Extreme thrombocytosis associated with malignancy

Spigel, Stuart C.; Mooney, Lewis R.

doi:10.1002/1097-0142(197701)39:1<339::aid-cncr2820390150>3.0.co;2-t

Cited by 21 publications

(7 citation statements)

References 9 publications

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“…The results suggest that thrombocytosis is a marker of advanced disease and may be the result of substances produced by the larger tumour load. In a few other reports, thrombocytosis has remitted following definitive radiotherapy, chemotherapy or surgical resection of the primary lesion [27].…”

Section: Discussionmentioning

confidence: 98%

Prognostic significance of thrombocytosis in patients with primary lung cancer

Pedersen

Milman²

1996

Eur Respir J

190

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In patients with malignancies, thrombocytosis has previously been related to disease stage, histological type, and survival. In the present study, the prevalence of thrombocytosis and the prognostic information provided by platelet counts were analysed in a large cohort of patients with primary lung cancer. At the time of diagnosis, pretreatment platelet counts were retrospectively recorded in 1,115 consecutive patients with histologically proven primary lung cancer. All patients were reviewed regarding histological type, tumour, node, metastasis (TNM) classification stage and survival. The prevalence of thrombocytosis in patients with lung cancer was compared with that in a series of 550 consecutive out-patients with benign lung disorders. In 269 surgically resected patients, postoperative platelet counts were recorded 1-3 months after resection of the tumour. In the follow-up period, thromboembolic episodes diagnosed either clinically or at autopsy were recorded. The overall prevalence of thrombocytosis (> 400 x 10(9) platelets.L-1) in the patients with lung cancer was 32%. The frequency of thrombocytosis was significantly higher compared with the control subjects (32 vs 6%; p < 0.0001). Platelet counts differed significantly among subgroups defined by the TNM classification, with the proportion of patients with > 400 x 10(9) platelets.L-1 greatest in the more advanced TNM stages (stage I and II 23% vs stage III and IV 37%; p < 0.0001). Patients with thrombocytosis had a significantly poorer survival than patients with normal platelet counts (p < 0.0001). In a multivariate survival analysis (Cox model), thrombocytosis continued to correlate strongly with poor survival even when adjusted for histological type, sex, age, and TNM stage (p < 0.001). In surgically resected patients, the frequency of preoperative and postoperative thrombocytosis differed significantly (23.0 vs 8.9%; p < 0.0001). Survival rate was significantly reduced in patients with preoperative thrombocytosis (p = 0.005). Thrombocytosis was not associated with an increased incidence of thromboembolism. In conclusion, thrombocytosis is an independent prognostic factor of survival in patients with primary lung cancer. We suggest that platelet counts should be included in future multivariate analyses of survival in patients with lung cancer.

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Section: Discussionmentioning

confidence: 98%

Prognostic significance of thrombocytosis in patients with primary lung cancer

Pedersen

Milman²

1996

Eur Respir J

190

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“…These features exist in patients with neoplasia and suggest increased humoral stimulation of thrombocytopoiesis in malignancy (37,38). Increased thrombocytopoietic activity has been observed in the serum of patients with malignancy (39) and platelet counts have been observed to fall following treatmentinduced regression of malignancy (5). Interestingly, several factors known to stimulate thrombocytopoiesis are known to also stimulate proliferation of other marrow cell lines (10,19) and fibrinogen synthesis (40--42).…”

Section: Discussionmentioning

confidence: 99%

The Platelet Count in Carcinoma of the Lung and Colon

Costantini

Zacharski

Möritz³

et al. 1990

Thromb Haemost

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SummaryPlatelet counts were evaluated in 714 patients with advanced non-small cell lung cancer (N-SCLC), small cell carcinoma of the lung (SCCL), and colon cancer entered to a clinical trial. Patients had not received prior chemotherapy. Platelet counts were not different in patients who had received radiation therapy prior to entry to the study. In comparison to the other tumor types, patients with N-SCLC demonstrated an increased prevalence of thrombocytosis (counts greater than 400,000/mm3), higher platelet counts at the time of entry to the study, higher over all mean platelet counts, relative preservation of high platelet levels during disease progression, and no relationship between platelet numbers and the amount of chemotherapy given. By contrast, platelet counts in patients with SCCL were negatively correlated with the absolute amount of cyclophosphamide and adriamycin given, and declined most dramatically with disease progression and death. Platelet numbers did not correlate with fibrinopep-tide A or fibrin split product levels suggesting that disseminated intravascular coagulation or fibrinolysis may have had less influence on platelet numbers than certain other factors. By contrast, significant correlations were found for all three tumor types between platelet numbers and other indicators of bone marrow function including anemia, total leukocyte count, and absolute neutrophil count; and the fibrinogen level. Based upon these findings, we postulate that the host response to malignancy, possibly in the form of production of bone marrow-stimulating cytokines, may play a prominent role in regulation of platelet counts in these (and perhaps other) neoplasms, and that a particularly prominent and persistent degree of marrow stimulation exists in patients with N-SCLC.

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“…Indeed, blood platelet numbers (platelet count) have been reported to have predictive value in various cancers. High platelet count is associated with poor survival in a large variety of cancers including malignant mesothelioma, gynaecological malignancies, lung, renal, gastric, colorectal and breast cancers ( Spigel & Mooney, 1977 ; Nakano et al ., 1986 ; Olesen & Thorshauge, 1988 ; Costantini et al ., 1990 ; Hernandez et al ., 1992 ; Lopes et al ., 1994 ; Zeimet et al ., 1994 ; Pedersen & Milman, 1996 ; 1998 ; Menczer et al ., 1998 ; Hefler et al ., 2000 ; Kerpsack & Finan, 2000 ; Ikeda et al ., 2002 ; O'Keefe et al ., 2002 ; Taucher et al ., 2003 ; Bozkurt et al ., 2004 ). The scope of this mini review is limited to the interactions between platelets and cancer cells deriving from solid, but not blood‐borne, tumours.…”

Section: Introductionmentioning

confidence: 99%

Platelet–cancer interactions: mechanisms and pharmacology of tumour cell‐induced platelet aggregation

Jurasz

Alonso-Escolano

Radomski

2004

British J Pharmacology

305

222

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During haematogenous metastasis, cancer cells migrate to the vasculature and interact with platelets resulting in tumour cell-induced platelet aggregation (TCIPA). We review: 1 The biological and clinical significance of TCIPA; 2 Molecular mechanisms involved in platelet aggregation by cancer cells; 3 Strategies for pharmacological regulation of these interactions. We conclude that pharmacological regulation of platelet-cancer cell interactions may reduce the impact of TCIPA on cancer biology.

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Extreme thrombocytosis associated with malignancy

Cited by 21 publications

References 9 publications

Prognostic significance of thrombocytosis in patients with primary lung cancer

Prognostic significance of thrombocytosis in patients with primary lung cancer

The Platelet Count in Carcinoma of the Lung and Colon

Platelet–cancer interactions: mechanisms and pharmacology of tumour cell‐induced platelet aggregation

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