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The recent advances in the investigation of tumor
immunobiology have suggested that cancer chemotherapy, in
addition to its well known cytotoxic activity, may play
modulatory effects on the endogenous production of cytokines
involved in the control of both tumor angiogenesis and antitumor
immunity. Cancer chemotherapy constantly acts with inhibitory
effects on anti-bacterial, anti-viral and anti- mycotic immune
responses, whereas its action on anticancer immunity, which is
mainly mediated by lymphocytes, has still to be better
investigated and defined.
The present study was carried out to evaluate the influence
of chemotherapy on lymphocyte count and its relation to the
clinical response in cancer patients suffering from the most
commonly frequent tumor histotypes, including lung, colorectal,
breast and prostate carcinomas. The study included 144
consecutive metastatic solid tumor patients. Lung cancer
patients were treated with cisplatin plus gemcitabine,
colorectal cancer patients received oxaliplatin plus
5-fluorouracil, while those affected by breast cancer or
prostate carcinoma were treated with taxotere alone.
An objective tumor regression was achieved in 66 out of 144
(46 percent) patients, whereas the remaining 78 patients had
only a stable disease (SD)or a progressive disease.
Independently of tumor histotype and chemotherapeutic regimen, a
lymphocytosis occurred in patients who achieved an objective
tumor regression in response to chemotherapy, and lymphocyte
mean count observed at the end of the chemotherapeutic treatment
was significantly higher with respect to the values seen before
the onset of treatment.
On the contrary, lymphocyte mean number decreased on
chemotherapy in patients with SD or PD, even though the decline
was statistically significant with respect to the pretreatment
values in the only patients who had a PD in response to
chemotherapy.
This study would suggest that chemotherapy itself may
paradoxically act, at least in part, as a cancer immunotherapy
by inducing lymphocytosis, as well as previously demonstrated
for the only immunotherapy with IL-2, probably by modulating the
cytokine network and correcting the altered endogenous
production of cytokines, responsible for cancer-related
immunodeficiency.
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