 42%) presented as either a ‘pure type’ (n = 5; 14%) or a ‘mixed type’ with either conventional or another nonconventional subtype (n = 10; 28%). Serrated lesions, as a group, were equally common (n = 15; 42%) and included three variants: traditional serrated adenoma-like (n = 10; 28%), sessile serrated lesion-like (n = 1; 3%), and serrated lesion, not otherwise specified (n = 4; 11%). Dysplastic lesions with increased Paneth cell differentiation (n = 4; 11%) and goblet cell deficient dysplasia (n = 2; 6%) were rare. Twelve (46%) of the 26 patients had only nonconventional dysplasia, whereas the remaining 14 patients (54%) had both nonconventional and conventional dysplasias. Nonconventional dysplasia was most often graded as low-grade dysplasia (81%), which was less common in conventional dysplasia (37%) (p = 0.003). When present alone, nonconventional dysplasia was predominantly found in the left colon (81%, p = 0.006) as a polypoid or raised lesion (75%, p
- Published
- 2019
11. Loss of expression of MLH1 in non-dysplastic crypts is a harbinger of neoplastic progression in sessile serrated adenomas/polyps
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Marina Kem, Mari Mino-Kenudson, Robert D. Odze, Joseph Misdraji, Masato Yozu, and Odise Cenaj
- Subjects
0301 basic medicine ,Adult ,Male ,congenital, hereditary, and neonatal diseases and abnormalities ,Pathology ,medicine.medical_specialty ,Histology ,Colonic Polyps ,Adenocarcinoma ,MLH1 ,digestive system ,Pathology and Forensic Medicine ,03 medical and health sciences ,Adenomatous Polyps ,Young Adult ,0302 clinical medicine ,Neoplastic progression ,Carcinoma ,Biomarkers, Tumor ,Medicine ,Humans ,neoplasms ,Aged ,Aged, 80 and over ,business.industry ,Serrated polyp ,nutritional and metabolic diseases ,General Medicine ,Middle Aged ,medicine.disease ,digestive system diseases ,030104 developmental biology ,Cell Transformation, Neoplastic ,Dysplasia ,030220 oncology & carcinogenesis ,Colonic Neoplasms ,Disease Progression ,Biomarker (medicine) ,Immunohistochemistry ,Female ,business ,MutL Protein Homolog 1 - Abstract
AIMS Dysplasia in colonic sessile serrated adenomas (SSAs)/sessile serrated polyps often shows loss of MLH1 expression as determined with immunohistochemistry, but the significance of loss of MLH1 expression in non-dysplastic crypts in these polyps is less well studied. The purpose of this study was to evaluate the prevalence of loss of MLH1 expression in non-dysplastic crypts in SSAs, and to evaluate its significance with regard to progression of these polyps. METHODS AND RESULTS Four hundred SSAs, including 158 SSAs without dysplasia, 219 SSAs with dysplasia (SSAD), and 23 SSAs with invasive adenocarcinoma (SSAC), were evaluated immunohistochemically for loss of MLH1 expression in both non-dysplastic and dysplastic portions of the polyps. Seventy-one of 400 (18%) SSAs showed loss of MLH1 expression in non-dysplastic crypts. The prevalence of MLH1-deficient non-dysplastic crypts was higher in polyps with dysplasia or carcinoma (7%, 22%, and 52% in SSAs, SSADs, and SSACs, respectively; P
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- 2019
12. Dabigatran-induced oesophagitis dissecans superficialis
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Masato Yozu and Suneeth Mathew
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medicine.medical_specialty ,business.industry ,Internal medicine ,medicine ,business ,Gastroenterology ,Pathology and Forensic Medicine ,Dabigatran ,medicine.drug - Published
- 2020
13. Essential Components of Melanoma Histopathological Reporting: The Surgical Oncologist’s Perspective
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Jon A. Mathy, Vinka Nurdjaja, and Masato Yozu
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Surgical oncologist ,medicine.medical_specialty ,business.industry ,Melanoma ,Perspective (graphical) ,Cancer ,Dermatology ,Review Article ,medicine.disease ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,lcsh:RC254-282 ,03 medical and health sciences ,0302 clinical medicine ,Oncology ,030220 oncology & carcinogenesis ,Cutaneous melanoma ,medicine ,Clinical significance ,030212 general & internal medicine ,Radiation treatment planning ,Intensive care medicine ,business - Abstract
Histopathological reporting plays a critical role in guiding the surgical oncologist’s management plan in treatment of primary cutaneous melanoma. The International Collaboration on Cancer Reporting (ICCR) espouses various components of structured histopathological reporting as “essential” or “recommended.” From a surgical oncologist’s perspective, we discuss the clinical relevance of each essential component, as well as prognostic and treatment implications with regard to treatment planning.
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- 2018
14. Heterotopic skin in meckel’s diverticulum – a case report
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Masato Yozu and Se Mi Kim
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Meckel's diverticulum ,business.industry ,Medicine ,Anatomy ,business ,medicine.disease ,Pathology and Forensic Medicine - Published
- 2019
15. Recurrent loss of heterozygosity correlates with clinical outcome in pancreatic neuroendocrine cancer
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Michael Findlay, Ben Lawrence, Braden Woodhouse, Esther Coats, Papaarangi Reid, Mik Black, Masato Yozu, Kimiora Henare, Richard Babor, Jonathan Koea, Sean M. Grimmond, Nicole Kramer, Nicholas Knowlton, Kate Parker, Saxon Connor, Paula Shields, Dragan Damianovich, Cherie Blenkiron, Peter Johnston, Andrew D. MacCormick, Vicky Fan, Marianne S. Elston, Helen Morrin, Peter Tsai, Bridget A. Robinson, Richard W. Carroll, Christopher Jackson, Sandra Fitzgerald, Patrick Yap, Nooriyah Poonawala, Tamsin Robb, Cristin G. Print, Mee Ling Yeong, Sarah M James, Reena Ramsaroop, John A. Windsor, and Adam Bartlett
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0301 basic medicine ,lcsh:QH426-470 ,lcsh:Medicine ,Aneuploidy ,Neuroendocrine tumors ,Gene mutation ,medicine.disease_cause ,Bioinformatics ,Article ,Loss of heterozygosity ,03 medical and health sciences ,0302 clinical medicine ,Pancreatic cancer ,Genetics ,medicine ,PTEN ,MEN1 ,Folliculin ,Molecular Biology ,Genetics (clinical) ,Mutation ,biology ,lcsh:R ,medicine.disease ,lcsh:Genetics ,030104 developmental biology ,030220 oncology & carcinogenesis ,DNA methylation ,Cancer research ,biology.protein - Abstract
Pancreatic neuroendocrine tumors (pNETs) are uncommon cancers arising from pancreatic islet cells. Here we report the analysis of gene mutation, copy number, and RNA expression of 57 sporadic well-differentiated pNETs. pNET genomes are dominated by aneuploidy, leading to concordant changes in RNA expression at the level of whole chromosomes and chromosome segments. We observed two distinct patterns of somatic pNET aneuploidy that are associated with tumor pathology and patient prognosis. Approximately 26% of the patients in this series had pNETs with genomes characterized by recurrent loss of heterozygosity (LoH) of 10 specific chromosomes, accompanied by bi-allelic MEN1 inactivation and generally poor clinical outcome. Another ~40% of patients had pNETs that lacked this recurrent LoH pattern but had chromosome 11 LoH, bi-allelic MEN1 inactivation, and universally good clinical outcome. The somatic aneuploidy allowed pathogenic germline variants (e.g., ATM) to be expressed unopposed, with RNA expression patterns showing inactivation of downstream tumor suppressor pathways. No prognostic associations were found with tumor morphology, single gene mutation, or expression of RNAs reflecting the activity of immune, differentiation, proliferative or tumor suppressor pathways. In pNETs, single gene mutations appear to be less important than aneuploidy, with MEN1 the only statistically significant recurrently mutated driver gene. In addition, only one pNET in the series had clearly actionable single nucleotide variants (SNVs) (in PTEN and FLCN) confirmed by corroborating RNA expression changes. The two clinically relevant patterns of LoH described here define a novel oncogenic mechanism and a plausible route to genomic precision oncology for this tumor type., Cancer: Frequent chromosome loss in rare pancreatic tumors The loss of entire chromosomes seems to be a fundamental driver of tumors arising from the hormone-producing cells of the pancreas. A team led by Cristin Print and Ben Lawrence from the University of Auckland, New Zealand, performed genomic and pathological analysis of 57 pancreatic neuroendocrine tumors, a rare form of cancer caused by the abnormal growth of hormone-producing islet cells within the pancreas. The researchers observed two distinct patterns of chromosome loss, with 26% of the samples missing one copy of 10 specific chromosomes and another 40% lacking a copy of chromosome 11. In both groups, the abnormal chromosome count prompts abnormal gene activity patterns, with recessive mutations unleashed and expressed unopposed. Single gene mutations seem to play only a minor role, suggesting that single gene-targeted drugs will provide little benefit in this disease setting, with more nuanced approaches required.
- Published
- 2017
- Full Text
- View/download PDF
16. Osteoclast-rich undifferentiated carcinoma of the bladder: A case report
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Sinead McCarthy and Masato Yozu
- Subjects
medicine.anatomical_structure ,Osteoclast ,business.industry ,medicine ,Cancer research ,Undifferentiated carcinoma ,business ,Pathology and Forensic Medicine - Published
- 2018
17. Biphasic gastric adeno-choriocarcinoma in a patient with known lynch syndrome – A case report
- Author
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Masato Yozu and Linda Leys
- Subjects
medicine.medical_specialty ,business.industry ,Internal medicine ,Choriocarcinoma ,medicine ,medicine.disease ,business ,Gastroenterology ,Lynch syndrome ,Pathology and Forensic Medicine - Published
- 2018
18. Gastric heterotopia-like duodenal polyps containing Brunner glands with abundant paneth cells and oxyntic cells are frequently associated with advanced left-sided colorectal polyps
- Author
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Masato Yozu and Jacklyn Ting
- Subjects
Gastric heterotopia ,Pathology ,medicine.medical_specialty ,business.industry ,Medicine ,Brunner Glands ,business ,Left sided ,Duodenal polyps ,Pathology and Forensic Medicine - Published
- 2018
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