Browsing by Author "Monthira Suntiparpluacha"

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    Association of estrogen receptor alpha and interleukin 6 polymorphisms with lymphovascular invasion, extranodal extension, and lower disease-free survival in thai breast cancer patients
    (2016-01-01) Doonyapat Sa-Nguanraksa; Monthira Suntiparpluacha; Anchalee Kulprom; Tanawan Kummalue; Tuenjai Chuangsuwanich; Panissadee Avirutnan; Pornchai O-Charoenrat; Mahidol University
    Breast cancer is the most frequent type of cancer diagnosed among women worldwide and also in Thailand. Estrogen and estrogen receptors exert important roles in its genesis and progression. Several cytokines have been reported to be involved in the microenvironment that promotes distant metastasis via modulation of immune and inflammatory responses to tumor cells. Estrogen receptor genetic polymorphisms and several cytokines have been reported to be associated with breast cancer susceptibility and aggressiveness. To investigate roles of genetic polymorphisms in estrogen receptor alpha (ESR1) and interleukin 6 (IL6), breast cancer patients and control subjects were recruited from the Division of Head, Neck and Breast Surgery (Siriraj Hospital, Bangkok, Thailand). Polymorphisms in ESR1 (rs3798577) and IL6 (rs1800795 and rs1800797) were evaluated by real-time PCR in 391 breast cancer patients and 79 healthy controls. Associations between genetic polymorphisms and clinicopathological data were determined. There was no association between genetic polymorphisms and breast cancer susceptibility. However the ESR1 rs3798577 CT genotype was associated with presence of lymphovascular invasion (OR=2.07, 95%CI 1.20-3.56, p=0.009) when compared to the TT genotype. IL6 rs1800795 CC genotype was associated with presence of extranodal extension (OR= 2.30, 95%CI 1.23-4.31, p=0.009) when compared to the GG genotype. Survival analysis showed that IL6 rs1800797 AG or AA genotypes were associated with lower disease-free survival. These findings indicate that polymorphisms in ESR1 and IL6 contribute to aggressiveness of breast cancer and may be used to identify high risk patients.
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    Dependency of Cholangiocarcinoma on Cyclin D–Dependent Kinase Activity
    (2019-11-01) Gunya Sittithumcharee; Orawan Suppramote; Kulthida Vaeteewoottacharn; Chumphon Sirisuksakun; Supawan Jamnongsong; Phatthamon Laphanuwat; Monthira Suntiparpluacha; Arriya Matha; Porncheera Chusorn; Pongsakorn Buraphat; Chumpot Kakanaporn; Komgrid Charngkaew; Atit Silsirivanit; Krittiya Korphaisarn; Somchai Limsrichamrern; Pinpat Tripatara; Chawalit Pairojkul; Sopit Wongkham; Somponnat Sampattavanich; Seiji Okada; Siwanon Jirawatnotai; Faculty of Medicine, Khon Kaen University; Kumamoto University; Khon Kaen University; Faculty of Medicine, Siriraj Hospital, Mahidol University
    © 2019 by the American Association for the Study of Liver Diseases. Cholangiocarcinoma (CCA) is a bile duct cancer with a very poor prognosis. Currently, there is no effective pharmacological treatment available for it. We showed that CCA ubiquitously relies on cyclin-dependent kinases 4 and 6 (CDK4/6) activity to proliferate. Primary CCA tissues express high levels of cyclin D1 and the specific marker of CDK4/6 activity, phospho-RB Ser780. Treatment of a 15-CCA cell line collection by pharmacological CDK4/6 inhibitors leads to reduced numbers of cells in the S-phase and senescence in most of the CCA cell lines. We found that expression of retinoblastoma protein (pRB) is required for activity of the CDK4/6 inhibitor, and that loss of pRB conferred CDK4/6 inhibitor-drug resistance. We also identified that sensitivity of CCA to CDK4/6 inhibition is associated with the activated KRAS signature. Effectiveness of CDK4/6 inhibition for CCA was confirmed in the three-dimensional spheroid-, xenograft-, and patient-derived xenograft models. Last, we identified a list of genes whose expressions can be used to predict response to the CDK4/6 inhibitor. Conclusion: We investigated a ubiquitous dependency of CCA on CDK4/6 activity and the universal response to CDK4/6 inhibition. We propose that the CDK4/6-pRB pathway is a suitable therapeutic target for CCA treatment.