Folate One-carbon Malnutrition as the Metabostemness Risk Factor of Malignancy Tumor Development of NSCLC Patients

NCT ID: NCT03504098

Last Updated: 2019-05-29

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

Total Enrollment

300 participants

Study Classification

OBSERVATIONAL

Study Start Date

2017-08-01

Study Completion Date

2020-07-31

Brief Summary

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Non-small cell lung cancer (NSCLC) accounts for more than two-thirds of lung cancer, which is the leading cause of cancer deaths in Taiwan. The overall prognosis of NSCLC is poor with low 5-year survival rates. Recent advances suggest that malignancy NSCLC cancers are the cancer stem cell (CSC) diseases. The stemness potentials of CSC with epithelial-mesenchymal transdifferentiation ensure their invasion and disseminate to metastsis organs. The self-renewal property of CSC mediates intrinsic drug resistance to cytotoxicity therapy and promoted aggressive relapse tumour. Metabolic reprogramming on bioenergetics of malignant cancer cells has been proposed as the key mediator in the stemness CSC development. Malignancy cells uptake glucose for fermented glycolysis to produce lactate which release resulted in acidified microenvironment to trigger the mTOR and sonic hedgehog metabolic stress signaling in supporting CSC stemness potentials. The metabostemness of cancer cells is the new-dimensional hallmark of malignancy tumour, which may serve as the diagnostic markers for the early detection of malignancy cancers. Folate-mediated one carbon metabolism coordinates glucose into amino acid metabolism to tailor the fuel metabolites in supporting macromolecule synthesis and to sustain the bioenergetics requirement. Acting as the metabolic stressor, low folate intake is associated with increased risks of lung cancers. Folate and one-carbon nutrient status of NSCLC patients in Taiwan, however, has not been assessed. The role of low folate metabolic stress (LFMS) in metabostemness marker and metastasis potentials of malignancy NSCLC is unexplored. The causal effect and the working mechanisms by which LFMS promoted NSCLC malignancy remain elusive.

Detailed Description

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Conditions

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Lung Cancer, Nonsmall Cell

Study Design

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Observational Model Type

CASE_ONLY

Study Time Perspective

PROSPECTIVE

Study Groups

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Lung cancer patients tumor

Using to analysis metabolomic markers, one carbon folate nutrition levels in lung cancer patients.

No interventions assigned to this group

Lung cancer patients blood

Using to analysis folate, B12, homocysteine levels in plasma and RBC. Using to analysis cDNA gene test in buffy coat.

nutrition consult

Intervention Type BEHAVIORAL

Post-lung cancer operation diet pattern

Lung cancer patients

Supply nutrition counseling

nutrition consult

Intervention Type BEHAVIORAL

Post-lung cancer operation diet pattern

Interventions

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nutrition consult

Post-lung cancer operation diet pattern

Intervention Type BEHAVIORAL

Eligibility Criteria

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Inclusion Criteria

* Surgeon diagnosed as the first time having non-small cell lung cancer from the surgical clinic of National Taiwan University Hospital

Exclusion Criteria

* Patients Suffer from major diseases such as heart, liver, kidney, or peripheral arterial disease, or having mental illness
* Diabetes and non-lung cancer patients
* Pregnancy, breast-feeding pregnant women
Minimum Eligible Age

20 Years

Maximum Eligible Age

90 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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National Taiwan University Hospital

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Chin-Pao Cheng

Role: PRINCIPAL_INVESTIGATOR

National Taiwan University Hospital

Locations

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National Taiwan University Hospital

Taipei, , Taiwan

Site Status RECRUITING

Countries

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Taiwan

Central Contacts

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Jin-Shing Chen

Role: CONTACT

8862-2312345670918

Rwei-Fen S.Huang

Role: CONTACT

8862-29052512

Facility Contacts

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Jin-Shing Chen

Role: primary

8862-23123456-70918

Other Identifiers

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201701123RINC

Identifier Type: -

Identifier Source: org_study_id

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