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Anticancer Immunotherapy by MFAP5 Blockade Inhibits Fibrosis and Enhances Chemosensitivity in Ovarian and Pancreatic

Tsz-Lun Yeung1, Cecilia S Leung1,2, Kay-Pong Yip3

  • 1Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|July 24, 2019
PubMed
Abstract

Insights

Targeting microfibril-associated protein 5 (MFAP5) with a novel antibody suppressed tumor growth by reducing fibrosis and normalizing blood vessels. This approach enhanced chemotherapy effectiveness in ovarian and pancreatic cancer models.

Area of Science:

  • Oncology
  • Immunology
  • Biochemistry

Background:

  • The tumor microenvironment significantly influences cancer progression.
  • Strategies to counteract microenvironment-driven malignant phenotypes require further exploration.

Purpose of the Study:

  • To evaluate the therapeutic potential of a new monoclonal antibody (mAb) targeting microfibril-associated protein 5 (MFAP5).
  • To assess the efficacy of anti-MFAP5 therapy in ovarian and pancreatic cancer models.

Main Methods:

  • Development of MFAP5-specific monoclonal antibodies using hybridoma technology.
  • Kinetic analysis, epitope mapping, and in vitro functional assays.
  • In vivo evaluation of anti-MFAP5 antibody clone 130A in ovarian and pancreatic tumor-bearing mice.

Main Results:

  • Selected antibody clone 130A demonstrated high affinity and specificity for MFAP5.
  • Clone 130A reduced MFAP5-induced collagen production by cancer-associated fibroblasts (CAFs).
  • The antibody suppressed intratumoral microvessel leakiness and improved paclitaxel bioavailability.

Conclusions:

  • MFAP5 blockade via immunotherapy inhibits fibrosis and normalizes tumor vasculature.
  • This approach enhances chemosensitivity in ovarian and pancreatic cancers.
  • Anti-MFAP5 antibodies represent a potential novel therapeutic strategy.

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