The Efficacy and Safety of Caffeic Acid for Esophageal Cancer

NCT ID: NCT03070262

Last Updated: 2020-11-27

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Clinical Phase

PHASE3

Total Enrollment

300 participants

Study Classification

INTERVENTIONAL

Study Start Date

2017-01-31

Study Completion Date

2021-12-31

Brief Summary

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Caffeic acid can target inhibit GASC1 (gene amplified in squamous cell carcinoma 1, also known as KDM4C and JMJD2C) expression and GASC1 is confirmed to be a new oncogene in several cancers including esophageal cancer. This study aims to investigate the efficiency and safety of coffeic acid in chinese advanced esophageal squamous cell cancer (ESCC).

Detailed Description

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Background: More than half of global esophageal cancer cases came from China.80 percentage patients were diagnosed with advanced disease and suffered from the poor outcome.With the development of target therapy among cancers,the overall survival and life quality of patients has been continuous improved recently.However,there had little reports focusing on target therapy in esophageal cancer . Caffeic acid as an ordinary drug is used for thrombocytopenia when patient received chemotherapy. Newly studies shown caffeic acid can target inhibit GASC1 expression, and GASC1 is confirmed to be a new oncogene in esophageal cancer.

Aim: to investigate the efficiency and safety of caffeic acid in chinese advanced esophageal squamous cell cancer.

Methods: 240 advanced ESCC patients will be randomized to two arms: Arm A (receiving coffeic acid treatment) or Arm B (placebo group). In Arm A, patients will receive coffeic acid treatment: 300mg, tid, po, continue to progress disease (PD) or die or the intolerant adverse events; in Arm B, the same shape placebo tablets will be deliveried to patients. 1 years follow-up for both groups patients.Patients in both arms can receive any other ways of anti cancer therapy in the same time.

Primary endpoints: OS Second endpoints: PFS

Conditions

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Esophagus Cancer

Keywords

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esophageal cancer caffeic acid

Study Design

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Allocation Method

RANDOMIZED

Intervention Model

PARALLEL

Primary Study Purpose

TREATMENT

Blinding Strategy

QUADRUPLE

Participants Caregivers Investigators Outcome Assessors

Study Groups

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CA group

caffeic acid (300mg, tid, po) continue given until progression of disease or death, or patients are unable to bear the side effects

Group Type EXPERIMENTAL

CA

Intervention Type DRUG

caffeic acid, 300mg, tid, po

placebo group

the same shape placebo tablets continue given until progression of disease or death, or patients are unable to bear the side effects

Group Type PLACEBO_COMPARATOR

placebo group

Intervention Type DRUG

placebo tablet, 3 tablets, tid, po

Interventions

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CA

caffeic acid, 300mg, tid, po

Intervention Type DRUG

placebo group

placebo tablet, 3 tablets, tid, po

Intervention Type DRUG

Eligibility Criteria

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Inclusion Criteria

* Chinese
* esophageal squamous cell cancer
* stage IV or disease recurrence
* chemotherapy, or radiotherapy, or palliative care is going on

Exclusion Criteria

* PS (performance status): ≥ 3
* severe hepatic and renal dysfunction
* hypercoagulability
* thrombocytosis
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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Anyang Tumor Hospital

OTHER

Sponsor Role collaborator

150th Hospital of PLA

OTHER_GOV

Sponsor Role collaborator

The First Affiliated Hospital of Henan University of Science and Technology

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Shegan Gao, PhD

Role: STUDY_CHAIR

The Clinical Medical College, The First Affiliated Hospital of Henan Science and Technology

Locations

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The Clinical Medical College, The First Affiliated Hospital of Henan University of Science and Technology

Luoyang, Henan, China

Site Status

Countries

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China

References

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Reference Type BACKGROUND
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Pedersen MT, Kooistra SM, Radzisheuskaya A, Laugesen A, Johansen JV, Hayward DG, Nilsson J, Agger K, Helin K. Continual removal of H3K9 promoter methylation by Jmjd2 demethylases is vital for ESC self-renewal and early development. EMBO J. 2016 Jul 15;35(14):1550-64. doi: 10.15252/embj.201593317. Epub 2016 Jun 6.

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Ye Q, Holowatyj A, Wu J, Liu H, Zhang L, Suzuki T, Yang ZQ. Genetic alterations of KDM4 subfamily and therapeutic effect of novel demethylase inhibitor in breast cancer. Am J Cancer Res. 2015 Mar 15;5(4):1519-30. eCollection 2015.

Reference Type RESULT
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Ozaki Y, Fujiwara K, Ikeda M, Ozaki T, Terui T, Soma M, Inazawa J, Nagase H. The oncogenic role of GASC1 in chemically induced mouse skin cancer. Mamm Genome. 2015 Dec;26(11-12):591-7. doi: 10.1007/s00335-015-9592-9. Epub 2015 Aug 7.

Reference Type RESULT
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Reference Type RESULT
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Reference Type RESULT
PMID: 24224128 (View on PubMed)

Berdel B, Nieminen K, Soini Y, Tengstrom M, Malinen M, Kosma VM, Palvimo JJ, Mannermaa A. Histone demethylase GASC1--a potential prognostic and predictive marker in invasive breast cancer. BMC Cancer. 2012 Nov 14;12:516. doi: 10.1186/1471-2407-12-516.

Reference Type RESULT
PMID: 23148692 (View on PubMed)

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Reference Type RESULT
PMID: 19784073 (View on PubMed)

Yuan X, Kong J, Ma Z, Li N, Jia R, Liu Y, Zhou F, Zhan Q, Liu G, Gao S. KDM4C, a H3K9me3 Histone Demethylase, is Involved in the Maintenance of Human ESCC-Initiating Cells by Epigenetically Enhancing SOX2 Expression. Neoplasia. 2016 Oct;18(10):594-609. doi: 10.1016/j.neo.2016.08.005. Epub 2016 Sep 19.

Reference Type RESULT
PMID: 27742014 (View on PubMed)

Tyszka-Czochara M, Konieczny P, Majka M. Caffeic Acid Expands Anti-Tumor Effect of Metformin in Human Metastatic Cervical Carcinoma HTB-34 Cells: Implications of AMPK Activation and Impairment of Fatty Acids De Novo Biosynthesis. Int J Mol Sci. 2017 Feb 21;18(2):462. doi: 10.3390/ijms18020462.

Reference Type RESULT
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Bonuccelli G, De Francesco EM, de Boer R, Tanowitz HB, Lisanti MP. NADH autofluorescence, a new metabolic biomarker for cancer stem cells: Identification of Vitamin C and CAPE as natural products targeting "stemness". Oncotarget. 2017 Mar 28;8(13):20667-20678. doi: 10.18632/oncotarget.15400.

Reference Type RESULT
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Chung LC, Chiang KC, Feng TH, Chang KS, Chuang ST, Chen YJ, Tsui KH, Lee JC, Juang HH. Caffeic acid phenethyl ester upregulates N-myc downstream regulated gene 1 via ERK pathway to inhibit human oral cancer cell growth in vitro and in vivo. Mol Nutr Food Res. 2017 Sep;61(9). doi: 10.1002/mnfr.201600842. Epub 2017 Mar 20.

Reference Type RESULT
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Dziedzic A, Kubina R, Kabala-Dzik A, Tanasiewicz M. Induction of Cell Cycle Arrest and Apoptotic Response of Head and Neck Squamous Carcinoma Cells (Detroit 562) by Caffeic Acid and Caffeic Acid Phenethyl Ester Derivative. Evid Based Complement Alternat Med. 2017;2017:6793456. doi: 10.1155/2017/6793456. Epub 2017 Jan 12.

Reference Type RESULT
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Sirota R, Gibson D, Kohen R. The timing of caffeic acid treatment with cisplatin determines sensitization or resistance of ovarian carcinoma cell lines. Redox Biol. 2017 Apr;11:170-175. doi: 10.1016/j.redox.2016.12.006. Epub 2016 Dec 7.

Reference Type RESULT
PMID: 27951496 (View on PubMed)

Other Identifiers

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GiCAEC-LY001

Identifier Type: -

Identifier Source: org_study_id