Prevalence of factor V Leiden, FII G20210A, FXIII Val34Leu and MTHFR C677T polymorphisms in cancer patients with and without venous thrombosis

Ramacciotti, Eduardo; Wolosker, Nelson; Puech-Leão, Pedro; Zeratti, Eduardo Antônio; Gusson, Paula Regina; Giglio, Auro del; Franco, Rendrik F.

doi:10.1016/s0049-3848(03)00179-8

Cited by 47 publications

(34 citation statements)

References 14 publications

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“…We found no association between the risk for thrombosis and known risk factors for venous thrombosis, nor with elevated levels of factor VIII, IX or XI. This is consistent with our previous data [17] and data from Ramacciotti and colleagues [18], who also did not find an association between gene polymorphisms tested, i.e., Factor V Leiden, factor II G20210A, factor XIII val 34leu and Methylene tetrahydrofolate reductase (MTHFR) C677T, and the risk of venous thrombosis in cancer patients. In agreement with these findings, Riordan and colleagues [19] found a low prevalence of factor V Leiden gene mutation in 28 cancer patients with catheter-related venous thrombosis.…”

Section: Discussionsupporting

confidence: 93%

Risk factors for catheter-related thrombosis in cancer patients

Tesselaar¹,

Ouwerkerk²,

Nooy³

et al. 2004

European Journal of Cancer

108

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We investigated the risk factors for venous thrombosis in cancer patients with implantable ports undergoing chemotherapy. One hundred and seventy one ports were placed in a central (''chest ports'') and 84 in a peripheral vein (''arm ports''), 181 received prophylactic nadroparin and 10 coumarin. Clinically overt thrombosis was confirmed by ultrasound or angiography. Catheter-related thrombosis incidence without anticoagulants was 28% in arm and 33% in chest ports, but with anticoagulants this was 32% in arm and only 1% in chest ports (odds ratio (OR) 34.8 95% confidence interval (CI) 7.3-165). Left-sided placement compared with rightsided and catheter tip position in the superior vena cava compared with right atrium were associated with a 3.5 respectively 2.6-fold increased risk. Thrombosis was associated with elevated homocysteine levels (OR = 3.8, 95% CI 1.3-11.3), but not with factor V Leiden or prothrombin 20210A gene mutations, or high concentration of factor VIII, IX or XI. Prophylaxis with anticoagulants is recommended for chest, but not for arm ports. Determination of plasma homocysteine levels may identify patients at an increased risk for thrombosis.

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Section: Discussionsupporting

confidence: 93%

Risk factors for catheter-related thrombosis in cancer patients

Tesselaar¹,

Ouwerkerk²,

Nooy³

et al. 2004

European Journal of Cancer

108

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“…Previously, few studies had investigated the role of FVL in cancer-related VTE. Initial results from small cancer cohorts, including 75-353 patients, reported either no 40,41 or a 2-to 4.4-fold higher risk 24,42 of VTE in cancer patients with FVL compared to those without the FVL mutation. In a large population-based VTE case-control study with cancer diagnoses registered during 5 years prior to the inclusion date, Blom and colleagues found a 2.4-fold and 12-fold higher VTE risk in individuals with FVL and cancer compared to those with cancer without the mutation, and those without cancer and the mutation, respectively.…”

Section: Discussionmentioning

confidence: 99%

Joint effects of cancer and variants in the factor 5 gene on the risk of venous thromboembolism

et al. 2016

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“…Factor V Leiden—a genetic variant that is resistant to inactivation by activated protein C—confers an increased risk of VTE with an odds ratio of 3.49 in the healthy population 31. While some studies suggest a two‐ to five‐fold increased risk of VTE in cancer patients with Factor V Leiden,32, 33, 34 other cohort studies were unable to confirm this association 35, 36, 37. Similarly, polymorphisms in other coagulation‐related genes, such as FII G20210A, FIII ‐603A/G, FIII +5466A>G, FXIII Val34Leu, and methylenetetrahydrofolate reductase C667T, showed no effect on VTE incidence in patients with and without cancer 34, 35, 36, 38, 39.…”

Section: Host‐specific Geneticsmentioning

confidence: 99%

“…While some studies suggest a two‐ to five‐fold increased risk of VTE in cancer patients with Factor V Leiden,32, 33, 34 other cohort studies were unable to confirm this association 35, 36, 37. Similarly, polymorphisms in other coagulation‐related genes, such as FII G20210A, FIII ‐603A/G, FIII +5466A>G, FXIII Val34Leu, and methylenetetrahydrofolate reductase C667T, showed no effect on VTE incidence in patients with and without cancer 34, 35, 36, 38, 39. Altogether, these studies suggest that host‐specific mutations and SNPs in coagulation factors are not main contributors of VTE in cancer patients, and therefore should not be considered as potential biomarkers.…”

Section: Host‐specific Geneticsmentioning

confidence: 99%

Cancer‐associated thrombosis: The search for the holy grail continues

Ünlü

Versteeg

2018

Research and Practice in Thrombosis and Haemostasis

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Cancer patients have an increased risk of developing venous thromboembolism (VTE), a condition that is associated with increased morbidity and mortality. Although risk assessment tools have been developed, it is still very challenging to predict which cancer patients will suffer from VTE. The scope of this review is to summarize and discuss studies focusing on the link between genetic alterations and risk of cancer‐associated thrombosis (CAT). Thus far, classical risk factors that contribute to VTE have been tried as risk factors of CAT, with low success. In support, hypercoagulant plasma profiles in patients with CAT differ from those with only VTE, indicating other risk factors that contribute to VTE in cancer. As germline mutations do not significantly contribute to elevated risk of VTE, somatic mutations in tumors may significantly associate with and contribute to CAT. As it is very time‐consuming to investigate each and every mutation, an unbiased approach is warranted. In this light we discuss our own recent unbiased proof‐of‐principle study using RNA sequencing in isolated colorectal cancer cells. Our work has uncovered candidate genes that associate with VTE in colorectal cancer, and these gene profiles associated with VTE more significantly than classical parameters such as platelet counts, D‐dimer, and P‐selectin levels. Genes associated with VTE could be linked to pathways being involved in coagulation, inflammation and methionine degradation. We conclude that tumor cell‐specific gene expression profiles and/or mutational status has superior potential as predictors of VTE in cancer patients.

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Prevalence of factor V Leiden, FII G20210A, FXIII Val34Leu and MTHFR C677T polymorphisms in cancer patients with and without venous thrombosis

Cited by 47 publications

References 14 publications

Risk factors for catheter-related thrombosis in cancer patients

Risk factors for catheter-related thrombosis in cancer patients

Joint effects of cancer and variants in the factor 5 gene on the risk of venous thromboembolism

Cancer‐associated thrombosis: The search for the holy grail continues

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