Yoshida A, Tsuta K, Wakai S, Arai Y, Asamura H, Shibata T, Furuta K, Kohno T, Kushima R. Immunohistochemical detection of ROS1 is useful for identifying ROS1 rearrangements in lung cancers / Mod Pathol, v.27, issue 5, November, 2014, pp.711-20
Sentences:
CD74-ROS1 and EZR-ROS1 fusions were significantly associated with at least focal globular immunoreactivity and plasma membranous accentuation, respectively, and these patterns were specific to ROS1-rearranged cases.

Li H, Pan Y, Wang R, Li Y, Sun Y, Chen H. Response to crizotinib observed in metastatic mediastinum lymph node from a non-small cell lung cancer patient harboring EZR–ROS1 fusion / J Cancer Res Clin Oncol., v.141, issue 1, January, 2015, pp.185-7
Sentences:
To the best of our knowledge, this is the first report about NSCLC patient with EZR–ROS1 fusion gene type responding to crizotinib.

Inoue M, Toki H, Matsui J, Togashi Y, Dobashi A, Fukumura R, Gondo Y, Minowa O, Tanaka N, Mori S, Takeuchi K, Noda T. Mouse models for ROS1-fusion-positive lung cancers and their application to the analysis of multikinase inhibitor efficiency / Carcinogenesis, v.37, issue 5, May, 2016, pp.452-60
Sentences:
Although at least 12 partner genes for ROS1 have been identified in human NSCLCs so far, only one TG mouse lung cancer model (EZR-ROS1 TG mouse) has been established

Lim SM, Kim EY, Kim HR, Ali SM, Greenbowe JR, Shim HS, Chang H, Lim S, Paik S, Cho BC. Genomic profiling of lung adenocarcinoma patients reveals therapeutic targets and confers clinical benefit when standard molecular testing is negative / Oncotarget., v.7, issue 17, March, 2016, pp.24172-78
Sentences:
As per NCCN guidelines, targetable GAs were identified in 16 patients (31%) (BRAF mutation [n=1], EGFR mutation [n=8], ERBB2 mutation [n=4], MET amplification [n=1], KIF5B-RET rearrangement [n=2], CCDC6-RET rearrangement [n=1], CD74-ROS1 rearrangement [n=1], EZR-ROS1 rearrangement [n=5], and SLC34A2-ROS1 rearrangement [n=1]).

Davare MA, Davare MA, Davare MA, Davare MA, Davare MA, Saborowski A, Saborowski A, Saborowski A, Saborowski A, Saborowski A, Eide CA, Eide CA, Eide CA, Eide CA, Eide CA, Tognon C, Tognon C, Tognon C, Tognon C, Tognon C, Smith RL, Smith RL, Smith RL, Smith RL, Smith RL, Elferich J, Elferich J, Elferich J, Elferich J, Elferich J, Agarwal A, Agarwal A, Agarwal A, Agarwal A, Agarwal A, Tyner JW, Tyner JW, Tyner JW, Tyner JW, Tyner JW, Shinde UP, Shinde UP, Shinde UP, Shinde UP, Shinde UP, Lowe SW, Lowe SW, Lowe SW, Lowe SW, Lowe SW, Druker BJ, Druker BJ, Druker BJ, Druker BJ, Druker BJ. Foretinib is a potent inhibitor of oncogenic ROS1 fusion proteins / Proc Natl Acad Sci U S A., v.110, issue 48, November, 2013, pp.196519-24
Sentences:
Other ROS1 fusions include CD74–ROS1, EZR–ROS1, LRIG3–ROS1, SDC4–ROS1, and TPM3–ROS1

Arai Y, Totoki Y, Takahashi H, Nakamura H, Hama N, Kohno T, Tsuta K, Yoshida A, Asamura H, Mutoh M, Hosoda F, Tsuda H, Shibata T. Mouse Model for ROS1-Rearranged Lung Cancer / PLoS One, v.8, issue 2, February, 2013, pp.e56010
Sentences:
The present study shows that EZR-ROS1 plays an essential role in the oncogenesis of NSCLC harboring the fusion gene.

Solomon B. Validating ROS1 Rearrangements As a Therapeutic Target in Non–Small-Cell Lung Cancer / J Clin Oncol., v.33, issue 9, March, 2015, pp.972-4
Sentences:
At least 11 fusion partners have been identified in NSCLC, including CD74-ROS1, SDC4-ROS1, EZR-ROS1, and SLC34A2-ROS1, all of which maintain a constant breakpoint in ROS1, preserving the kinase domain and resulting in aberrant ROS1 expression with constitutive kinase activity.

Keefe JG, Sukov WR, Knudson RA, Nguyen LP, Williamson C, Sinnwell JP, Ketterling RP. Development of five dual-color, double-fusion fluorescence in situ hybridization assays for the detection of common MLL translocation partners / J Mol Diagn, v.12, issue 4, June, 2010, pp.441-52
Sentences:
Five translocations account for approximately 80% of MLL rearrangements: t(4;11)(q21;q23), AFF1/MLL; t(6;11)(q27;q23), MLLT4/MLL; t(9;11)(p22;q23), MLLT3/MLL; t(11;19)(q23;p13.1), MLL/ELL; and t(11;19)(q23;p13.3), MLL/MLLT1.

König M, Reichel M, Marschalek R, Haas OA, Strehl S. A highly specific and sensitive fluorescence in situ hybridization assay for the detection of t(4;11)(q21;q23) and concurrent submicroscopic deletions in acute leukaemias / N Engl J Med., v.116, issue 4, March, 2002, pp.758-64
Sentences:
On the molecular level, the MLL gene on 11q23 is fused to the AF4 gene in the 4q21 region, resulting in a chimaeric MLL/AF4 fusion transcript.

Frestedt JL, Hilden JM, Moore RO, Kersey JH. Differential expression of AF4/FEL mRNA in human tissues / Genet Anal., v.12, issue 3-4, January, 1996, pp.147-9
Sentences:
AF4 mRNA is highly expressed in normal placental tissue which correlates with the newborn age of patients presenting with leukemia characterized by the MLL/AF4 gene rearrangement.

Pane F, Intrieri M, Izzo B, Quintarelli C, Vitale D, Migliorati R, Sebastio L, Salvatore F. A novel MLL/AF4 fusion gene lacking the AF4 transactivating domain in infant acute lymphoblastic leukemia / Blood, v.100, issue 12, December, 2002, pp.4247-8
Sentences:
Because the MLL partner fragment included a sequence homologous toAF4 exon 11, we designed a new antisense primer on this exon to amplify the junction sequences of MLL/AF4cDNA, transcribed from the new MLL/AF4 fusion gene.

Domer PH, Fakharzadeh SS, Chen CS, Jockel J, Johansen L, Silverman GA, Kersey JH, Korsmeyer SJ. Acute mixed-lineage leukemia t(4;11)(q21;q23) generates an MLL-AF4 fusion product / Proc Natl Acad Sci U S A., v.90, issue 16, August, 1993, pp.7884-8
Sentences:
The composition of the complete MLL-AF4 fusion product argues that it may act through either a gain-of-function or a dominant negative mechanism in leukemogenesis.

Caslini C, Serna A, Rossi V, Introna M, Biondi A. Modulation of cell cycle by graded expression of MLL-AF4 fusion oncoprotein / Leukemia., v.18, issue 6, June, 2004, pp.1064-71
Sentences:
Our results demonstrate a dosage-dependent effect of MLL-AF4 fusion oncoprotein on cell cycle progression, with increasing expression levels resulting in the accumulation in G1, prolonged doubling time, both findings that might be responsible for the increased resistance to etoposide-mediated cytotoxicity.

Bertrand FE, Spengeman JD, Shah N, LeBien TW. B-cell development in the presence of the MLL/AF4 oncoprotein proceeds in the absence of HOX A7 and HOX A9 expression / Leukemia., v.17, issue 12, December, 2003, pp.2454-9
Sentences:
Infant acute lymphoblastic leukemia (ALL) is frequently characterized by the t(4;11)(q21;q23) cytogenetic abnormality encoding the MLL/AF4 oncogene, increased HOX gene expression and a pro-B/monocytoid phenotype.

Yamamoto S, Zaitsu M, Ishii E, Yatsuki H, Mizutani S, Eguchi M, Ihara K, Okamura T, Hara T, Miyazaki S. High frequency of fusion transcripts of exon 11 and exon 4/5 in AF-4 gene is observed in cord blood, as well as leukemic cells from infant leukemia patients with t(4;11)(q21;q23) / Leukemia., v.12, issue 9, September, 1998, pp.1398-403
Sentences:
We analyzed the presence and frequency of the MLL/AF-4 rearrangement in normal cord blood.

Divoky V, Trka JM, Watzinger F, Lion T. Cryptic splice site activation during RNA processing of MLL/AF4 chimeric transcripts in infants with t(4;11) positive ALL / Gene, v.247, issue 1-2, April, 2000, pp.111-8
Sentences:
Co-expression of multiple variants of the MLL/AF4 fusion transcript is a common phenomenon in patients with acute lymphoblastic leukemia (ALL) with t(4;11)(q21;q23).

Blütters-Sawatzki R, Borkhardt A, Grathwohl J, Repp R, Rheinisch-Becker I, Bohle RM, Lampert F. Secondary acute myeloid leukemia with translocation (4;11) and MLL/AF4 rearrangement in a 15-year-old boy treated for common acute lymphoblastic leukemia 11 years earlier / Ann Hematol., v.70, issue 1, January, 1995, pp.31-5
Sentences:
A polymerase chain reaction assay of a peripheral blood sample recognized the mRNA fusion region for the MLL/AF4 rearrangement, i.e., the molecular equivalent of the translocation (4;11)(q21,q23).

Bizarro S, Cerveira N, Correia C, Lisboa S, Peixoto A, Norton L, Teixeira MR. Molecular characterization of a rare MLL-AF4 (MLL-AFF1) fusion rearrangement in infant leukemia / Cancer Genet Cytogenet., v.178, issue 1, October, 2007, pp.61-4
Sentences:
We characterize at both the DNA and RNA level a rare MLL-AF4 fusion transcript identified in a 15-month-old girl with acute lymphoblastic leukemia.

Benedikt A, Baltruschat S, Scholz B, Bursen A, Arrey TN, Meyer B, Varagnolo L, Müller AM, Karas M, Dingermann T, Marschalek R. The leukemogenic AF4-MLL fusion protein causes P-TEFb kinase activation and altered epigenetic signatures / Leukemia., v.25, issue 1, January, 2011, pp.135-44
Sentences:
Expression of the AF4-MLL fusion protein in murine hematopoietic progenitor/stem cells results in the development of proB acute lymphoblastic leukemia

McMahon M. RAF translocations expand cancer targets / Nat Med., v.16, issue 7, December, 2014, pp.749-750
Sentences:
The SCL45A3-BRAF fusion mRNA encodes a 329–amino acid protein that comprises only a C-terminal fragment of BRAF. By contrast, the ESRP1-RAF2 and AGTRAP-BRAF fusions encode proteins with substantial contribution of N-terminal sequences from the RAF fusion partner.

Lee J, Ou SH. Towards the goal of personalized medicine in gastric cancer--time to move beyond HER2 inhibition. Part II: Targeting gene mutations and gene amplifications and the angiogenesis pathway / Discov Med., v.16, issue 86, August, 2013, pp.7-14
Sentences:
AGTRAP-BRAF transcript is generated from the fusion of exon 5 of AGTRAP to exon 8 of BRAF with a 597 amino acid AGTRAP-BRAF fusion protein

Nakaoku T, Tsuta K, Ichikawa H, Shiraishi K, Sakamoto H, Enari M, Furuta K, Shimada Y, Ogiwara H, Watanabe S, Nokihara H, Yasuda K, Hiramoto M, Nammo T, Ishigame T, Schetter AJ, Okayama H, Harris CC, Kim YH, Mishima M, Yokota J, Yoshida T, Kohno T. Druggable Oncogene Fusions in Invasive Mucinous Lung Adenocarcinoma / Clin Cancer Res, v.20, issue 12, June, 2014, pp.3087-93
Sentences:
These features suggested that the fusion was constitutively active, as in the cases of the ESRP1-BRAF and AGTRAP-BRAF fusions in other cancers

Lee NV, Lira ME, Pavlicek A, Ye J, Buckman D, Bagrodia S, Srinivasa SP, Zhao Y, Aparicio S, Rejto PA, Christensen JG, Ching KA. A novel SND1-BRAF fusion confers resistance to c-Met inhibitor PF-04217903 in GTL16 cells through [corrected] MAPK activation / PLoS One, v.7, issue 6, June, 2012, pp.e39653
Sentences:
Similarly, various fusions of BRAF have been implicated in cancer such as pediatric astrocytomas (KIAA1549-BRAF; exons 9/11) [24], melanocytic nevi (FCHSD1-BRAF; exon 9) [25], papillary thyroid carcinomas (AKAP9-BRAF; exon 9) [26], prostate cancer (SLC45A-BRAF; exon 8) [27], and gastric cancer (AGTRAP-BRAF; exon 8)

Tan P, Yeoh KG. Genetics and Molecular Pathogenesis of Gastric Adenocarcinoma / Gastroenterology., v.149, issue 5, October, 2015, pp.1153-1162
Sentences:
An RNA-sequencing study in 2010 revealed for the first time the presence of rare RAF-fusion genes in GC and prostate cancers (eg, AGTRAP-BRAF), and preclinical models expressing these RAF fusions were shown sensitive to treatment by sorafinib, originally designed as a RAF inhibitor

Spans L, Clinckemalie L, Helsen C, Vanderschueren D, Boonen S, Lerut E, Joniau S, Claessens F. The genomic landscape of prostate cancer / Int J Mol Sci., v.14, issue 6, May, 2013, pp.10822-51
Sentences:
Paired-end transcriptome sequencing identified several other rearrangements involving genes of the RAF kinase pathway: SLC45A3-BRAF, AGTRAP-BRAF, ESRP1-RAF1, EPB41-BRAF and RAF1-ESRP1