Letter to the Editor: No immunophenotyping in peripheral blood of prostate cancer patients treated with neoadjuvant Ritu
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Journal of Translational Medicine Open Access
LETTER TO THE EDITOR
Letter to the Editor: No immunophenotyping in peripheral blood of prostate cancer patients treated with neoadjuvant Rituximab? Paulius Bosas1, Gintaras Zaleskis2* , Vita Pasukoniene2,3 and Feliksas Jankevicius1
Dear Editor, The paper by Ryan et al. [1] in your recent issue addresses intriguing data on Rituximab (Rx) immunomodulation in prostate cancer (PCa) neoadjuvant setting. The report on the first 8 participants from author’s trial (NCT01804712) is appreciated since the complexity of similar studies quite often results in a termination or withdrawal. However, we would like to point out some downsides in the above-mentioned publication. The cornerstone statement that “…high B cell density is associated with biochemical failure” refers to the author’s own previous publication [2]. However, this reference has nothing to do with biochemical failure. Even the higher density of B cells in recurrent tumors cannot be considered a surrogate parameter of biochemical failure. Growing tumors can passively induce recruitment of immune cells into the prostate microenvironment as a result of concomitant inflammation [3]. The relationship between tumor infiltrating cells and clinical outcomes for PCa is still debatable. The authors concluded that Rx treatment applied prior to prostatectomy reduced tumor infiltration density of B and T-cells. However, Rx is well known to specifically deplete a T cell subset which also co-express CD20+ [4, 5]. As a matter of fact, the double positive CD20+CD3+ lymphocyte was demonstrated This comment refers to the article available at https://doi.org/10.1186/s1296 7-020-02370-4. *Correspondence: [email protected] 2 Laboratory of Immunology, National Cancer Institute, P. Baublio 3b, Vilnius, Lithuania Full list of author information is available at the end of the article
to be a specific marker of therapeutic response in rheumatoid arthritis patients receiving Rx [5]. Isn’t it possible that similar mechanisms were involved in PCa patients treated with Rx? The statement that there was a demonstration of “the inter-dependence between B and T-cells in prostate cancer…” is also questionable since the authors do not provide any evidence of double positive CD20+CD3+ lymphocyte absence in tumorous tissue. One can notice that CD20+ B cell and CD 3+ T cell infiltration scores in tumor tissue provided in Tables 2 and 3 of the paper are almost identical. This raises the question if an alternative explanation of the phenomenon might also be valid. Could it be that some specific B cell phenotype conversions or infiltration patterns were induced by Rx treatment? Unexpectedly, the peripheral blood T and B subset monitoring were not reported in this paper, although the peripheral blood B cell enumeration was originally planned as a secondary outcome measure (NCT01804712). Four out of 8 patients (Fig. 3) exhibited PSA rise while being on Rx treatment for only 29 days (one patient displayed a steep 40% PSA increase). We would suggest
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