X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Medicine  (293)
Type of Medium
Publisher
Person/Organisation
Language
Years
FID
Subjects(RVK)
  • Medicine  (293)
RVK
  • 1
    Online Resource
    Online Resource
    Pembrolizumab versus paclitaxel for previously treated, advanced gastric or gastro-oesophageal junction cancer (KEYNOTE-061): a randomised, open-label, controlled, phase 3 trial
    Elsevier BV ; 2018
    In:  The Lancet Vol. 392, No. 10142 ( 2018-07), p. 123-133
    Details
    In: The Lancet, Elsevier BV, Vol. 392, No. 10142 ( 2018-07), p. 123-133
    Type of Medium: Online Resource
    ISSN: 0140-6736
    URL: Article
    DOI: 10.1016/S0140-6736(18)31257-1
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2067452-1
    detail.hit.zdb_id: 3306-6
    detail.hit.zdb_id: 1476593-7
    SSG: 5,21
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 2
    Online Resource
    Online Resource
    The prognostic role of soluble transforming growth factor-β related with soluble programmed death-ligand 1 in biliary tract cancer.
    American Society of Clinical Oncology (ASCO) ; 2019
    In:  Journal of Clinical Oncology Vol. 37, No. 15_suppl ( 2019-05-20), p. 4094-4094
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 37, No. 15_suppl ( 2019-05-20), p. 4094-4094
    Abstract: 4094 Background: We previously reported that soluble programmed death-Ligand 1 (sPD-L1) at pre-chemotherapy indicated the prognostic value for overall survival (OS) and the dynamics of sPD-L1 during palliative chemotherapy correlated with disease burden in biliary tract cancer (BTC). Transforming growth factor (TGF) -β attenuates tumor response to PD1/PD-L1 inhibitors. Strategy of dual targeting of PD1/PD-L1 and TGF-β is now under investigation. This study aimed to evaluate the association between soluble TGF-β (sTGF-β) and sPD-L1, dynamics during chemotherapy and its prognostic role in BTC. Methods: Study population consisted of 90 BTC patients treated with first line chemotherapy. Blood samples at pre-and post-chemotherapy and at disease progression (PD) were prospectively collected. Plasma sTGF-β and sPD-L1 levels were measured by using an enzyme-linked immunosorbent assay. Results: The median progression free survival (PFS) and OS of all patients was 6.9 months (m) (95% CI, 5.2-8.6) and 11.5 m (95% CI, 9.4-13.6). The best response was CR in 7 (7.8%), PR in 20 (22.2%), SD in 52 (57.8%), and PD in 11 patients (12.2%). The mean baseline sTGF-β and sPD-L1 were 16.4 ng/ml and 1.3 ng/ml. There was a positive association between sTGF-β and sPD-L1 in terms of baseline levels and changes after chemotherapy (at pre-chemo, Pearson correlation = 0.578, p 〈 0.001; change after chemotherapy, Pearson correlation = 0.542, p 〈 0.001). Patients with higher pre-chemotherapy sPD-L1 ( 〉 1.3 ng/ml) showed worse OS (9.2 vs 16.2 m, p 〈 0.001). Both sPD-L1 (1.8 vs 1.0 ng/ml, p 〈 0.001) and sTGF-β (20.5 vs 11.6 ng/ml, p 〈 0.001) were increased significantly at the time of PD compared with pre-chemotherapy. Regarding changes after chemotherapy, increased sTGF-β after chemotherapy (Δ 〉 3.2 ng/ml) had worse prognosis (PFS: 5.1 vs 7.3 m, p = 0.024; OS: 9.2 vs 12.3 m, p = 0.028). This prognostic value of change of sTGF-β after chemotherapy was also significant in multivariable analysis with other clinical factors (PFS: HR = 1.78, p = 0.022; OS: HR = 1.86, p = 0.018). Conclusions: In BTC, there is a positive association between sTGF-β and sPD-L1 value in terms of baseline levels and changes after chemotherapy. sTGF-β could be associated with the survival, particularly, increased value after chemotherapy indicates worse prognosis.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2019.37.15_suppl.4094
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2019
    detail.hit.zdb_id: 2005181-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 3
    Online Resource
    Online Resource
    Dynamics of soluble programmed death-ligand 1 (soluble PDL1) during chemotherapy and its prognostic implication in cancer patients.
    American Society of Clinical Oncology (ASCO) ; 2017
    In:  Journal of Clinical Oncology Vol. 35, No. 15_suppl ( 2017-05-20), p. 11542-11542
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 35, No. 15_suppl ( 2017-05-20), p. 11542-11542
    Abstract: 11542 Background: The soluble form Programmed Death-Ligand 1(sPDL1) is suggested to have immunosuppressive activity and under investigation as candidate biomarker for immuno-oncology drug development. In this study, we measured the serum sPDL1 at pre-and post-chemotherapy and evaluated its prognostic implication and dynamics during chemotherapy in biliary tract cancer (BTC) patients. Methods: From 90 advanced BTC patients (training cohort 42 patients, validation cohort 48 patients) who were candidates for palliative 1 st -line chemotherapy, blood was collected at pre-and post-chemotherapy. sPDL1 was measured using an enzyme-linked immunosorbent assay. Response to chemotherapy, overall survival (OS) and other prognostic factors including neutrophil-lymphocyte ratio (NLR) were also obtained. Results: OS of all patients was 11.5 months (95% CI; 9.7-16.2). The best response was CR in 7 patients (7.8%), PR 20 patients (22.2%), SD 52 patients (57.8%) and PD 11 patients (12.2%). Median sPDL1 at pre-chemotherapy was 0.97 ng/mL (range 0.6-1.9). Patients with high pre-chemo sPDL1 (≥ 1.30 ng/mL) showed worse OS than patients with low pre-chemo sPDL1 (9.1 vs. 12.5 months, p =0.003). In multivariate analysis, high pre-chemo sPDL1 (HR 1.96, 95% CI; 1.2-3.9, p = 0.011) and pre-chemo NLR (HR 1.82, 95% CI; 1.1-3.0, p = 0.020) were independent poor prognostic factors for OS. Post-chemotherapy sPDL1 and its changes compared with pre-chemotherapy were not significantly different across tumor response groups. However, at the time of disease progression, sPDL1 was increased significantly compared with pre-chemo sPDL1 (1.59 ng/mL vs 0.72 ng/mL, p = 0.003). In PR group, sPDL1 at pre-chemo, post-chemo, and PD was 1.19, 0.98, and 2.77 ng/mL, respectively. In SD group, sPDL1 at pre-chemo, post-chemo, and PD was 1.16, 1.19, and 1.83 ng/mL, respectively. In PD group, sPDL1 at pre-chemo and PD was 0.62, and 1.04 ng/mL. Conclusions: sPDL1 at pre-chemotherapy confers the prognostic value for OS in BTC patients under palliative chemotherapy. The dynamics of sPDL1 during chemotherapy correlates with disease progression.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2017.35.15_suppl.11542
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2017
    detail.hit.zdb_id: 2005181-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 4
    Online Resource
    Online Resource
    Phase Ib study of binimetinib (MEK162) in combination with capecitabine in gemcitabine-pretreated advanced biliary tract cancer.
    American Society of Clinical Oncology (ASCO) ; 2018
    In:  Journal of Clinical Oncology Vol. 36, No. 15_suppl ( 2018-05-20), p. 4079-4079
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 36, No. 15_suppl ( 2018-05-20), p. 4079-4079
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2018.36.15_suppl.4079
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2018
    detail.hit.zdb_id: 2005181-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 5
    Online Resource
    Online Resource
    Enhanced antitumor effect of binimetinib in combination with capecitabine for biliary tract cancer patients with mutations in the RAS/RAF/MEK/ERK pathway: phase Ib study
    Springer Science and Business Media LLC ; 2019
    In:  British Journal of Cancer Vol. 121, No. 4 ( 2019-8), p. 332-339
    Details
    In: British Journal of Cancer, Springer Science and Business Media LLC, Vol. 121, No. 4 ( 2019-8), p. 332-339
    Type of Medium: Online Resource
    ISSN: 0007-0920 , 1532-1827
    URL: Article
    DOI: 10.1038/s41416-019-0523-5
    RVK:
    XA 33500
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
    detail.hit.zdb_id: 2002452-6
    detail.hit.zdb_id: 80075-2
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 6
    Online Resource
    Online Resource
    Abstract 2110: WEE1 inhibition could reverse trastuzumab resistance by downregulation of PD-L1 in HER2-positive cancers
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 2110-2110
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 2110-2110
    Abstract: Background: Trastuzumab in combination with chemotherapy is a standard of care for patients with HER2-positive breast and gastric cancer. Resistance mechanism to trastuzumab, anti-HER2 therapy, includes multiple pathways. Cancer cells could evade immune surveillance through high expression of programmed cell death ligand 1 (PD-L1) on cancer or immune cells. Among resistance mechanisms to trastuzumab, the role of PD-L1 modulation has not yet been discovered in HER2-positive cancers. WEE1 is involved in cell cycle progression and DNA damage response (DDR), and, interestingly, beyond DDR, it could modulate immunes. We aimed to evaluate the role of PD-L1 in trastuzumab resistance in HER2-positive cancers with/without immune cells and to explore WEE1 inhibitor as a trastuzumab resistance overcoming strategy by modulation of PD-L1. Methods: Four trastuzumab-resistant (HR) cells (SNU216HR, N87HR, SNU2670HR, SNU2773HR) were established from 2 HER2-amplified gastric cancer cells (SNU216, NCI-N87) and 2 HER2-amplified biliary tract cancer cells (SNU2670, SNU2773). For WEE1 inhibition, AZD1775 was used. MTT assay, colony formation assay, cell cycle analysis by FACS Calibur flow cytometer, and western blot were done. Results: All four HR cells showed PD-L1 upregulation compared with parental cells. When PD-L1 was knocked-down by transfection with si-PD-L1, anti-growth/proliferation effects were observed in MTT assay and colony forming assay. PD-L1 itself may promote cancer cell growth without interacting with immune cells. AZD1775 downregulated PD-L1 expression and induced cell cycle arrest at sub-G1 and G2/M phases in all 4 HR cells. The synergistic anti-proliferative effects were found in all 4 HR cells with co-treatment of trastuzumab and AZD1775. Conclusion: PD-L1 upregulation may contribute to trastuzumab resistance in HER2-positive cancer cells. Targeting WEE1-PD-L1 pathway might be a candidate strategy to overcome trastuzumab resistance in HER2-positive cancers. Citation Format: Meihua Jin, Ah-Rong Nam, Ji-Eun Park, Ju-Hee Bang, Kyoung-Seok Oh, Do-Youn Oh, Yung-Jue Bang. WEE1 inhibition could reverse trastuzumab resistance by downregulation of PD-L1 in HER2-positive cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2110.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-2110
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 7
    Online Resource
    Online Resource
    Abstract 5869: Resistance mechanism against trastuzumab in HER2-positive cancer cells and its negation by Src inhibition
    American Association for Cancer Research (AACR) ; 2017
    In:  Cancer Research Vol. 77, No. 13_Supplement ( 2017-07-01), p. 5869-5869
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 77, No. 13_Supplement ( 2017-07-01), p. 5869-5869
    Abstract: Background: Trastuzumab in combination with chemotherapy is a standard of care for patients with HER2-positive breast and gastric cancer. Resistance mechanism to trastuzumab, anti-HER2 therapy, includes multiple pathways. Among them, Src is not well known especially in HER2-positive gastric and biliary tract cancers. We investigated the role of Src involved in trastuzumab resistance and explored the potential of Src inhibition as a trastuzumab resistance overcoming strategy. Methods: Four trastuzumab-resistant (HR) cells (SNU216HR, N87HR, SNU2670HR, SNU2773HR) were established from 2 HER2-amplified gastric cancer cells (SNU216, NCI-N87) and 2 HER2-amplified biliary tract cancer cells (SNU2670, SNU2773). For Src inhibition, bosutinib was used. MTT assay, colony formation assay, cell cycle analysis by FACS Calibur flow cytometer, and cell migration assay were done. Animal experiments were conducted to test anti-tumor effect of bosutinib using SNU2670 and SNU2670HR xenograft models. Results: SNU2670HR/NCI-N87HR cells showed pSrc activation, in contrast, SNU216HR/SNU2773HR cells exhibited decreased pSrc expression. In these pSrc decreased HR cells, pFAK was elevated. Bosutinib downregulated Src-FAK signaling more obviously in Src activated HR cells than parental cells. In pSrc decreased HR cells, bosutinib reduced Src-dependent FAK phosphorylation to affect cell fate. Bosutinib inhibited the growth of both parental cells and HR cells, and induced apoptosis and G1 arrest in HR cells. Bosutinib suppressed HR cell migration more effectively compared with parental cells. Bosutinib exhibited potent tumor growth inhibition in both SNU2670 and SNU2670HR xenograft models and more significantly suppressed tumor growth in HR models. Conclusion: Src activation may contribute to trastuzumab resistance in part in HER2-positive gastric and biliary tract cancer cells. Targeting Src might be a candidate strategy to overcome trastuzumab resistance in HER2-positive cancers. Citation Format: Meihua Jin, Ah Rong Nam, Ji Eun Park, Ju Hee Bang, Yung Jue Bang, Do Youn Oh. Resistance mechanism against trastuzumab in HER2-positive cancer cells and its negation by Src inhibition [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5869. doi:10.1158/1538-7445.AM2017-5869
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2017-5869
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2017
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 8
    Online Resource
    Online Resource
    Abstract 3599: Resistance mechanisms to HER2-targeting treatment in HER2-positive gastric cancer
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 3599-3599
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 3599-3599
    Abstract: Background: HER2 is the first validated therapeutic target in advanced gastric cancer (GC). Trastuzumab in combination with chemotherapy is used as a first-line treatment of GC. The resistance mechanisms to trastuzumab have not been widely known in GC. We investigated the resistance mechanisms to HER2-targeting agents in HER2-positive gastric cancer cells. Methods: SNU216 and NCI-N87 are HER2 amplified gastric cancer cells. Using these cells, we established trastuzumab-resistant cells (SNU216-HR, N87-HR) and dacomitinib (panHER inhibitor)-resistant cells (SNU216-PR). Acquired resistance of the established cell lines was verified by MTT assay and western blotting. We compared various receptor tyrosine kinase activities and protein expression levels between parental and resistant cells by RTK arrays and western blotting. We used many targeted agents (HER family inhibitor, PI3K inhibitor, mTOR inhibitor, MEK inhibitor, Src inhibitor, HSP90 inhibitor, etc) to overcome the resistance. Results: Resistant cells displayed more rapid growth rate and different morphology compared with parent cells. Resistant cells showed increased levels of pEGFR, pHER2, pHER3, pMET, pIGF1R, pAXL, pSTAT3, pAKT, pFAK, and TS compared with the parental cells in western blot. With the treatment of trastuzumab, HR cells showed elevated levels of EGFR, pHER2, AXL, pAXL, pMEK, pSRC, pSTAT3, pAKT, pERK and TS compared with the parental cells. With the treatment of dacominitib, PR cells showed elevated levels of pEGFR, pAXL, pIGF1R, pMEK, pSRC, pERK and TS compared with the parental cells in western blot. The RTK arrays also showed the similar findings. These resistant cells were more sensitive to Src inhibitor and PI3K inhibitor than parent cells. Conclusion: Resistance mechanisms to HER2-targeting strategy in gastric cancer include activation of HER, MET, FAK and Src pathway. Targeting these pathways is needed to overcome resistance. Citation Format: Kyo Hwa Kang, Ah-Rong Nam, Ji Eun Park, Ju-Hee Bang, Jin Ling, Mei Hua Jin, Tae Yong Kim, Sae-Won Han, Sang-Hyun Song, Seock-Ah Im, Tae-You Kim, Do-Youn Oh, Yung-Jue Bang. Resistance mechanisms to HER2-targeting treatment in HER2-positive gastric cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3599. doi:10.1158/1538-7445.AM2015-3599
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-3599
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 9
    Online Resource
    Online Resource
    Abstract 3496: GC1118, a novel anti-EGFR andtibody, shows more potent antitumor activity regardless of KRAS mutation or high-affinity lignad stimulation compared with cetuximab in gastric cancer
    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 3496-3496
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 3496-3496
    Abstract: Background: EGFR overexpression in gastric cancer (GC) has been reported in about 30% of patients. However, cetuximab and panitumulab, anti-EGFR antibodies, have failed to improve overall survival of GC patients compared with standard chemotherapy alone. GC1118 is a novel anti-EGFR antibody with distinct binding epitope compared to cetuximab or panitumumab, and has superior inhibitory activity against high-affinity EGFR ligands (Mol Cancer Ther 2016). In this study, GC1118 was tested to evaluate the antitumor effects in gastric cancer cells. Methods: Using a total of 15 kinds of GC cell lines (SNU-1, SNU-5, SNU-16, SNU-216, SNU-484, SNU-601, SNU-620, SNU-638, SNU-668, SNU-719, AGS, MKN-28, MKN-45, NCI-N87, and KATO-), GC1118, cetuximab, cisplatin, and 5-FU were tested. Cells were treated with or without high-affinity EGFR ligands, EGF 20ng/mL or HB-EGF 100ng/mL. Result: GC1118 exhibited more potent antigrowth effects in the majority of GC cells than cetuximab in colony forming assay and MTT assay, regardless of KRAS mutation status of cells. The synergistic efficacy was observed when cells were treated with GC1118 in combination with cytotoxic chemotherapeutic agents (cisplatin or 5FU) in colony formation assay and migration assay compared to each treatment alone, even under the EGFR-ligand stimulation condition. GC1118 significantly blocked the p-AKT or p-ERK signaling under the presence of ligand induced-EGFR activation. However, cetuximab failed to block p-AKT or p-ERK that was upregulated by EGF or HB-EGF. Moreover, this signal-blocking activity was more potent in case of GC1118 compared with cetuximab in the chemotherapy combination experiment. Conclusion: GC1118 showed more potent antitumor effects in GC compared with cetuximab. In combination with cytotoxic chemotherapy, GC1118 also has more potent activity compared with cetuximab regardless of KRAS mutation status or high-affinity ligand stimulation condition. This study supports further clinical development of GC1118 in gastric cancer. Citation Format: Ji Eun Park, Mei Hua Jin, Ah-Rong Nam, Ju-Hee Bang, Do-Youn Oh, Yung-Jue Bang. GC1118, a novel anti-EGFR andtibody, shows more potent antitumor activity regardless of KRAS mutation or high-affinity lignad stimulation compared with cetuximab in gastric cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3496.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2018-3496
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
  • 10
    Online Resource
    Online Resource
    The role of soluble TGF-beta and its dynamics for predicting the prognosis in unresectable pancreatic cancer patients treated with chemotherapy.
    American Society of Clinical Oncology (ASCO) ; 2018
    In:  Journal of Clinical Oncology Vol. 36, No. 4_suppl ( 2018-02-01), p. 288-288
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 36, No. 4_suppl ( 2018-02-01), p. 288-288
    Abstract: 288 Background: Transforming growth factor-beta (TGF-β) is a multifunctional regulatory factor. Here, we measured serum soluble TGF-β (sTGF-β) levels and evaluated its dynamics and prognostic capabilities during chemotherapy in unresectable pancreatic cancer patients. Methods: Sixty patients treated with FOLFIRINOX as the first-line palliative chemotherapy were prospectively enrolled. We prospectively collected blood samples at the time of diagnosis, first response assessment, and disease progression and measured serum sTGF-β using an enzyme-linked immunosorbent assay. Results: The patients’ median overall survival (OS) and progression free survival (PFS) were 10.3 (95% confidence interval [CI], 8.5–12.1) and 6.5 (95% CI, 4.9–8.1) months, respectively. Patients with low sTGF-β at diagnosis ( 〈 31.2ng/mL) had better OS and PFS than patients with high sTGF-β, respectively (OS, 13.7 vs. 9.2 months; hazard ratio [HR], 2.602; P =0.004; PFS, 9.0 vs. 5.8 months; HR, 2.010; P =0.034). At the time of disease progression, sTGF-β was increased compared with that of diagnosis (mean 26.4 vs. 23.9ng/mL). Especially, in patients with a partial response, sTGF-β was significantly increased at disease progression (mean 25.7 vs. 31.0ng/mL; P =0.049). Conclusions: Pre-treatment sTGF-β levels serve as a prognostic indicator in unresectable pancreatic cancer patients treated with FOLFIRINOX chemotherapy. Likewise, the dynamics of sTGF-β during chemotherapy have prognostic value.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2018.36.4_suppl.288
    RVK:
    XA 52760
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2018
    detail.hit.zdb_id: 2005181-5
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Online Resource
    Open Access Request
    Availability (electronic / print)
Nothing or not found what you are looking for? Please check your search query or use the Interlibrary Loan Search.
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages