Induction of thrombocytosis and leukocytosis by tumour is a part of complex propagative strategy of malignancy. Activated leukocytes and thrombocytes produce several cytokines and enzymes that are crucial for tumour growth, invasion and dissemination. Therefore, leukocytosis and thrombocytosis might be a negative prognostic factor in malignancies.
Thrombocyte and leukocyte count were determined before the beginning of treatment. Patients with recent bleeding, elevated CRP or treated with best-supportive care were excluded. Relationship between thrombocytosis, leukocytosis and known negative prognostic factors was assessed. The impact of thrombocytosis and leukocytosis on progression-free survival (PFS) was determined. Chi- squared test, Kaplan- Meier and Cox- regression statistical analysis were used.
500 patients with breast cancer (BC), ovarian cancer (OC), colorectal cancer (CrC), head and neck tumours (H&N) or lung cancer (LC) were included to our retrospective study. Thrombocytosis was more frequent in patients with metastatic cancer (whole population of patients) (17.4%, 95%CI :8.1125-26.7381, p = 0.0001); in patients with CrC (27%, 95% CI: 4.1554-47.9434, p = 0.0111); in patients with OC (27.7%, 95%CI: 6.5334- 46.4296, p = 0.0063) and in patients with H&N (46.9%, 95%CI: -9.5975-72.7755, p = 0.0459). Grading, estrogen- receptor (ER) progesteron- receptor (PR) and her2 status had no impact on frequency of thrombocytosis. Thrombocytosis had no impact on PFS. Leukocytosis was more frequent among patients with metastatic malignancies (10.6 %, 95%CI: 1.4352- 19.9713, p = 0.0174). This result reflected only in the subgroup of patients with H&N (46.9%, 95%CI: -9.5975- 72.7755, p = 0.0459). Grading, PR and her2 status had no impact on frequency of leukocytosis. Leukocytosis was more frequent in BC patients with negative ER status (18.7%, 95%CI: 1.0068- 40.1859, p = 0.0158). Leukocytosis shortened PFS in patients with LC (hazard ratio 2.1126, 95%CI:1.2712- 3.5109, p = 0.0014).
Leukocytosis might be a negative prognostic factor in patients with LC. More studies are needed to identify the subpopulation of leukocytes responsible for this effect.
Clinical trial identification
Legal entity responsible for the study
Faculty Hospital Trencin, Department of Oncology.
Has not received any funding.
All authors have declared no conflicts of interest.