Epidemiology and Etiology of AML
(2021) In Hematologic Malignancies p.1-22- Abstract
Acute myeloid leukemia (AML) is a grave disease with an incidence of 4 per 100,000 a year. It can present in all ages, but the median age is 70 years. One-third of such patients have secondary AML, that is, AML following chemoradiotherapy or a transformation from previous myelodysplastic syndrome (MDS) or myeloproliferative neoplasia. A combination of genetic, epigenetic, and environmental factors may be responsible for the development of most cases of AML. The pathogenesis of AML is characterized by the serial acquisition of somatic mutations and several genes are recurrently mutated in AML. Exposures to benzene, cigarette smoking, pesticides, embalming fluids, accidental or professional ionization radiation, therapeutic radiotherapy,... (More)
Acute myeloid leukemia (AML) is a grave disease with an incidence of 4 per 100,000 a year. It can present in all ages, but the median age is 70 years. One-third of such patients have secondary AML, that is, AML following chemoradiotherapy or a transformation from previous myelodysplastic syndrome (MDS) or myeloproliferative neoplasia. A combination of genetic, epigenetic, and environmental factors may be responsible for the development of most cases of AML. The pathogenesis of AML is characterized by the serial acquisition of somatic mutations and several genes are recurrently mutated in AML. Exposures to benzene, cigarette smoking, pesticides, embalming fluids, accidental or professional ionization radiation, therapeutic radiotherapy, and radioactive I-131 therapy can cause AML with or without a preceding MDS phase. Alkylating agents (e.g., melphalan, cyclophosphamide), topoisomerase-II inhibitors (e.g., etoposide, doxorubicin), and other drugs (e.g., azathioprine) are described to be associated with the development of therapy-related AML (t-AML). Furthermore, about 5–15% of adults and 4–13% of pediatric patients with MDS or AML carry germline pathogenic variants in cancer susceptibility genes. Individuals with clonal hematopoiesis (CHIP) progress to AML at a rate of about 1% per year. Higher age of onset, obesity, previous autoimmune disease, and antecedent MDS or MPN are associated with a risk for developing AML.
(Less)
- author
- Juliusson, Gunnar LU ; Lazarevic, Vladimir LU and Lehmann, Sören
- organization
- publishing date
- 2021
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- keywords
- Benzene, Diagnosis, Exposure, Hereditary conditions, Incidence, Mutations, Prevalence, Secondary AML, Sex, Survival, t-AML
- host publication
- Acute Myeloid Leukemia
- series title
- Hematologic Malignancies
- editor
- Röllig, Christoph and Ossenkoppele, Gert J.
- pages
- 22 pages
- publisher
- Springer Science and Business Media B.V.
- external identifiers
-
- scopus:85106496515
- ISSN
- 2197-9774
- 2197-9766
- ISBN
- 978-3-030-72678-2
- 978-3-030-72676-8
- DOI
- 10.1007/978-3-030-72676-8_1
- language
- English
- LU publication?
- yes
- id
- 717b7c46-5247-473a-b141-582f8bbe4c68
- date added to LUP
- 2021-06-06 08:14:26
- date last changed
- 2024-06-15 12:08:02
@inbook{717b7c46-5247-473a-b141-582f8bbe4c68,
abstract = {{<p>Acute myeloid leukemia (AML) is a grave disease with an incidence of 4 per 100,000 a year. It can present in all ages, but the median age is 70 years. One-third of such patients have secondary AML, that is, AML following chemoradiotherapy or a transformation from previous myelodysplastic syndrome (MDS) or myeloproliferative neoplasia. A combination of genetic, epigenetic, and environmental factors may be responsible for the development of most cases of AML. The pathogenesis of AML is characterized by the serial acquisition of somatic mutations and several genes are recurrently mutated in AML. Exposures to benzene, cigarette smoking, pesticides, embalming fluids, accidental or professional ionization radiation, therapeutic radiotherapy, and radioactive I-131 therapy can cause AML with or without a preceding MDS phase. Alkylating agents (e.g., melphalan, cyclophosphamide), topoisomerase-II inhibitors (e.g., etoposide, doxorubicin), and other drugs (e.g., azathioprine) are described to be associated with the development of therapy-related AML (t-AML). Furthermore, about 5–15% of adults and 4–13% of pediatric patients with MDS or AML carry germline pathogenic variants in cancer susceptibility genes. Individuals with clonal hematopoiesis (CHIP) progress to AML at a rate of about 1% per year. Higher age of onset, obesity, previous autoimmune disease, and antecedent MDS or MPN are associated with a risk for developing AML.</p>}},
author = {{Juliusson, Gunnar and Lazarevic, Vladimir and Lehmann, Sören}},
booktitle = {{Acute Myeloid Leukemia}},
editor = {{Röllig, Christoph and Ossenkoppele, Gert J.}},
isbn = {{978-3-030-72678-2}},
issn = {{2197-9774}},
keywords = {{Benzene; Diagnosis; Exposure; Hereditary conditions; Incidence; Mutations; Prevalence; Secondary AML; Sex; Survival; t-AML}},
language = {{eng}},
pages = {{1--22}},
publisher = {{Springer Science and Business Media B.V.}},
series = {{Hematologic Malignancies}},
title = {{Epidemiology and Etiology of AML}},
url = {{http://dx.doi.org/10.1007/978-3-030-72676-8_1}},
doi = {{10.1007/978-3-030-72676-8_1}},
year = {{2021}},
}