Abstract
Fusion genes are structural chromosomal rearrangements resulting in the exchange of DNA sequences between genes. This results in the formation of a new combined gene. They have been implicated in carcinogenesis in a number of different cancers, though they have been understudied in high grade serous ovarian cancer. This study used high throughput tools to compare the transcriptome of high grade serous ovarian cancer and normal fallopian tubes in the interest of identifying unique fusion transcripts within each group. Indeed, we found that there were significantly more fusion transcripts in the cancer samples relative to the normal fallopian tubes. Following this, the role of fusion transcripts in chemo-response and overall survival was investigated. This led to the identification of fusion transcripts significantly associated with overall survival. Validation was performed with different analytical platforms and different algorithms to find fusion transcripts.
Highlights
Though much effort has been invested in defining the biology and natural history of ovarian cancer, standard treatment and prognosis has not changed much since the addition of platinum based chemotherapy [1]
Sci. 2021, 22, 4791 chromosome 6, AL445985.1—SPATA13 is found on chromosome 13, and PFKF3Bo3f —20 LNC02649 is found on chromosome 10
The The Cancer Genome Atlas (TCGA) allowed investigators to examine the genomic underpinnings of ovarian cancer, and such analyses have helped identify a molecular subset of patients (HRD) which benefit from targeted therapy (PARP inhibitors)
Summary
Though much effort has been invested in defining the biology and natural history of ovarian cancer, standard treatment and prognosis has not changed much since the addition of platinum based chemotherapy [1]. A notable exception is a subset of ovarian cancer patients with deficiencies in DNA repair who have enjoyed new targeted therapies with significant gains in progression free survival [2,3,4,5]. The Cancer Genome Atlas (TCGA) made great strides in defining the genomic profile of high grade serous ovarian cancers. Beyond and/or because of a high preponderance of TP53 mutations and homologous recombination deficiency, the genomic profile was marked by disarray, especially in contrast with other cancer types, such as glioblastoma multiforme [6]. It is necessary to expand the repertoire of examined genomic features in high grade serous ovarian cancer. Fusion genes represent an understudied genomic feature of high grade serous ovarian cancer
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