2017
DOI: 10.1016/j.ygyno.2016.12.002
|View full text |Cite
|
Sign up to set email alerts
|

Genotype-matched treatment for patients with advanced type I epithelial ovarian cancer (EOC)

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

1
13
0

Year Published

2017
2017
2024
2024

Publication Types

Select...
4
4

Relationship

0
8

Authors

Journals

citations
Cited by 29 publications
(14 citation statements)
references
References 30 publications
1
13
0
Order By: Relevance
“…Advancements in genomic and proteomic approaches have improved methods for the identification of candidate biomarkers and helped to develop effective screening strategies for early detection [5]. Molecular profiling and individualized OC treatment have provided optimism regarding the role of individualized medicine for oncological patients [6].…”
Section: Introductionmentioning
confidence: 99%
“…Advancements in genomic and proteomic approaches have improved methods for the identification of candidate biomarkers and helped to develop effective screening strategies for early detection [5]. Molecular profiling and individualized OC treatment have provided optimism regarding the role of individualized medicine for oncological patients [6].…”
Section: Introductionmentioning
confidence: 99%
“…Firstly, we identified potential targetable genomic mutations in CCC using an extensive literature search (24,25). Patients with CCC (64%) had ≥1 somatic mutation (24).…”
Section: Candidate Mutated Genes For Enhancing the Therapeutic Ratio mentioning
confidence: 99%
“…Patients with CCC (64%) had ≥1 somatic mutation (24). These included ARID1A; PIK3CA; PTEN; KRAS proto-oncogene, GTPase (KRAS); NRAS proto-oncogene, GTPase; B-Raf proto-oncogene, serine/threonine kinase (BRAF); zincfinger protein 217; AKT serine/threonine kinase (AKT); TP53; Wnt/β-catenin (CTNNB1); microsatellite instability; mutL homolog 1; SRC proto-oncogene, non-receptor tyrosine kinase; ETS proto-oncogene 1, transcription factor; protein kinase DNA-activated, catalytic polypeptide; APC membrane recruitment protein 1; AT-rich interaction domain 2; B cell CLL/lymphoma 11A; CREB binding protein; erb-b2 receptor tyrosine kinase 2 (ERBB2); exostosin glycosyltransferase 1; Fanconi anemia complementation group D2; mutS homolog 6 (MSH6), neurofibromin 1 (NF1); notch 1 (NOTCH1), nuclear mitotic apparatus protein 1; phosphodiesterase 4D interacting protein; protein phosphatase 2 scaffold subunit Aalpha (PPP2R1A); ring finger protein 213; spectrin repeat containing nuclear envelope protein 1; CUB and Sushi multiple domains 3; latrophilin 3; LDL receptor related protein 1B; speckle type BTB/POZ protein (SPOP); speckle type BTB/POZ protein (KMT2D) and TP53 (21,(24)(25)(26)(27). The genetic mutations related to chromatin remodeling, DNA repair signaling, PI3K-AKT-mTOR, Notch signaling and CTNNB1 pathway may be involved in CCC biology (27).…”
Section: Candidate Mutated Genes For Enhancing the Therapeutic Ratio mentioning
confidence: 99%
“…Those retrospective, yet to be validated analyses have generated hypotheses that have to be evaluated prospectively to be proven clinically useful. Currently, profiling objectives are toward the identification and validation of biomarkers in prospective clinical trials . With advancing technology, costs should become less prohibitive and may be augmented by the development of customized, subtype‐specific panels for defined populations.…”
Section: When Should Effective Treatment Be Introduced Interrupted mentioning
confidence: 99%