Proceedings of the Texas A&M Medical Student Grand Rounds

Targeting CSF-1/CSF-1R to Decrease Metastasis and Inflammation in Gastric Cancer

July 27, 2021 Megh Gore

Megh Gore

Introduction. Gastric cancer, the fifth most common cancer in the world and the third most common cause of cancer-related deaths, is often diagnosed in later stages leading to increased morbidity and mortality.1 Factors such as H. pylori, smoking, alcohol, and genetics play a role in the increase incidence and poor prognosis of gastric cancer.1 A factor of this poor prognosis is the increase in number of tumor associated macrophages (TAMs), due to increased prolonged levels of H. pylori, lactate, and Colony Stimulating Factor-1 (CSF-1).1,2 An increase in levels of M2 TAMs lead to increased angiogenesis, tumor growth, and metastasis.1,3 By identifying increased levels of and inhibiting the CSF-1/CSF-1R axis, it may be possible to improve gastric cancer outcomes. Methods. Immunohistochemical studies were done on 148 tissue samples collected during surgery on gastric cancer patients using avidin-biotin-peroxidase methods, primary antibodies, and goat polyclonal antibodies against CSF-1.4 Samples were also analyzed using PCR after reverse transcription analysis to measure CSF-1 and CSF-1R levels in the tissue samples.4 Patients were then sorted into high and low categories for both CSF-1 and CSF-1R and their 5-year survival was measured at 10-month intervals.4 In a phase Ia/b study, patients with solid tumors were treated with Emactuzumab, a monoclonal antibody to CSF-1R, either as a monotherapy or in combination with paclitaxel.5 Optimal biological dose as well as biopsies to detect tumor progression and M2 macrophage levels were taken before and during treatment.5 Results. Immunohistochemical analysis shows an increased level of both CSF-1 and CSF-1R in gastric cancer tissues.4 Patients who were classified to have high expression of CSF-1 or CSF-1R were found to have increased mortality over five years in comparison to those in the low expression groups.4 Patients treated with the monoclonal antibody showed no maximum tolerated dose and no antitumor activity as a monotherapy or in combination with paclitaxel.5 Treatment with Emactuzumab showed a decrease in M2 TAMs. Conclusions. The CSF-1/CSF-1R axis is elevated in gastric cancer tissues, signaling an important association. While a monoclonal antibody to CSF-1R did not decrease tumor size or inhibit cancer growth, the decrease in M2 macrophage numbers shows a promising avenue for an adjunct cancer therapy. Additionally, the relationship between elevated CSF-1 and gastric cancer may be able to serve as an important clinical tool, helping with early diagnosis.

  1.  Vinasco K, Mitchell HM, Kaakoush NO, Castaño-Rodríguez N. Microbial carcinogenesis: Lactic acid bacteria in gastric cancer. Biochim Biophys Acta Rev Cancer. 2019;1872(2):188309. doi:10.1016/j.bbcan.2019.07.004
  2. Gambardella V, Castillo J, Tarazona N, et al. The role of tumor-associated macrophages in gastric cancer development and their potential as a therapeutic target. Cancer Treat Rev. 2020;86:102015. doi:10.1016/j.ctrv.2020.102015
  3. Yin S, Huang J, Li Z, et al. The Prognostic and Clinicopathological Significance of Tumor-Associated Macrophages in Patients with Gastric Cancer: A Meta-Analysis. PLoS One. 2017;12(1):e0170042. Published 2017 Jan 12. doi:10.1371/journal.pone.0170042
  4. Okugawa Y, Toiyama Y, Ichikawa T, et al. Colony-stimulating factor-1 and colony-stimulating factor-1 receptor co-expression is associated with disease progression in gastric cancer. Int J Oncol. 2018;53(2):737-749. doi:10.3892/ijo.2018.4406
  5. Gomez-Roca CA, Italiano A, Le Tourneau C, et al. Phase I study of emactuzumab single agent or in combination with paclitaxel in patients with advanced/metastatic solid tumors reveals depletion of immunosuppressive M2-like macrophages. Ann Oncol. 2019;30(8):1381-1392. doi:10.1093/annonc/mdz163

 

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