Table 3.

Examples of molecular and cytogenetic lesions (hematology-context) detectable in apparently healthy individuals and correlation with proposed terminology.

Term	Molecular correlate	Examples	at Risk for
CHIP	Early mutations and cytogenetic lesions that may be detected in healthy individuals (passenger lesions⁎)	TET2 mutation	Myeloid neoplasms
		DNMT3A mutation	Myeloid neoplasms
		GNAS mutations	Myeloid neoplasms
		ASXL1 mutations	Myeloid neoplasms
		SF3B1 mutations	Myeloid neoplasms
		PPM1D mutations	Myeloid neoplasms
		IGH-rearrangement	B cell neoplasms
		TCR-rearrangement	T cell neoplasms
		-Y	BM neoplasms
CHOP	Disease-determining mutations and related karyotype anomalies (driver lesions⁎)	BCR-ABL1 p210	CML
		JAK2 V617F	MPN
		FIP1L1-PDGFRA, del CHIC2	CEL/HES
		KIT D816V	SM
		RUNX1- RUNX1T1	AML
		CBFβ-MYH11	AML
		FLT3 ITD mutations	AML
		KRAS, HRAS mutations	AML
		BCL2-IGJ(H)	FL
		IGH-CCND1	MCL
		− 7,+8,5q-, …	MDS/AML
		t(8;21), inv16, …	AML
		t(9;22)	CML
		t(14;18)	FL
		t(11;14)	MCL
		t(8;14)	Burkitt NHL

^⁎Depending on germline patterns, affected cells and organs, and additional lesions, so-called passenger lesions may become drivers of oncogenesis, and vice versa, some of the drivers may be detected over decades without visible signs of tumor formation. Therefore, the terms ‘driver’ and ‘passengers’ lesions (mutations) should be used with caution and always in the context of the overall situation in each patient. Abbreviations: CHIP, clonal hematopoiesis of indeterminate clinical potential; CHOP, clonal hematopoiesis with substantial oncogenic potential; CML, Ph + chronic myeloid leukemia; CEL, chronic eosinophilic leukemia; HES, hypereosinophilic syndrome; SM, systemic mastocytosis; AML, acute myeloid leukemia; FL, follicular lymphoma; MCL, mantle cell lymphoma; TCR, T cell receptor; IGH, immunoglobulin heavy chain gene.