The main MPN cancer types fall into two broad categories: Philadelphia chromosome–positive (chronic myeloid leukemia, CML) and Philadelphia chromosome–negative (polycythemia vera, essential thrombocythemia, and myelofibrosis). Each has distinct blood-cell overproduction patterns, clinical features, and standard treatment approaches.

Chronic myeloid leukemia (CML)

• What it is: A clonal disorder defined by the BCR::ABL1 fusion gene (Philadelphia chromosome, an abnormal gene that drives CML).
• Main cells affected: Overproduction of mature and immature white blood cell (neutrophils, basophils, eosinophils).
• Key feature: The presence of BCR::ABL1 is a diagnostic indicator. [1][3][4]

Polycythemia vera (PV)

• What it is: A Philadelphia-negative MPN most often associated with JAK2 mutations.
• Main cells affcted: Overproduction of red blood cells, with frequent elevations in white cells and platelets.
• Key features: High hemoglobin/hematocrit, aquagenic pruritus, risk of blood clots, and sometimes splenomegaly. [1]

Essential thrombocythemia (ET)

• What it is: An MPN defined by persistently elevated platelet counts, often associated with JAK2, CALR, or MPL mutations.
• Main cells affected: Platelets.
• Key features: The risk of both clotting and bleeding is common. Some people also report microvascular symptoms such as headache, erythromelalgia, or visual changes.”. [1]

Primary myelofibrosis (PMF)

• What it is: PMS is characterized by scarring in the marrow and abnormal blood production.
• Main cells involved: Variable; patients can present with anemia, leukocytosis, or thrombocytosis, which may later develop into marrow failure.
• Key features: Large spleen (splenomegaly), severe constitutional symptoms (fatigue, weight loss, night sweats), and risk of transformation to acute leukemia. [1][5]

Together, these MPN cancer types illustrate the heterogeneity of the group: from the highly targetable, mutation-defined CML to the symptom-driven Philadelphia-negative disorders, where risk of thrombosis, fibrosis, or leukemic transformation shapes management. [1]

Beyond the “classic” myeloproliferative neoplasms (MPNs), there is a smaller set of very rare MPN or MPN-adjacent disorders. They’re grouped together because the bone marrow produces too many myeloid cells, and the specific label depends on which blood cell line is predominantly expanded (for example, certain white blood cells).[3][5]

Chronic neutrophilic leukemia (CNL) is a BCR::ABL1–negative entity marked by persistent neutrophilia/leukocytosis with a hypercellular marrow and generally preserved neutrophil maturation; a key diagnostic clue is that CSF3R mutations are common and are part of modern diagnostic frameworks. [3]

Chronic eosinophilic leukemia (CEL) is the parallel concept on the eosinophil side—persistent eosinophilia that requires careful evaluation to confirm a clonal/myeloid-neoplasm process and to distinguish it from reactive causes. [3]

Because these conditions are uncommon and can mimic more benign explanations, workup typically relies on blood and bone marrow testing plus molecular studies to secure the right classification (including “MPN-unclassifiable” when features don’t cleanly fit a single category). [3][5]

MPNs are diagnosed by combining several sources of information, not by any single “positive/negative” test. Clinicians consider symptoms and exam findings, review persistent patterns on routine blood tests (like a CBC and blood smear), and—when needed—use a bone marrow aspirate/biopsy to see how blood cells are being produced and whether the marrow appearance fits an MPN framework. [1]

Genetic testing is often a central part of the workup because it helps support clonality and refine the subtype. Depending on the clinical picture, testing may include markers that distinguish specific entities (for example, BCR::ABL1 for CML) and common MPN “driver” mutations such as JAK2, CALR, and MPL. In certain situations, clinicians also evaluate additional molecular targets relevant to rarer MPN-adjacent disorders (e.g., CSF3R in CNL or PDGFRA/PDGFRB-rearranged eosinophilic neoplasms). [1]

Other labs may be added to clarify specific scenarios—for example, serum erythropoietin (EPO) can help interpret an erythrocytosis workup when PV is being considered. [1]

Ultimately, the final diagnosis still depends on the clinician, who integrates your history, exam, trends over time, bone marrow findings, and molecular/cytogenetic results—and rules out reactive causes or overlap conditions—before assigning the most appropriate subtype. [1]

Symptoms overlap across MPN cancer types, but certain patterns and risks tend to cluster within each subtype. Recognizing these helps prioritize tests and guide treatment.

General common symptoms of MPNs

Many MPNs are asymptomatic early and are picked up on a routine CBC; when symptoms occur, they commonly include fatigue, night sweats/weight loss, and spleen-related early satiety or abdominal fullness. [6][1]

Specific symptoms for each MPN

CML: Often asymptomatic; if symptomatic, fatigue and splenomegaly-related early satiety/fullness are typical. [6]

PV: Aquagenic pruritus, erythromelalgia, and “hyperviscosity-type” symptoms (headache/blurred vision) are common. [7][8]

ET: Vasomotor/microvascular symptoms (headache, dizziness, visual changes, paresthesias) and sometimes bruising/bleeding. [1]

PMF: Prominent constitutional symptoms plus early satiety/abdominal fullness; bone pain can occur. [1]

Rarer entities: CNL may present with fatigue, night sweats, weight loss and splenomegaly; eosinophilic neoplasms/CEL-spectrum may present with symptoms driven by tissue/organ involvement. [1]

General complications of MPNs

Across MPNs, clinicians monitor for thrombosis and bleeding, symptomatic splenomegaly, and disease progression/transformations over time. [9][10]

Specific complications for each MPN

CML: Risk of progression to advanced phases without effective therapy; TKIs have markedly improved long-term survival and disease control. [6][11]

PV: Arterial/venous thrombosis is a major complication; longer-term risks include evolution to myelofibrosis or acute leukemia. [7][12]

ET: Both thrombosis and bleeding; extreme thrombocytosis can increase bleeding risk via acquired von Willebrand syndrome. [1][13]

PMF: Progressive marrow failure–related problems (e.g., anemia/infections), portal-hypertension complications in some cases, and leukemic transformation risk. [10][14]

Rarer entities: CNL can be complicated by infections and transformation; eosinophilic neoplasms can cause organ damage from eosinophil infiltration (with prognosis and complications varying by subtype). [1]

Reminder for patient-facing accuracy: these symptom/complication patterns are helpful for orientation, but the final diagnosis and subtype assignment still depend on the clinician integrating labs, marrow findings, and molecular results in context. [1]

1. What are the main MPN cancer types?

Main types include polycythemia vera (PV), essential thrombocythemia (ET), myelofibrosis (MF, including PMF), and chronic myeloid leukemia (CML). PV/ET/MF are often described as BCR::ABL1–negative MPNs, while CML is BCR::ABL1–positive. Less common subtypes include chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia–NOS (CEL-NOS), and MPN, unclassifiable. [1][15]

2. How are these MPNs different from one another?

They differ by the main blood cell line affected (e.g., red cells in PV, platelets in ET, fibrosis in MF) and key molecular drivers (e.g., BCR::ABL1 in CML; JAK2 /CALR / MPL in many PV/ET/MF cases). These features support diagnosis and management decisions. [1]

3. What symptoms should patients watch for?

Symptoms vary, but may include fatigue, night sweats, headaches, itching (including after showering), burning/red hands or feet, easy bruising/bleeding, and abdominal fullness from an enlarged spleen. Some people have no symptoms and are diagnosed from abnormal blood counts. Seek urgent care for possible clot symptoms (e.g., chest pain, shortness of breath, one-sided leg swelling/pain) or significant bleeding. [4]

4. Can MPNs turn into leukemia?

In some patients, PV, ET, or MF can progress to a more aggressive phase, including acute myeloid leukemia (AML). Risk varies by subtype, molecular features, and prior treatments. Follow-up typically includes periodic blood tests and, when clinically indicated, bone marrow evaluation. [1][5]

MPN — Myeloproliferative neoplasm

MPNs — Myeloproliferative neoplasms

CML — Chronic myeloid leukemia

PV — Polycythemia vera

ET — Essential thrombocythemia

MF — Myelofibrosis

PMF — Primary myelofibrosis

BCR::ABL1 — BCR–ABL1 fusion gene (Philadelphia chromosome–associated)

JAK2 — Janus kinase 2

CALR — Calreticulin

MPL — Myeloproliferative leukemia virus oncogene (thrombopoietin receptor)

TKIs — Tyrosine kinase inhibitors

CNL — Chronic neutrophilic leukemia

CSF3R — Colony stimulating factor 3 receptor

CEL — Chronic eosinophilic leukemia

CEL-NOS — Chronic eosinophilic leukemia, not otherwise specified

PDGFRA — Platelet-derived growth factor receptor alpha

PDGFRB — Platelet-derived growth factor receptor beta

CBC — Complete blood count

EPO — Erythropoietin

AML — Acute myeloid leukemia

FAQs — Frequently asked question

1. Thapa, B., Fazal, S., Parsi, M., & Rogers, H. J. (2023). Myeloproliferative neoplasms. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK531464/
2. Leukaemia Foundation. (n.d.). Myeloproliferative neoplasms. Retrieved February 3, 2026, from https://www.leukaemia.org.au/blood-cancer/types-of-blood-cancer/myeloproliferative-neoplasms/
3. National Cancer Institute. (n.d.). Chronic myeloproliferative neoplasms treatment (PDQ®)–Patient version. Retrieved February 3, 2026, from https://www.cancer.gov/types/myeloproliferative/patient/chronic-treatment-pdq
4. National Cancer Institute. (n.d.). Chronic myeloid leukemia treatment (PDQ®)–Patient version. Retrieved February 3, 2026, from https://www.cancer.gov/types/leukemia/patient/cml-treatment-pdq
5. Anderson, L. A., & McMullin, M. F. (2014). Epidemiology of MPN: What do we know? Current Hematologic Malignancy Reports, 9, 340–349. https://doi.org/10.1007/s11899-014-0228-z
6. Eden, R. E., & Coviello, J. M. (2023). Chronic myelogenous leukemia. In StatPearls [Internet]. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK531459/
7. Siegel, F. P., Tauscher, J., & Petrides, P. E. (2013). Aquagenic pruritus in polycythemia vera: Characteristics and influence on quality of life in 441 patients. American Journal of Hematology, 88(8), 665–669. https://doi.org/10.1002/ajh.23474
8. Tefferi, A. (2023). Primary myelofibrosis: 2023 update on diagnosis, risk-stratification, and management. American Journal of Hematology, 98(5), 801–821. https://doi.org/10.1002/ajh.26857
9. Barbui, T., Ghirardi, A., Carobbio, A., De Stefano, V., Rambaldi, A., Tefferi, A., & Vannucchi, A. M. (2024). Thrombosis in myeloproliferative neoplasms: a viewpoint on its impact on myelofibrosis, mortality, and solid tumors. Blood cancer journal, 14(1), 188. https://doi.org/10.1038/s41408-024-01169-6
10. Mughal, T. I., Vaddi, K., Sarlis, N. J., & Verstovsek, S. (2014). Myelofibrosis-associated complications: pathogenesis, clinical manifestations, and effects on outcomes. International journal of general medicine, 7, 89–101. https://doi.org/10.2147/IJGM.S51800
11. Awada, H., Voso, M. T., Guglielmelli, P., & Gurnari, C. (2020). Essential Thrombocythemia and Acquired von Willebrand Syndrome: The Shadowlands between Thrombosis and Bleeding. Cancers, 12(7), 1746. https://doi.org/10.3390/cancers12071746
12. Cuthbert, D., & Stein, B. L. (2019). Polycythemia Vera-Associated Complications: Pathogenesis, Clinical Manifestations, And Effects On Outcomes. Journal of blood medicine, 10, 359–371. https://doi.org/10.2147/JBM.S189922
13. Awada, H., Voso, M. T., Guglielmelli, P., & Gurnari, C. (2020). Essential Thrombocythemia and Acquired von Willebrand Syndrome: The Shadowlands between Thrombosis and Bleeding. Cancers, 12(7), 1746. https://doi.org/10.3390/cancers12071746
14. Tefferi A. (2023). Primary myelofibrosis: 2023 update on diagnosis, risk-stratification, and management. American journal of hematology, 98(5), 801–821. https://doi.org/10.1002/ajh.26857
15. Barbui, T., Thiele, J., Gisslinger, H., Kvasnicka, H. M., Vannucchi, A. M., Guglielmelli, P., Orazi, A., & Tefferi, A. (2018). The 2016 WHO classification and diagnostic criteria for myeloproliferative neoplasms: document summary and in-depth discussion. Blood cancer journal, 8(2), 15. https://doi.org/10.1038/s41408-018-0054-y