China
Africa
Explore chapters and articles related to this topic
EML4-ALK Fusion Gene and Therapy with ALK-Targeted Agents in Non-Small Cell Lung Cancer
Published in Sherry X. Yang, Janet E. Dancey, Handbook of Therapeutic Biomarkers in Cancer, 2021
Francisco E. Vera-Badillo, Janet E. Dancey
ROS1 was first discovered as the oncogene product of an avian sarcoma RNA tumor virus [77]. ROS1 is activated by chromosomal rearrangement in a variety of human cancers, including NSCLC, cholangiocarcinoma, gastric cancer, ovarian cancer, and glioblastoma [78–82]. Rearrangements lead to the fusion of a portion of ROS1 that includes the entire tyrosine kinase domain with 1 of 12 different partner proteins [83]. The resulting ROS1 fusion kinases are constitutively activated and drive cellular transformation. ROS1 rearrangements occur in 1% to 2% of NSCLC via a genetic translocation between ROS1 and other genes, the most common of which is CD74 [84–86].
Systemic Therapy (Targeted Therapy and Immunotherapy) for Thyroid Cancers
Published in Madan Laxman Kapre, Thyroid Surgery, 2020
Another genetic translocation involved in thyroid carcinogenesis is PAX8-PPARγ. This translocation leads to the fusion between the PAX8 gene and the peroxisome proliferator–activated receptor (PPARγ) gene. PAX8–PPARγ has an inactivating effect on the wild-type tumor suppressor PPARγ and transactivates certain PAX8-responsive genes [16]. This translocation occurs in about 40%–60% of FTC [12].
Molecular Diagnostics of Chronic Myeloid Leukemia: Precision Medicine via Gold Nanoparticles
Published in Il-Jin Kim, Companion Diagnostics (CDx) in Precision Medicine, 2019
Raquel Vinhas, Alexandra R. Fernandes, Pedro V. Baptista
This type of leukemia is caused by the Philadelphia chromosome (Ph), a balanced genetic translocation, t(9;22)(q34.1;q11.2), involving the fusion of the Abelson gene (ABL1) from chromosome 9 with the breakpoint cluster region (BCR) gene on chromosome 22 originating the hallmark BCR-ABL1 fusion transcript that encodes a constitutively overexpressed BCR-ABL1 tyrosine kinase.22 Since the BCR gene harbors at least six potential breakpoint regions, the product of the BCR–ABL1 fusion oncogene may exist in six forms of different molecular weight (Fig. 11.1).
Personalized patient care with aggressive hematological malignancies in non-responders to first-line treatment
Published in Expert Review of Precision Medicine and Drug Development, 2021
Katsuhiro Miura, Noriyoshi Iriyama, Yoshihiro Hatta, Masami Takei
ALCL is the third most common PTCL that uniformly overexpresses CD30. Among ALCL cases, overexpression of ALK derived from genetic translocation is found in variable incidence, mostly in children and young adults [98]. Historically, ALK has been a favorable prognostic biomarker, but it can be a therapeutic target for molecular inhibitors [99]. Brentuximab vedotin, an antibody–drug conjugate targeting CD30, was the treatment of choice for second-line ALCL treatment, with high response rates and long-term remission duration even among patients without HSCT consolidation in the phase 2 study, which enrolled 58 patients with R/R systemic ALCL [100,101]. Brentuximab vedotin also has an activity for R/R CD30-positive PTCL-NOS or AITL, with a modest efficacy [102]. However, brentuximab vedotin is now administered as the first-line treatment (BV+CHP) for these patients since the ECHELON-2 trial demonstrated excellent clinical outcomes [103]. Therefore, salvage treatment for ALCL/CD30-positive lymphomas depends on the patient’s AKL status, brentuximab vedotin exposure, or authorized indications per local agencies.