September 2026
M	T	W	T	F	S	S
	1	2	3	4	5	6
7	8	9	10	11	12	13
14	15	16	17	18	19	20
21	22	23	24	25	26	27
28	29	30

Sally Mandour: The Diagnostic Challenge of Hypocellular Bone Marrow Failure

Sally Mandour/LinkedIn

Aug 13, 2026, 08:23

Sally Mandour: The Diagnostic Challenge of Hypocellular Bone Marrow Failure

Sally Mandour, Associate Professor, Head of Hematology Unit at Clinical Pathology Department of National Liver Institute, Monofeya University, shared a post on LinkedIn:

“Aplastic Anaemia is defined by the presence of pancytopenia with an empty bone marrow , by exclusion of marrow aplasia due to direct effect of chemotherapy or radiotherapy or any underlying pathological marrow condition.

Diagnosis difficulty is due to the number of marrow failure syndromes having a similar presentation.

Aplastic Anaemia vs. Hypoplastic MDS: Two Empty Marrows, Two Very Different Diseases

Both present with pancytopenia and a ’empty,’ fat-replaced marrow.
Both are driven by an oligoclonal CD8+ T-cell attack on haematopoietic stem cells. On a low-power view.

But one is an autoimmune bone marrow failure state. The other is a clonal neoplasm

5 differentiating tips:

Dysplasia — subtle dysgranulopoiesis, megakaryocyte atypia, or ring sideroblasts favour MDS-h; a ‘clean’ hypoplastic marrow favours AA.
Blasts — even a mildly increased blast percentage tips the scale toward MDS-h.
Cytogenetics — clonal abnormalities (del(5q), del(7q), trisomy 8, del(20q)) support MDS-h; a normal karyotype supports AA (though AA is not always normal either).
Molecular profile — BCOR/BCORL1 and PIGA mutations are typically ‘benign passengers’ in AA and predict a good response to immunosuppression. TP53, RUNX1, and multi-hit mutations point toward MDS-h/high-risk disease.
PNH clone — a sizeable PNH clone (flow cytometry: CD55/CD59/FLAER) supports immune-mediated AA rather than MDS-h.”

Sally Mandour: The Diagnostic Challenge of Hypocellular Bone Marrow Failure