RecruitingNCT06393140

The Study on the Mechanism of Radiotherapy-elicited Immune Response


Sponsor

Fudan University

Enrollment

200 participants

Start Date

Jul 1, 2022

Study Type

OBSERVATIONAL

Conditions

Summary

Radiotherapy plays an important role in multidisciplinary treatment of esophageal cancer. Data from many laboratories indicate that local radiation produces systemic, immune-mediated anti¬tumour and, potentially, antimetastatic effects. Additionally, the combination of local radiotherapy and immune-modulation can augment local tumour control and cause distant (abscopal) antitumour effects through increased tumour-antigen release and antigen-presenting cell (APC) cross-presentation, improved dendritic-cell (DC) function, and enhanced T cell priming. The generation of an effective antitumor immune response requires the presentation of tumor antigens to naïve CD8+ cells in tumor-draining lymph nodes (TDLN) . Tumor-draining lymph nodes, however, are often subject to the immunosuppressive activity of tumor-derived factors, such as cytokines and other bioactive molecules from tumor cells and their associated leukocytes in the primary tumor site that contribute to the overriding of effective rejection mechanisms. Thus, in TDLN a T cell tolerance rather than a T cell activation often occurs, thereby preventing immune attack and facilitating local tumor progression.


Eligibility

Min Age: 18 Years

Inclusion Criteria4

  • new diagnosis locoregional esophageal cancer;
  • pathologic diagnosis is squamous carcinoma;
  • Patients had received either neoadjuvant or definitive radiotherapy
  • tumor and lymph node tissue can be collected and can be conducted with single cell RNA (scRNA)-sequencing and other sequencings.

Exclusion Criteria3

  • Pregnant or lactating women.
  • Unable or rejection to receive radiotherapy or unable to comply with study requirements or follow-up schedule.
  • Inability to provide informed consent.

Locations(1)

Fudan University Shanghai cancer center

Shanghai, China

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NCT06393140


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