Table 1. Clinical and pathologic characteristics of patients with AA and HL.

Patient #	HL subtype	Bone marrow histology at AA diagnosis	Cytogenetics	T-cell receptor rearrangement	NGS for myeloid malignancy-associated mutations	PNH flow cytometry	HLA alleles	Inherited marrow failure testing, if available
Patient 1	n/a	Markedly hypocellular (5% cellularity) with markedly decreased trilineage hematopoiesis.	46,XY[20] (diagnosis); evolved to 46,XY,der(21)t(3;21)(q11.2;p13)[12] after immunosuppression	Polyclonal	Negative	Negative	A*01:01, A*24:07, B*35:02, C*04:01, DR*11:04	n/a
Patient 2	nodular sclerosis	Markedly hypocellular marrow (<5% cellularity) with markedly decreased trilineage hematopoiesis.	46,XY [20]	Polyclonal	Negative	Negative	A* 68:02, A*02:01; B* 14:02, B*18:01, C*08:02, C*07:01, DR* 13:03, 08:01	Chromosome breakage: normal; Lymphocyte telomere length: very high
Patient 3	nodular sclerosis	Markedly hypocellular marrow (<5% cellularity) with markedly decreased trilineage hematopoiesis.	46,XY[1]; poor growth	n/a	n/a	Negative	A*2, 24; B*39, 51; Cw*7, 15, DR*4, 13, DQ*6, 8	n/a
Patient 4	nodular sclerosis	Hypocellular marrow (20%), with foci of erythropoiesis and myelopoiesis.	Normala	n/a	n/a	n/a	A*1, 3; B*35, 57; Cw*02:02; Cw*06:02	n/a

HL, Hodgkin Lymphoma; AA, Idiopathic Acquired Aplastic Anemia; NGS, Next-Generation Sequencing; HLA, Human Leukocyte Antigen; PNH, Paroxysmal Nocturnal Hemoglobinuria.

^aFor patient 4, results of metaphase cytogenetics from the time of AA diagnosis are not available, however, karyotype after immunosuppression was normal (46,XY,inv(9)(p11q13)c[20]).