Chronic myeloproliferative neoplasms and subsequent cancer risk: a Danish population-based cohort study

Frederiksen, Henrik; Farkas, Dóra Körmendiné; Christiansen, Christian Fynbo; Hasselbalch, Hans Carl; Sørensen, Henrik Toft

doi:10.1182/blood-2011-04-348755

Cited by 152 publications

(175 citation statements)

References 26 publications

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“…Accordingly, myelofibrosis may be featured by clinical, biochemical, and molecular evidence of an aberrant and dysfunctional immune system, 4,48-51 implying a potential risk of autoimmune/autoinflammatory diseases and, in addition, an increased risk of second cancer. 4,52,53 Several observations are supportive for this hypothesis. First, several studies have shown that inflammatory diseases may precede or develop during the course of ET, PV, and myelofibrosis.…”

Section: Does Chronic Inflammation Trigger Clonal Evolution Autoimmusupporting

confidence: 60%

Perspectives on chronic inflammation in essential thrombocythemia, polycythemia vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and development of accelerated atherosclerosis and second cancer?

Hasselbalch

2012

Blood

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279

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The morbidity and mortality of patients with the chronic Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia, polycythemia vera, and primary myelofibrosis are mainly caused by cardiovascular diseases, thrombohemorrhagic complications, and bone marrow failure because of myelofibrosis and leukemic transformation. In the general population, chronic inflammation is considered of major importance for the development of atherosclerosis and cancer. MPNs are characterized by a state of chronic inflammation, which is proposed to be the common denominator for the development of "premature atherosclerosis," clonal evolution, and second cancer in patients with MPNs. Chronic inflammation may both initiate clonal evolution and catalyze its expansion from early disease stage to the myelofibrotic burnt-out phase. Furthermore, chronic inflammation may also add to the severity of cardiovascular disease burden by accelerating the development of atherosclerosis, which is well described and recognized in other chronic inflammatory diseases. A link between chronic inflammation, atherosclerosis, and second cancer in MPNs favors early intervention at the time of diagnosis (statins and interferon-␣2), the aims being to dampen chronic inflammation and clonal evolution and thereby also diminish concurrent diseasemediated chronic inflammation and its consequences (accelerated atherosclerosis and second cancer).

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Section: Does Chronic Inflammation Trigger Clonal Evolution Autoimmusupporting

confidence: 60%

Perspectives on chronic inflammation in essential thrombocythemia, polycythemia vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and development of accelerated atherosclerosis and second cancer?

Hasselbalch

2012

Blood

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279

301

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“…In the background, more frequent occurrence of nonhematological malignancies was revealed to be responsible for this adverse survival in our classic MPN cohort. BCR-ABL1 chromosome-negative and positive MPN patients were previously described to present with an increased risk of developing a subsequent nonhematologic cancer (33). According to the general assumption, these subsequent nonhematologic tumors were simply attributed to the application of myelosuppressive regimens.…”

Section: Discussionmentioning

confidence: 99%

Co-occurrence of Myeloproliferative Neoplasms and Solid Tumors Is Attributed to a Synergism Between Cytoreductive Therapy and the Common TERT Polymorphism rs2736100

Krähling

Balassa

Kiss

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: The germline telomerase reverse transcriptase (TERT) rs2736100_C variant was identified as a susceptibility factor for a variety of solid tumors and recently for myeloproliferative neoplasms (MPN).Methods: LightCycler melting curve analysis was applied to detect risk alleles of TERT rs2736100_C and Janus kinase 2 (JAK2) rs12343867_C tagging 46/1 haplotype in 584 BCR-ABL1-negative MPN, 308 acute, and 86 chronic myeloid leukemia (AML and CML) patients and 400 healthy individuals.Results: TERT rs2736100_C showed an increased allele frequency in BCR-ABL1-negative MPN patients compared with controls (62.7%AE2.8% vs. 48.8%AE3.5%, P < 0.0001) regardless of molecular background or disease type, but not in CML or AML. Combined TERT and JAK2 hetero-or homozygosity conferred even higher risk for classic MPN. Common complications (throm-

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“…In Passamonti study, age > 65 years was determined to be a risk factor for developing SPM including leukemia [32] . A Danish study demonstrated that the probability of non hematologic and hematologic malignancies was higher in younger patients (2049 years vs 5069 and > 70 years) [13] . Such conflicting results may be accounted by the differences in the characteristics of patients and other risk factors for SPM in different studies.…”

Section: Discussionmentioning

confidence: 99%

“…The log rank test was statistically significant with a P-value of < 0.01. [13] . Another retrospective study from Italy (n = 331) showed cumulative incidence of SPM of 13% from the time of diagnosis of ET [17] .…”

Section: Discussionmentioning

confidence: 99%

“…The probability of transformation to leukemia is 1%5% during the first decade but increases significantly in the subsequent decades [2,6] . Additionally, patients with ET may also develop lymphoid malignancies such as nonHodgkin's lymphoma (NHL) and solid organ malignancies [13,14] . The treatment with cytotoxic chemotherapy decreases the incidence of thrombohemorrhagic events but may increase the risk of hematological SPM [2] .…”

Section: Introductionmentioning

confidence: 99%

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Risk of second primary malignancies in a population-based study of adult patients with essential thrombocythemia

Shrestha¹,

Giri²,

Pathak³

et al. 2016

WJCO

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AIM:To determine the risk of second primary malignancy (SPM) and survival of patients with essential thrombocythemia (ET). METHODS:We identified all patients with ET diagnosed during 2001 to 2011 from the Surveillance, Epidemiology and End Results (SEER) 18 database. Actuarial and relative survival methods were used to calculate the survival statistics. We utilized the SEER 13 database to calculate SPM. We used multiple primary standardized incidence ratio (SIR) session of the SEER*Stat software (version 8.1.5) to calculate SIR and excess risk of SPM for ET patients. RESULTS:Age standardized five-year cause-specific survival was greater for patients < 50 years vs those ≥ 50 years (99.4% vs 93.5%, P < 0.01). Five-year cause- Shrestha R, Giri S, Pathak R, Bhatt VR. Risk of second primary malignancies in a population-based study of adult patients with essential thrombocythemia. World J Clin Oncol

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Chronic myeloproliferative neoplasms and subsequent cancer risk: a Danish population-based cohort study

Cited by 152 publications

References 26 publications

Perspectives on chronic inflammation in essential thrombocythemia, polycythemia vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and development of accelerated atherosclerosis and second cancer?

Perspectives on chronic inflammation in essential thrombocythemia, polycythemia vera, and myelofibrosis: is chronic inflammation a trigger and driver of clonal evolution and development of accelerated atherosclerosis and second cancer?

Co-occurrence of Myeloproliferative Neoplasms and Solid Tumors Is Attributed to a Synergism Between Cytoreductive Therapy and the Common TERT Polymorphism rs2736100

Risk of second primary malignancies in a population-based study of adult patients with essential thrombocythemia

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