Search Results
Search for other papers by Debora Degl'Innocenti in
Google Scholar
PubMed
Search for other papers by Paola Romeo in
Google Scholar
PubMed
Search for other papers by Eva Tarantino in
Google Scholar
PubMed
Molecular Mechanisms Unit, Nuclear Medicine Division, Scientific Directorate, Department of Experimental Oncology and Molecular Medicine
Search for other papers by Marialuisa Sensi in
Google Scholar
PubMed
Search for other papers by Giuliana Cassinelli in
Google Scholar
PubMed
Search for other papers by Veronica Catalano in
Google Scholar
PubMed
Search for other papers by Cinzia Lanzi in
Google Scholar
PubMed
Search for other papers by Federica Perrone in
Google Scholar
PubMed
Search for other papers by Silvana Pilotti in
Google Scholar
PubMed
Search for other papers by Ettore Seregni in
Google Scholar
PubMed
Search for other papers by Marco A Pierotti in
Google Scholar
PubMed
Search for other papers by Angela Greco in
Google Scholar
PubMed
Search for other papers by Maria Grazia Borrello in
Google Scholar
PubMed
thyroid tissues for a total of 13 non-neoplastic thyroids and 69 PTCs, including different subtypes. For both datasets, information about the genetic alteration of the neoplastic samples was available. In the first dataset, a cDNA array generated in our
Departments of, Pathology, Surgical Oncology, Pathology and Histotechnology, Department of Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aobaku, Sendai, Japan
Search for other papers by Akiko Ebata in
Google Scholar
PubMed
Search for other papers by Takashi Suzuki in
Google Scholar
PubMed
Search for other papers by Kiyoshi Takagi in
Google Scholar
PubMed
Search for other papers by Yasuhiro Miki in
Google Scholar
PubMed
Search for other papers by Yoshiaki Onodera in
Google Scholar
PubMed
Search for other papers by Yasuhiro Nakamura in
Google Scholar
PubMed
Search for other papers by Fumiyoshi Fujishima in
Google Scholar
PubMed
Search for other papers by Kazuyuki Ishida in
Google Scholar
PubMed
Search for other papers by Mika Watanabe in
Google Scholar
PubMed
Departments of, Pathology, Surgical Oncology, Pathology and Histotechnology, Department of Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aobaku, Sendai, Japan
Search for other papers by Kentaro Tamaki in
Google Scholar
PubMed
Search for other papers by Takanori Ishida in
Google Scholar
PubMed
Search for other papers by Noriaki Ohuchi in
Google Scholar
PubMed
Departments of, Pathology, Surgical Oncology, Pathology and Histotechnology, Department of Pathology, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aobaku, Sendai, Japan
Search for other papers by Hironobu Sasano in
Google Scholar
PubMed
lesions of atypical ductal hyperplasia (ADH), DCIS and IDC, and reported that genetic alterations accumulate during cancer progression from ADH to DCIS and finally to IDC ( Amari et al . 1999 ). However, several groups reported a close association of
Institut National de la Santé et de la Recherche Médicale, Université Lyon 1, Unité Fonctionnelle de Biologie Cellulaire, UMR 664, Lyon F-69372, France
Search for other papers by Stéphanie Durand in
Google Scholar
PubMed
Institut National de la Santé et de la Recherche Médicale, Université Lyon 1, Unité Fonctionnelle de Biologie Cellulaire, UMR 664, Lyon F-69372, France
Search for other papers by Carole Ferraro-Peyret in
Google Scholar
PubMed
Search for other papers by Mireille Joufre in
Google Scholar
PubMed
Search for other papers by Annie Chave in
Google Scholar
PubMed
Institut National de la Santé et de la Recherche Médicale, Université Lyon 1, Unité Fonctionnelle de Biologie Cellulaire, UMR 664, Lyon F-69372, France
Search for other papers by Françoise Borson-Chazot in
Google Scholar
PubMed
Institut National de la Santé et de la Recherche Médicale, Université Lyon 1, Unité Fonctionnelle de Biologie Cellulaire, UMR 664, Lyon F-69372, France
Search for other papers by Samia Selmi-Ruby in
Google Scholar
PubMed
Institut National de la Santé et de la Recherche Médicale, Université Lyon 1, Unité Fonctionnelle de Biologie Cellulaire, UMR 664, Lyon F-69372, France
Institut National de la Santé et de la Recherche Médicale, Université Lyon 1, Unité Fonctionnelle de Biologie Cellulaire, UMR 664, Lyon F-69372, France
Search for other papers by Bernard Rousset in
Google Scholar
PubMed
another tyrosine kinase receptor) and different fusion partners leads to the expression of chimeric proteins with constitutive activity on different signaling cascades including the MAPK cascade. This genetic alteration has a low incidence in PTC
Search for other papers by Nancy D Perrier in
Google Scholar
PubMed
Search for other papers by Andrew Arnold in
Google Scholar
PubMed
Search for other papers by Jessica Costa-Guda in
Google Scholar
PubMed
Search for other papers by Naifa L Busaidy in
Google Scholar
PubMed
Search for other papers by Ha Nguyen in
Google Scholar
PubMed
Search for other papers by Hubert H Chuang in
Google Scholar
PubMed
Search for other papers by Maria Luisa Brandi in
Google Scholar
PubMed
specific genetic alterations and combinations thereof. Promising therapies can then be further tested in PDX models. Pathologic reporting Since pathology details are fundamental for appropriate cancer staging and treatment, the need for a standard
Department of Internal Medicine, CHA Bundang Medical Center, CHA University, Seongnam, Korea
Search for other papers by Young Shin Song in
Google Scholar
PubMed
Search for other papers by Seong-Keun Yoo in
Google Scholar
PubMed
Search for other papers by Hwan Hee Kim in
Google Scholar
PubMed
Search for other papers by Gyeongseo Jung in
Google Scholar
PubMed
Search for other papers by Ah-Reum Oh in
Google Scholar
PubMed
Search for other papers by Ji-Young Cha in
Google Scholar
PubMed
Search for other papers by Su-jin Kim in
Google Scholar
PubMed
Search for other papers by Sun Wook Cho in
Google Scholar
PubMed
Department of Surgery, Seoul National University College of Medicine, Seoul, Korea
Search for other papers by Kyu Eun Lee in
Google Scholar
PubMed
Search for other papers by Jeong-Sun Seo in
Google Scholar
PubMed
Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul, Korea
Center for Medical Innovation, Seoul National University Hospital, Seoul, Korea
Search for other papers by Young Joo Park in
Google Scholar
PubMed
fusions were then excluded (Supplementary Table 1, see section on supplementary data given at the end of this article). The driver genetic alterations were defined as the significantly mutated genes and driver fusions, according to definitions in a TCGA
Search for other papers by Yeon-Sook Choi in
Google Scholar
PubMed
Search for other papers by Hyemi Kwon in
Google Scholar
PubMed
Search for other papers by Mi-Hyeon You in
Google Scholar
PubMed
Search for other papers by Tae Yong Kim in
Google Scholar
PubMed
Search for other papers by Won Bae Kim in
Google Scholar
PubMed
Search for other papers by Young Kee Shong in
Google Scholar
PubMed
Search for other papers by Min Ji Jeon in
Google Scholar
PubMed
Search for other papers by Won Gu Kim in
Google Scholar
PubMed
. 2005 , Kurata et al. 2016 , Subbiah et al. 2018 , Kim et al. 2020 , Lee & Park 2021 ). The BRAF V600E mutation is one of the common genetic alterations in ATC, accounting for 20–50% of cases ( Xing 2013 , Jeon et al. 2016 , Subbiah et al
Search for other papers by Alfred King-yin Lam in
Google Scholar
PubMed
Search for other papers by Nassim Saremi in
Google Scholar
PubMed
. Other than BRAFV600E -like tumours and RAS -like tumours, the other papillary thyroid carcinomas are labelled as non- BRAF –non- RAS tumours. They were seen with other genetic alterations such as EIF1AX ( eukaryotic translation initiation factor 1A
Search for other papers by Maria Chiara Zatelli in
Google Scholar
PubMed
Search for other papers by Elia Guadagno in
Google Scholar
PubMed
Search for other papers by Erika Messina in
Google Scholar
PubMed
Search for other papers by Fabio Lo Calzo in
Google Scholar
PubMed
Search for other papers by Antongiulio Faggiano in
Google Scholar
PubMed
Search for other papers by Annamaria Colao in
Google Scholar
PubMed
Search for other papers by NIKE Group in
Google Scholar
PubMed
sporadic pancreatic NETs disclosed the presence of genetic alterations affecting DNA damage and repair, chromatin remodeling, telomere maintenance and mammalian target of rapamycin (mTOR) signaling ( Scarpa et al. 2017 ), providing a significant
Search for other papers by Vanida A Serna in
Google Scholar
PubMed
Search for other papers by Xin Wu in
Google Scholar
PubMed
Division of Reproductive Science in Medicine, Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
Search for other papers by Wenan Qiang in
Google Scholar
PubMed
Search for other papers by Justin Thomas in
Google Scholar
PubMed
Search for other papers by Michael L Blumenfeld in
Google Scholar
PubMed
Search for other papers by Takeshi Kurita in
Google Scholar
PubMed
al . 2014 , Wang et al . 2014 ). Recent comprehensive genome analyses identified four major LM subtypes with unique genetic alterations ( Mehine et al . 2013 , 2016 ), namely, MED12 mutant (MED12-LM) ( Mäkinen et al . 2011 ), HMGA2
Search for other papers by Antonella Verrienti in
Google Scholar
PubMed
Search for other papers by Giovanni Tallini in
Google Scholar
PubMed
Search for other papers by Chiara Colato in
Google Scholar
PubMed
Search for other papers by Amélie Boichard in
Google Scholar
PubMed
Search for other papers by Saula Checquolo in
Google Scholar
PubMed
Search for other papers by Valeria Pecce in
Google Scholar
PubMed
Search for other papers by Marialuisa Sponziello in
Google Scholar
PubMed
Search for other papers by Francesca Rosignolo in
Google Scholar
PubMed
Search for other papers by Dario de Biase in
Google Scholar
PubMed
Search for other papers by Kerry Rhoden in
Google Scholar
PubMed
Search for other papers by Gian Piero Casadei in
Google Scholar
PubMed
Search for other papers by Diego Russo in
Google Scholar
PubMed
Search for other papers by Michela Visani in
Google Scholar
PubMed
Search for other papers by Giorgia Acquaviva in
Google Scholar
PubMed
Search for other papers by Marco Ferdeghini in
Google Scholar
PubMed
Search for other papers by Sebastiano Filetti in
Google Scholar
PubMed
Search for other papers by Cosimo Durante in
Google Scholar
PubMed
). Nevertheless, in a small proportion of sporadic MTCs, no genetic alterations are detected. Small-molecule inhibitors of receptor tyrosine kinases (TKIs) are one of the most promising approaches for treating MTCs. Indeed, encouraging results have emerged from