16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.

com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Received: 15 August 2022 Revised: 22 September 2022 Accepted: 26 September 2022
DOI: 10.1111/ejh.13872

REVIEW

Auer rods and faggot cells: A review of the history,

significance and mimics of two morphological curiosities
of enduring relevance

Tushar Sehgal 1 | Prashant Sharma 2

1
Department of Laboratory Medicine, All India
Institute of Medical Sciences (AIIMS), New Abstract
Delhi, India
Myeloid differentiation in blasts is distinguished by the presence of one or more
2
Hematology Department, Postgraduate
Institute of Medical Education and Research
needle-shaped crystalline structures called Auer rods. Auer rods manifest either alone
(PGIMER), Chandigarh, India or as faggot cells (containing bundles of Auer rods) in various types of acute myeloid

Correspondence leukemia (AML), myelodysplastic syndromes (MDS) and myelodysplastic/

Prashant Sharma, Hematology Department,
Level 5, Research Block A, Postgraduate
Institute of Medical Education and Research
(PGIMER), Sector 12, Chandigarh 160012,
India.
Email: sharma.prashant@pgimer.edu.in;
prashant.sh@gmail.com
myeloproliferative neoplasms (MDS/MPN). Their presence largely portends a better
prognosis in AML (as markers of maturation/differentiation) and upstages cases of
MDS and MDS/MPN. Observation of these rods in residual blasts in treated cases of
AML indicates an absence of remission. This article traces their historical discovery
and examines their pathogenetic intricacies, as well as our current understanding of
their relevance in myeloid neoplasms. Studies evaluating their prognostic impact in
AML and MDS are catalogued. We also discuss a variety of other hematological and
non-hematological neoplasms where structures potentially mistakable for Auer rods
have been described. Even as the diagnostic approach to hematological malignancies
has evolved from a morphology + cytochemistry + immunophenotyping-dependent
one in the last century to a predominantly molecular genetics-based classification
currently, and even as high-throughput sequencing and structural variation detection
techniques surpass morphology in detecting clinically-relevant sub-categories of
similar-appearing tumours, we review these curious microscopic structures that have
withstood the test of time with respect to their diagnostic relevance.

KEYWORDS
acute myeloid leukemia, brightfield microscopy, hematological malignancies, intracellular
inclusions, myeloperoxidase

1 | I N T RO DU CT I O N rod- or needle- or spindle-shaped azurophilic cytoplasmic inclusions.1

The eponymous term ‘Auer rod’, described initially as a refractile rod-like
body in wet-film preparations of blood, is named after Dr. John Auer.1 In
1903, while working in Dr. William Osler's ward in the Johns Hopkins
Hospital, Dr. Auer observed a 21-year-old man with fever, epistaxis and
1
throat infection. Examination revealed anemia and splenomegaly. His
total leukocyte count was 139
109/L with 92% immature leukemic
cells. About 10% of these cells contained one to three, 1–6 μm long
Although these rod-containing cells were initially interpreted as ‘large
lymphocytes’, their description matches that of myeloblasts. Such inclu-
sions being previously undescribed, Auer deemed his observations wor-
thy of publishing (after due authorization from Drs. Osler and Thomas
McRae).1 He postulated that ‘the data are only strong enough to render
a comparison justifiable’ between human intracellular parasites and the
‘leukemia granules’ he described. He referred to the Leishman-Donovan
body, but conceded that the comparison was highly speculative.1

Eur J Haematol. 2022;1–10. wileyonlinelibrary.com/journal/ejh © 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. 1

2 SEHGAL AND SHARMA
Subsequently, in 1913, Roth found Auer bodies in the myelo-
blasts of a tuberculosis patient, concluding that they represented an
2
unusual form of the tubercle bacillus. This error was resolved when,
on applying the Koch's postulates, attempts to transmit Auer bodies
by inoculation experiments or grow them on various cultures media
were unsuccessful.1 Other researchers rapidly validated the link
2
between Auer rods and leukemic cells. Though most often observed
in myeloblasts, these rods were also seen in polymorphonuclear
3
leukocytes in acute myeloid leukemia (AML). In addition, they were
reported in acute monocytic leukemia, thus establishing that Auer
4,5
rods can occur in granulocytic as well as monocytic AMLs.
2 | STRUCTURE, BIOGENESIS AND
MORPHOLOGY
In 1917, Rosenthal first demonstrated a positive histochemical oxi-
dase reaction on Auer rods in myelogenous leukemia cells.2 In 1923,
Richter revealed the histochemical distinctions between mitochondria,
Russell fuchsin bodies, azure granules and Auer bodies, establishing
them as pathognomonic signs of myelogenous leukemia.2 Kibler's
cytochemical analysis showed that Auer bodies were almost entirely
comprised of a Sudanophilic substance.2 Locquin and Bessis studied
the histochemical structures of Auer bodies and Charcot crystals and
concluded that both are primarily composed of nucleoprotein and are
structurally identical.2 This last conclusion was based upon their
closely overlapping refractive indices (nα for Auer rods was 1.459–
1.461 and for Charcot crystals was 1.457–1.461). Spectroscopic anal-
ysis demonstrated that Auer bodies have an ultraviolet absorption
between 2600 and 2800 Å.2
In 1950, Ackerman's extensive histochemical study of cytoplas-
mic granules revealed that an altered acidic pH in the immature cells
led to the refusion of their azurophilic granules into Auer bodies
instead of their normal maturation into specific granules.1
Cytochemically, Auer rods were positive for peroxidase, periodic
acid-Schiff (PAS) and Sudan black B, along with acid and alkaline
phosphatase stains, and negative for lipase, glycogen
DNA/nucleic acid stains.5,6 Electron microscopically, Ito interpreted
Auer bodies to comprise a fused mass of granules within the endo-
plasmic reticular system.2 Electron microscopic studies also revealed
structural similarities between Auer rods and cytoplasmic granules,
supporting their origin from azurophilic granules and therefore being
1
composed of fused lysosomes.
3 | PHI BODIES
A related but less frequently observed intracytoplasmic structure, the
Phi body, has also been described as characteristic of AML. First
recognised in a publication by Hanker et al. in 1978, these new types
of rods were single or multiple, fusiform or thin, and were frequently
distinguishable from the thicker Auer rods.7 Phi bodies are not visua-
lised well with Romanowsky stains but are apparent in a peroxidase
16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
reaction using 3,30 diaminobenzidine (DAB).7 Hanker called the cyto-
chemical reaction he described hydroxyperoxidase (HPO), because
DAB has myeloperoxidase (MPO) and catalase activity.8,9 When using
DAB, it was difficult to distinguish between Auer rods and Phi bodies
because both were strongly positive with this reagent. Experiments at
pH 9.7 and inhibition by 3-amino 1,2,4-triazole, a known catalase
inhibitor, supported Phi bodies' formation from catalase-containing
granules.7 Gong et al. proposed an alternative method in 2009 that
simplified HPO staining and increased the detection rate of Phi bodies
over previous results.10 Improved HPO staining was used to stain
128 bone marrow or peripheral blood smears from patients with mye-
loid and lymphoid malignancies.10 They demonstrated that the shape
of bundle-like Phi bodies could be long or short while nubbly Phi bod-
ies were frequently oval and smooth. Bundle-like Phi bodies were
detected in 42.9% of AML-M1, 83.3% of M2, 92.0% of M3, 52.3% of
M4 and 33.3% of M5, while nubbly Phi bodies were detected in
28.6% of M1, 66.7% of M2, 11.1% of M3, 33.3% of M4 and 20.0% of
M5. M3 had a significantly higher detection rate of bundle-like or
club-like Phi bodies than the other groups. The detection rate of nub-
bly Phi bodies was higher in the combined M1 + M2 group than in
the M3 group.10
4 | MORPHOLOGICAL RELEVANCE OF
AUER RODS IN AML
The near-universally applied World Health Organization (WHO) classi-
fication of tumours of the hematopoietic and lymphoid tissues clas-
sifies AML and its related precursor neoplasms into various
subcategories, based predominantly on their molecular genetic and
cytogenetic abnormalities.11 This continually updated classification
also takes into account the clinical background (e.g., in therapy-related
or extramedullary myeloid neoplasms), the immunophenotype (e.g., in
mixed-phenotype acute leukemia), predisposing genetic conditions
(e.g., Down syndrome-related AML or AML with germline predisposi-
tion) and, if all other inputs are unrevealing, places neoplasms into the
and predominantly morphology-based AML, not otherwise specified
(NOS).11 Even in this scenario, where morphology's most critical role
is to enumerate blasts or their equivalents and to screen for and quan-
tify the dysplastic cells and lineages, and where the final diagnosis
relies heavily on ancillary investigations, Auer rods and faggots (bun-
dles of Auer rods) have retained their significance. As morphological
hallmarks of AML, Auer rods are found in AML subtypes M1, M2, M3,
M4, M5 and M6 but are not present or are very rare in AML M0 or
M7 of the French–American–British (FAB) classification.12 They are
most often found in and are most numerous in acute promyelocytic
leukemia (APL, the older terminology being FAB-M3), where they are
arranged in bundles in cells named ‘faggot cells’.11 In most situations,
APL with t(15;17)(q22;qI2); PML::RARA features distinctive cells with
bundles of Auer rods (‘faggot cells’) irregularly scattered in the cyto-
plasm. Auer rods in classical (hypergranular) APL are usually more
prominent than in other types of AML. They also have a characteristic
ultrastructural morphology, showing hexagonally arranged tubular

SEHGAL AND SHARMA
structures with a specific 250 nm periodicity in contrast to Auer rods'
6–20 nm laminar periodicities in other AML subtypes.11,13
Rarely, MPO-negative APL occurs, either due to mutation in the
gene encoding the enzyme or when the neoplasm develops in a per-
son with congenital MPO-deficiency, a relatively mild immunodefi-
ciency disorder. In such APL cases, the Auer rods are MPO-negative
as well, and they are seen as thin, unstained areas (negatively-stained
shadows).14
Auer rods are also frequently found in AML with t(8;21)(q22;
q22); RUNX1::RUNX1T1, where they appear in the form of single long,
sharp rods with tapered ends. They may also be detected in mature
neutrophils.11 Auer rods are present in approximately one-third of the
cases of AML with t(6;9)(p23;q34)DEK::NUP214, which is variably
associated with monocytic features, basophilia and multilineage dys-
11
plasia. In the predominantly morphology-based AML, NOS group,
the AML with maturation subtype frequently shows Auer rods. In
other subtypes of AML, NOS group, Auer rods are seen occasionally.
Auer rods in granulocytic sarcomas are extremely difficult to detect in
15
hematoxylin-and-eosin-stained sections.
5 | PROGNOSTIC SIGNIFICANCE IN AML
AND MDS
Auer rods, as markers of differentiation, have been extensively stud-
ied as potential indicators of prognosis in AML and MDS.16–26 In gen-
eral, in AML, their presence has been found to correlate with a better
prognosis in terms of both remission induction and the remission's
duration/stability. Table 1 lists the salient findings of larger studies
studying this phenomenon. This superior prognosis may be due to the
origin of Auer rods from azurophilic granules, suggesting that cases of
AML with Auer rods show a tendency to differentiate.
MDS are a group of clonal hematopoietic stem cell diseases char-
acterised by cytopenias, dysplasia in one or more of the significant
myeloid lineages, ineffective haematopoiesis, genetic abnormalities
and an increased risk of developing AML. Auer rods are included in
the list of findings that indicate dysgranulopoiesis in all recent editions
of the WHO classification.11,27 In addition, they represent evidence of
MDS with excess blasts-2 (MDS-EB-2), regardless of the blast per-
centage.27 Cases of MDS-EB2 with Auer rods but <5% blasts in the
bone marrow and <1% in the peripheral blood are associated with a
worse prognosis as compared to the lower-risk category that they
would have been assigned to in the absence of Auer rods. However,
compared to MDS-EB-2 with increased blasts but without Auer rods,
they have consistently been shown to have a better prognosis
(Table 1).16–19,21–24
Post-therapy in AML, the persistence of Auer rods, specifically
within blasts, indicates an absence of remission.28 However, their
presence in non-blast cells may not portend the same grim situation.
Likewise, in APL who have undergone induction therapy, the
persistence of Auer rods within residual dysplastic neutrophils is not
consistent with the absence of remission, as they may represent
maturing promyelocytes that have lost their replicative potential.29
16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
3
Zassadowski et al. have reported an unusual correlation between the
presence of Auer rods in APL cells at diagnosis and outcome: they
found that patients with higher Auer rod-positive cells tended to have
a higher risk of relapse.30
6 | RE L E V A N C E I N O T H E R M Y E L O I D
NE OP LAS M S
Chronic myelomonocytic leukemia (CMML) is a hematological malig-
nancy with overlapping features of both a myeloproliferative neo-
plasm (MPN) and a myelodysplastic syndrome (MDS).31 Its
diagnostic criteria and sub-classification have been in flux in the
past. Based on the percentage of blasts and promonocytes in the
blood and bone marrow, CMML was subclassified by the WHO in
2016 into CMML-0, 1 and 2, wherein the presence of Auer rods was
only compatible with CMML-2 (akin to MDS-EB2).31 However, a
recent overview of the upcoming WHO 5th edition (2022) divides
CMML cases into only two subcategories: CMML-1 and CMML-2.32
Auer rods are not mentioned in this review, and it is unclear whether
this omission is for brevity or because they have been removed as a
diagnostic consideration.32 A parallel International Consensus Classi-
fication (ICC) of Myeloid Neoplasms and Acute Leukemias, with its
authors comprising many of the experts of the previous WHO 2016
edition, also reverts to the 2-tier system of subclassifying CMML but
still mentions Auer rods as indicative of CMML-2 in its summary
paper.33
Juvenile myelomonocytic leukemia (JMML) is a rare, aggressive
pediatric malignancy characterised by uncontrolled proliferation of
granulocytic and monocytic lineage cells with minimal to mild myelo-
dysplasia. JMML was classified by WHO 2016 under MDS/MPN;
however, a recent overview of the upcoming WHO 5th edition (2022)
places this neoplasm under the MPN.32 ICC has moved JMML to a
group of pediatric and/or germline mutation-associated disorders.33
Auer rods have been rarely reported in JMML.34 The reported case
was of a 2-year-old boy with splenomegaly, anemia, thrombocytope-
nia, leukocytosis and 5%–6% blood/marrow myeloblasts showing
Auer rods. Marked dysgranulopoiesis and dyserythropoiesis were also
noted along with t(3;5)(q25;q35) and a disease-related somatic NRAS
mutation. Thus, the case represented an exceptional JMML with Auer
rods and marked myelodysplasia.34 Pabari et al. described four unique
cases of NRAS-mutated JMML and JMML-like myeloproliferations,
two with somatic mutations and two with germline mutations. One
case had Auer rods.35
Mayer et al. in 1978 described Auer rods in the blasts in four
cases of what morphologically and cytogenetically appeared to be
chronic myeloid leukaemia (CML) in blast crisis with the Ph1 chromo-
some.36 Subsequent detailed cytological and cytochemical examina-
tion however, led to the revised diagnoses (according to the authors)
of an AML-M2, a pre-leukemia (i.e., MDS) progressing to an AML-M2
and an acute promyelocytic leukemia. The last case' diagnosis, as
deduced by the authors, was either a CML in blast crisis with Auer
rods or an acute myelomonocytic leukemia.36 In light of the now
 4

TABLE 1 Salient research studies evaluating the impact of the presence of Auer rods on the prognosis of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML)

First author,
S. no. journal, year Number and description of cases Observations/results Authors' conclusions
1 Wang, Annals of 112 adults with MDS-EB2 who underwent 90.5% of cases with Auer rods achieved marrow blast clearance after one cycle Auer rods in high-risk MDS
Hematology, myeloablative allo-HSCT between 2015 of combined therapy vis-à-vis 66.7% of those without (p = .036). correlated highly with clinical
2022.16 and 2020. Patients with Auer rods had significantly better 3-year OS than those without responses and were
32 cases had Auer rods; of them, 15 were them (p = .04). independent markers for
upgraded to EB-2 solely based on Auer Relapse rates and NRM were not statistically significantly different between the superior survival.
rods. two groups.
2 Huang, British Journal 516 consecutive, newly diagnosed MDS- MDS-EB2 with Auer rods had significantly higher reticulocyte, neutrophil and Auer rod+ve MDS-EB2 has a high
of Haematology, EB2 patients, including 59 (11%) with platelet counts, were more likely to show normal cytogenetics and not harbour frequency of AML-related
2019.17 Auer rods. Of these 59, 25 were complex karyotypes or MDS-defining cytogenetic abnormalities. mutations and may represent a
diagnosed as MDS-EB2 solely based on Patients with Auer rods were less often classified as very-high-risk in IPSS-R special subgroup biologically
Auer rods while 34 met blood and/or BM (p = .005), mainly due to lower blast% and more favourable cytogenetics. closer to AML.
blast criteria for MDS-EB2 with Auer NPM1, DNMT3A, NRAS and TET2 were most frequently mutated genes in These patients may benefit from
rods. These 59 were compared to 236 patients with Auer rods, while U2AF1, TP53 and SF3B1 were commonest in chemotherapy.
MDS-EB2 without Auer rods. those without.
No patient with Auer rods had TP53 mutations (17% in patients without Auer
rods).
Among patients receiving chemotherapy ± hypo-methylating drugs, those with
Auer rods had longer median survival as compared to those without (p = .254).
3 Schuler, Annals of 299 patients with high-risk MDS or AML 100% of patients with Auer rods achieved CR after intensive chemotherapy, vis- Auer rods predict survival and
Hematology, secondary to MDS from the Duesseldorf à-vis 49% of those without. response to intensive
2018.18 MDS registry, diagnosed between 1981 Median survival was 40 months in patients with Auer rods, vis-à-vis 7.8 months chemotherapy in high-risk MDS
and 2014 (diagnoses were adapted to in those without. and secondary AML.
WHO 2016). On multivariate analysis, presence of Auer rods was one of only 3 parameters
These patients received intensive influencing survival (the other two being achievement of CR, and blasts <30%).
chemotherapy at first diagnosis or at
disease progression. Seven of them had
Auer rods.
96 of them were compared with a matching
MDS patient who did not receive
intensive chemotherapy.
4 Germing, British Analysed subtypes of 558 RAEB patients: 26/302 patients were upgraded to RAEB-2 solely based on Auer rods. MDS RAEB-2 patients with Auer
Journal of 256 RAEB I and 302 RAEB II Highest risk of AML transformation (48%) was observed in those classified as rods, irrespective of their
Haematology, RAEB-2 due to a peripheral blast count >5% or Auer rods. marrow or peripheral blood
2005.19 No difference in prognosis between RAEB-2 patients defined based on a blast percentages, had no worse
peripheral blast count >5% versus those defined based on Auer rods only. prognosis than those without
Auer rods.
5 Haferlach, Leukemia & 41 AML with t(8;21) including 5 M1 and 36 Auer rods were detected in 28 patients (68%). Presence or absence of Auer rods
Lymphoma, 1996.20 M2 who underwent aggressive 16/28 had typical Auer rods (long, thin). was not associated with
chemotherapy. Dysgranulopoiesis detected in 37/41 (90%) cases. disease-free survival.
Overall, 90% complete remission rate, 60% disease-free survival at 2-years, 50%
overall survival at 6 years.
SEHGAL AND SHARMA

16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
 TABLE 1 (Continued)

First author,
S. no. journal, year Number and description of cases Observations/results Authors' conclusions
6 Seymour, Leukemia & Group 1: 29 RAEBt patients with Auer rods, Group 1 patients had no different clinical and hematologic parameters than MDS RAEBt patients with Auer
Lymphoma, 1995.21 but no other criteria for inclusion into patients with RAEB or RAEBt with or without Auer rods present. rods have better biology,
SEHGAL AND SHARMA

RAEBt (blood blasts <5%, marrow blasts They were more likely to have diploid cytogenetics, a lower incidence of adverse response to therapy and survive
<20%); Group 2: 40 RAEBt patients with cytogenetic abnormalities, significantly longer survival, and superior complete longer than patients without
Auer rods who additionally had >5% remission rates after intensive AML-like chemotherapy than Auer rod negative Auer rods.
blood blasts and/or >20% and ≤30% patients.
marrow blasts, and Group 3: 139 RAEBt
patients without Auer rods.
7 Michels, Cancer, 52 RAEBt patients (47 adults and five All 20 patients aged ≤45 years had Auer rods. Auer rods were commoner among
1989.22 children) Among those aged >45 years and who received induction chemotherapy, the younger patients, and in those
38 (73%) patients had Auer rods. survival of those with Auer rods was superior (median survivals of 15 and treated intensively, were
23 (44%) were included only because of the 9 months respectively, p = .05). associated with longer survival.
presence of Auer rods. No difference in survival between untreated RAEBt patients with or without
Auer rods.
8 Mertelsmann, Blood, 263 patients with AML or MDS diagnosed Auer rods were the single most important prognostic parameter, with CR rates of Auer rods predicted survival and
1980.23 as per FAB classification, including 31 68% in the Auer-rod-positive and 40% in the negative group (p < .0001). remission in AML and MDS.
RAEB, 14 CMML, 16 AML secondary to Patients with Auer rods had significantly longer survival (p < .0002), and longer
MDS, and 202 de novo aml remission duration among responders.
9 Aul, Cancer, 1989.24 67 patients with advanced MDS Two factors most strongly associated with successful remission induction were ‘Aggressive’ MDS (mainly RAEB
the presence of Auer rods and less than 30% blast count at initiation of and RAEBt) with Auer rods had
treatment. a higher likelihood of achieving
complete remission.
10 Ritter, Medical and 257 children from two European AML Auer rods were more frequent in FAB AML-M1 (63%) and M2 (78%) compared Auer rods indicated patients with
Pediatric Oncology, studies: BFM-78 and BFM-83. with M4 (47%) and M5 (5%). more favourable prognosis,
1989.25 129 (50%) children had Auer rods. Patients with Auer rods had significantly higher remission rates (p = .01) especially for AML-M1.
AML-BFM-83 showed significantly longer remission durations in Auer rod+ve
cases (p = .007).
In FAB AML-M1, Auer rods were highly predictive of induction therapy success
(p = .003) and duration of remission (p = .004), but not in other subtypes.
11 Kris, Leukemia 89 adults with acute non-lymphoblastic Auer rods were more likely in patients with normal or no evaluable metaphases Auer rods in the initial bone
Research, 1985.26 leukemia undergoing conventional than those with only abnormal or both normal and abnormal metaphases marrow predict greater
cytogenetic analyses and receiving (p = .03). response and longer survival in
protocol chemotherapy Auer rods in a pre-treatment marrow were associated with higher complete acute non-lymphoblastic
remission rates (p = .004), remission duration (p = .02), and median survival leukemia
(p = .01).
On multivariate analyses, pre-treatment presence/absence of Auer rods
significantly predicted response and survival.

Abbreviations: BFM, Berlin-Frankfurt-Munster; BM, bone marrow; CR, complete remission; EB, excess blast; FAB, French–American–British; HSCT, hematopoietic stem cell transplantation; IPSS-R, revised
international prognostic scoring system; NRM, non-relapse mortality; OS, overall survival; RAEB, refractory anemia with excess blasts; RAEBt, refractory anemia with excess blasts in transformation.
5

16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
 6

TABLE 2 Review of laboratory and clinical findings of patients with non-acute promyelocytic leukemia neoplasms showing faggot cells

S. Antecedant
no. Study Age/sex WBC/Hb/Pt Immunophenotyping Cytogenetics Molecular study disease Therapy Diagnosis
53
1 Choi et al. 32/female 2.4/105/119 CD13, CD33+, 45,XX,-7[5]/46,XX[15] NA None AIDA and CD based AML-MRC
CD34, HLADR+, CTx
cMPO+
2 Guérin 67/male 241/65/42 cMPO+, CD13+, 46,XY, complex Amplification of MYC NA CD based CTx AML
et al.54 CD33+, CD34 karyotype involving carried by double
fragmented minute chromosome
chromosome 11
3 Dmitrienko 17/male NA 90%: TdT+, CD34+, 46 XY[20] Normal NA High risk ALL protocol MPAL
et al.55 CD2+, CD7+, with suboptimal (T/Myeloid)
cCD3+, CD13, response followed by
CD15+, CD117+; 5% BMT
co-expressed
cMPO+, cCD3+
4 Gupta 19/male NA AML with CD19+, 45XY,t(8;21)(q22;q22) NA None CD based CTx AML-t(8;21)
et al.56 CD56+ [13]/46,idem,+8[07]
5 Sehgal 32/female 28.2/63/40 CD13+, CD7+, None Normal None CR after Hyper CVAD MPAL-T/
et al.57 CD117+, CD34+, protocol Myeloid
HLA-DR+, cMPO+,
CD2, cCD3+
6 Garrastazul- 36/male 22/98/42 CD13+, CD33+, Inv16[16]/hyperdiploidy CBFB -MYH11 None CR after induction CTx AML with inv
Sánchez CD123+, CD34+, [4/40] KIT [p.Asp816Val] (16)
et al.58 HLA-DR+, cMPO+
12.5%: CD4+, CD64+
7 Yanagisawa 62/male 4.9/81/149 CD33+, CD117+; 46, XY, t(7;11)(p15;p15) NUP98 -HOXA9 None CR after induction CTx AML with t
et al.59 CD13+, CD34+, [20] (7;11)
cMPO+, glycophorin
A+, HLA-DR
8 Ohnishi 13/male 143/52/64 CD13+, CD33, 47,XY,+4[20] NA NA CR after induction CTx AML M1
et al.60 CD34+, HLADR+ followed by BMT
9 Jerez 32/male 67.4/85/10 15% blasts: CD13+, 47,XY,+8,inv(16) CBFB-MYH11 NSHL treated with CR after induction CTx Therapy related
et al.61 CD33+, CD34+, (p13q22)[20] ABVD, HIV AML with +8
HLA-DR+, MPO + infection and inv (16)
60% blasts: CD13+,
CD14+, CD34,
CD64+, CD14+,
HLA-DR+,
lysozyme+
10 Ogura 62/male NA CD13+, CD33, 46,XY[20] NA Neuroschwannoma Azacitidine CTx MDS-RAEB2
et al.62 CD34+, HLADR+
SEHGAL AND SHARMA

16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
 16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
SEHGAL AND SHARMA 7

available (since 2017) diagnostic category of Ph-positive AML, it is

immunodeficiency virus; MDS, myelodysplastic syndrome; MPAL, mixed phenotype acute leukemia; MRC, myelodysplasia-related changes; NA, not available; NSHL, nodular sclerosis Hodgkin lymphoma; Pt.,
possible that these may have, after all, represented AML with

AML with inv

AML with inv

(p13.1q22)

(p13.1q22)

Abbreviations: ABVD, adriamycin, bleomycin, vinblastine, dacarbazine; AIDA, all-trans retinoic acid, idarubicin; AML, acute myeloid leukemia; BMT, allogeneic bone marrow transplantation; CD, cytarabine,
daunorubicin; CR, complete remission; CTx, chemotherapy; CVAD, cyclophosphamide, vincristine, doxorubicin (Adriamycin) and dexamethasone; DM, diabetes mellitus; Hb, hemoglobin (g/L); HIV, human
Auer rods.
Diagnosis
AML-M4

(16)

(16)
7 | AUER ROD-LIKE INCLUSIONS IN NON-
CR after induction CTx MYELOID DISORDERS

Died 2 days after

Auer rod-like inclusions may be seen in non-myeloid hematological or

remission
non-hematological neoplasms. They have been frequently reported in
Therapy

plasma cell neoplasms and medullary carcinomas of the thyroid, and

NA

less often in non-Hodgkin lymphomas, an early T-cell precursor acute

lymphoblastic leukemia (ETP-ALL) and prolymphocytic leukemia
(PLL).37–41 Steinmann first reported purple cytoplasmic Auer rod-like
Colonic adenoma,

needle-shaped inclusions in Giemsa-stained myelomatous plasma

Antecedant

cells.37 Metzgeroth t al. found that these needles possessed

disease

intense α-N-esterase activity, indicating their lysosomal origin.37,42

DM
None

None

Electron-microscopy demonstrated their close relationship to the

ultrastructural morphology of myeloid Auer rods by revealing internal
periodicities similar to those observed in neutrophil primary granules
KIT (p.Asp816Tyr)

and being composed predominantly of normal cellular enzymes.37

CBFB-MYH11 KIT
Molecular study

(p.Asp816Val)

While Auer rods in myeloid cells are comprised of enzymes

including MPO and/or chloroacetate esterase, the plasmacytic azuro-
philic inclusions are composed of myeloma cell-specific enzymes like
NA

α-N-esterase, acid phosphatase or β-glucuronidase. They must be

strictly distinguished from immunoglobulin/paraprotein crystals.37
platelet count (
109/L); RAEB, refractory anemia with excess blasts; WBC, white blood cell count (
109/L).
(p13.1q22),+22[20]

Factors predisposing to the appearance of Auer rod-like inclusions in

(p13.1q22), +22

myeloma remain unknown except that the paraprotein has been of

[17]/46,XX[3]

the κ-type in the overwhelming majority of the reported cases.37

47,XX,inv(16)

47,XY,inv(16)
Cytogenetics

Auer rod-like inclusions have rarely been reported in medullary

carcinoma of the thyroid.38 Cytological smears were found to be
NA

hypercellular with small cohesive cellular clusters and rare cells resem-
bling neoplastic myeloblasts that showed multiple eosinophilic rods.38
HLA-DR+, CD64+,

Auer rod-like inclusions may rarely be seen in B-cell neoplasms.

Immunophenotyping

CD38+, CD117+,

CD33+, CD117+,
CD11c+, cMPO+
CD56+ CD11c,
CD33+, CD34,

CD14, CD64

These rod-like inclusions are cytochemically negative for MPO,

and HLA-DR+,
CD13+, CD14+,

CD34+, CD13+,

CD34+, CD13+,

α-naphthyl acetate esterase and PAS. Immunostaining and flow cyto-

CD34

metric analysis confirmed monoclonal (κ-restricted) malignant lympho-

cytes in a patient with B-cell non-Hodgkin lymphoma infiltrating the
bone marrow.39 Auer rod-like inclusions have been reported in B-
PLL.40 Prolymphocytes with Auer rod-like inclusions from a PLL
20.8/106/55
WBC/Hb/Pt
323/82/38

patient reacted positively with anti-γ heavy chain and anti-κ light
9.4/95/37

chain antibodies. On transmission electron microscopy, the 1–2

microns long rods consisted of an electron-dense crystalline matrix,
with a 60 Å periodicity contained within a single unit membrane.40
28/female

65/female

Auer rods have been reported in ETP-ALL, a unique subtype of

Age/sex

12/male

precursor T-cell acute lymphoblastic leukemia with distinct immuno-

(Continued)

phenotypic and genetic features.41 In the reported case, the Auer rods
were weakly positive for MPO, sans cytoplasmic positivity in the cor-
Kim et al.64

Kim et al.65
et al.63

responding blasts, leading the authors to debate whether mixed-

Sehgal
Study

phenotype acute leukemia, T/myeloid might be a more appropriate

TABLE 2

designation.41 ETP-ALLs are closely associated with myeloid and stem

cell lineages and express both T-lymphoid and myeloid cell markers;
no.
11

12

13
S.

however, MPO staining is consistently negative. Even so, in their case,


8 SEHGAL AND SHARMA
with only 0.3% of blasts containing unequivocally (though weakly)
MPO-positive Auer rods, Rahman et al. averred that ETP-ALL was the
preferred diagnosis, citing the prior requirements of MPO-positivity
for recognising the myeloid lineage, which were 3.0% (as per FAB),
10% (as per EGIL and others) and 13% not being met.43–46
8 | F A G G O T C E L L S A ND T H E I R
OCCURRENCE IN NON-APL NEOPLASMS
The word ‘faggot’ is an archaic unit of measurement for a bundle of
sticks.47 This expression is used in hematology to describe a leukemic
promyelocyte. Faggot cells are leukemia cells containing bundles of
Auer rods.11 The word has previously seen other legitimate medical
applications. A body of Russian orthopaedic surgery literature from
the 1960s through the 1980s discusses the faggot method of manag-
ing cystic bone defects by laying down multiple thin plates of homo-
geneous grafted bone.48,49 Greenwood and Kerry described the use
of a faggot of fused glass capillaries to isolate peripheral blood
lymphocytes in 197250; a ‘faggot like assembly’ was defined for
bundles of lentinan triple helical chain polysaccharides by a 2010
Chinese paper,51 and an Indian urology text from 2014 describes a
faggot method of dilating urethral strictures by passing multiple
parallel bougies.52
Infrequently, faggot cells are also reported in patients with AML
other than APL (Table 2).53–65 These cases were diagnosed as AML
with inv(16) in four cases, mixed-phenotype acute leukemia
(T/Myeloid) in two cases, and one each of AML without maturation
(M1), AML with complex karyotype involving chromosome 11, MDS-
refractory anemia with excess blasts-2, AML with myelodysplasia-
related changes, AML-M4, AML with t(8;21) and AML with t(7;11).
Median age was 32 years (interquartile range [IQR] 13–67) and the
male to female ratio was 2.2:1. Median white blood cell (WBC)
count was 23
109/L (IQR 2.4–323), hemoglobin was 83.6 g/L
(IQR 52–106) and platelet count was 42
109/L (IQR 10–149). In all
cases, molecular studies confirmed the absence of t(15;17).
Antecedent diseases in 3/13 (23%) cases were nodular-sclerosis type
of Hodgkin lymphoma with human immunodeficiency virus infection,
neuroschwannoma and colonic adenoma with diabetes mellitus.
9 | C O N CL U S I O N
MPO-positive Auer rods indicate morphologic myeloid differentiation
in blasts. They also provide an indication of the prognosis and their
presence alters the grade of MDS. Inclusions resembling Auer rods
can sometimes be discovered in non-myeloid and non-hematological
tumours as well. Bundles of Auer rods, also known as faggot cells, are
considered essentially diagnostic of APL, however, this may not
always be the case as faggot cells have also been described in
non-promyelocytic leukemias. The continuing relevance of Auer rods,
faggot cells and to a lesser extent, Phi bodies in the era of
16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
high-throughput genomics is evidence that the laboratory diagnosis of
hematological malignancies remains a truly multi-modality science.
AUTHOR CONTRIBU TIONS
Tushar Sehgal contributed to the concept, design, literature search,
manuscript preparation, review, approval. Prashant Sharma contrib-
uted to the design, literature search, manuscript editing, review,
approval.
AC KNOW LEDG EME NT
None to declare.
CONFLIC T OF INT ER E ST
The authors declare no conflict of interest.
DATA AVAILABILITY STAT EMEN T
Data sharing is not applicable to this article as no new data were cre-
ated or analyzed in this study.
OR CID
Tushar Sehgal https://orcid.org/0000-0001-7481-5550
Prashant Sharma https://orcid.org/0000-0003-4741-3403
RE FE RE NCE S
1. Freeman JA. The ultrastructure and genesis of Auer bodies. Blood.
1960;15:449-465.
2. Freeman JA. Origin of Auer bodies. Blood. 1966;27(4):499-510.
3. Bainton DF, Friedlander LM, Shohet SB. Abnormalities in granule
formation in acute myelogenous leukemia. Blood. 1977;49(5):
693-704.
4. Ackerman GA. Microscopic and histochemical studies on the Auer
bodies in leukemic cells. Blood. 1950;5:847-863.
5. Goldberg AF. Acid phosphatase activity in Auer bodies. Blood. 1964;
24:305-308.
6. Cardullo L d S, Morilla R, Catovsky D. Significance of Phi bodies in
acute leukaemia. J Clin Pathol. 1981;34(2):153-157.
7. Hanker JS, Laszlo J, Moore JO. The light microscopic demonstra-
tion of hydroperoxidase-positive Phi bodies and rods in leuko-
cytes in acute myeloid leukemia. Histochemistry. 1978;58(4):
241-252.
8. Hanker JS, Ambrose WW, James CJ, et al. Facilitated light micro-
scopic cytochemical diagnosis of acute myelogenous leukemia. Cancer
Res. 1979;39(5):1635-1639.
9. Novikoff AB, Novikoff PM, Davis C, Quintana N. Studies on microper-
oxisomes. II. A cytochemical method for light and electron micros-
copy. J Histochem Cytochem. 1972;20(12):1006-1023.
10. Gong XB, Lu XG, Yan LJ, et al. Improvement of Phi bodies stain and
its clinical significance. Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2009;
17(1):222-225.
11. Arber DA, Brunning RD, Le Beau MM, Falini B. Acute myeloid leuke-
mia with recurrent cytogenetic abnormalities. In: Swerdlow SH,
Campo E, Harris NL, et al., eds. WHO Classification of Tumours of Hae-
matopoietic and Lymphoid Tissues. International Agency for Research
on Cancer; 2008:110-123.
12. Bennett JM, Catovsky D, Daniel MT, et al. Proposed revised criteria
for the classification of acute myeloid leukemia. A report of the
French-American-British Cooperative Group. Ann Intern Med. 1985;
103(4):620-625.

SEHGAL AND SHARMA
13. Pearson EC. Crystal structure of Auer rods in acute myeloblastic leu-
kaemia (AMyL). J Clin Pathol. 1986;39(5):569-572. https://doi.org/10.
1136/jcp.39.5.569
14. Rastogi P, Sharma S, Sreedharanunni S, et al. Myeloperoxidase defi-
cient acute promyelocytic leukemia: report of two cases. Indian J
Hematol Blood Transfus. 2018;34(2):372-374.
15. Byrd JC, Edenfield WJ, Shields DJ, Dawson NA. Extramedullary mye-
loid cell tumors in acute nonlymphocytic leukemia: a clinical review.
J Clin Oncol. 1995;13(7):1800-1816.
16. Wang Y, Shen Y, Qi J, et al. Prognostic impact of Auer rods for cytor-
eductive chemotherapy and myeloablative allogeneic stem cell trans-
plantation in adult patients with myelodysplastic syndrome with
excess blasts-2. Ann Hematol. 2022;101(7):1611-1615.
17. Huang H, Qin T, Xu Z, et al. Mutational features of myelodysplastic
syndromes with Auer rods reveal them are more akin to acute mye-
loid leukemia. Br J Haematol. 2020;188(5):796-800.
18. Schuler E, Zadrozny N, Blum S, et al. Long-term outcome of high risk
patients with myelodysplastic syndromes or secondary acute myeloid
leukemia receiving intensive chemotherapy. Ann Hematol. 2018;
97(12):2325-2332.
19. Germing U, Strupp C, Kuendgen A, et al. Refractory anaemia with
excess of blasts (RAEB): analysis of reclassification according to the
WHO proposals [published correction appears in Br J Haematol.
2006; 134(2):247]. Br J Haematol. 2006;132(2):162-167.
20. Haferlach T, Bennett JM, Löffler H, et al. Acute myeloid leukemia
with translocation (8;21). Cytomorphology, dysplasia and prognostic
factors in 41 cases. AML Cooperative Group and ECOG. Leuk Lym-
phoma. 1996;23(3–4):227-234.
21. Seymour JF, Estey EH. The contribution of Auer rods to the classifica-
tion and prognosis of myelodysplastic syndromes. Leuk Lymphoma.
1995;17(1–2):79-85.
22. Michels SD, Saumur J, Arthur DC, Robison LL, Brunning RD. Refrac-
tory anemia with excess of blasts in transformation hematologic and
clinical study of 52 patients. Cancer. 1989;64(11):2340-2346.
23. Mertelsmann R, Tzvi Thaler H, To L, et al. Morphological classifica-
tion, response to therapy, and survival in 263 adult patients with
acute nonlymphoblastic leukemia. Blood. 1980;56(5):773-781.
24. Aul C, Schneider W. The role of low-dose cytosine arabinoside and
aggressive chemotherapy in advanced myelodysplastic syndromes.
Cancer. 1989;64(9):1812-1818.
25. Ritter J, Vormoor J, Creutzig U, Schellong G. Prognostic significance
of Auer rods in childhood acute myelogenous leukemia: results of the
studies AML-BFM-78 and -83. Med Pediatr Oncol. 1989;17(3):
202-209.
26. Kris MG, Mertelsmann R, Jhanwar S, et al. Relationship of Auer rods
and chromosome findings to outcome in eighty-nine adults with
acute nonlymphoblastic leukemia. Leuk Res. 1985;9(10):1231-1235.
27. Hasserjian RP, Orazi A, Germing U, et al. Myelodysplastic syndromes:
overview. In: Swerdlow SH, Campo E, Harris NL, et al., eds. WHO
Classification of Tumours of Haematopoietic and Lymphoid Tissues.
International Agency for Research on Cancer; 2008:95-105.
28. Döhner H, Estey E, Grimwade D, et al. Diagnosis and management of
AML in adults: 2017 ELN recommendations from an international
expert panel. Blood. 2017;129(4):424-447.
29. Virk H, Khaire N, Sreedharanunni S, Naseem S, Malhotra P, Sharma P.
Significance of dysplastic neutrophils with multiple Auer rods in post-
therapy acute promyelocytic leukemia. Indian J Hematol Blood Trans-
fus. 2022;38(1):199-201.
30. Zassadowski F, Ades L, Schlageter MH, et al. Auer rods and differenti-
ation in acute promyelocytic leukemia. Br J Haematol. 2008;142(6):
998-1000.
31. Orazi A, Bennett JM, Germing U, et al. Chronic myelomonocytic leu-
kaemia. In: Swerdlow SH, Campo E, Harris NL, et al., eds. WHO Classi-
fication of Tumours of Haematopoietic and Lymphoid Tissues.
International Agency for Research on Cancer; 2008:80-84.
16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
9
32. Alaggio R, Amador C, Anagnostopoulos I, et al. The 5th edition of the
World Health Organization Classification of Haematolymphoid
Tumours: lymphoid neoplasms. Leukemia. 2022;36(7):1720-1748.
33. Arber DA, Orazi A, Hasserjian RP, et al. International consensus classi-
fication of myeloid neoplasms and acute leukemias: integrating mor-
phologic, clinical, and genomic data. Blood. 2022;140(11):1200-1228.
34. Li W, Cooley LD, August K. Juvenile myelomonocytic leukemia with t
(3;5)(q25;q35), Auer rods and marked myelodysplasia. Pathol Res
Pract. 2018;214(6):919-923.
35. Pabari R, Chun K, Naqvi A. The clinical landscape of NRAS-mutated
juvenile myelomonocytic leukemia-like myeloproliferation includes
children with costello syndrome [published online ahead of print,
2022 Jun 3]. J Pediatr Hematol Oncol. 2022. doi:10.1097/MPH.
0000000000002492
36. Mayer S, Falkenrodt A, Albert A, et al. Corps d'Auer et chromosome
Ph 1: pseudo-leucémies myéloïdes chroniques? [Auer bodies and Ph1
chromosome: chronic myeloid pseudoleukemia?]. Nouv Rev Fr Hema-
tol (1978). 1982;24(5):307-312.
37. Hütter G, Nowak D, Blau IW, Thiel E. Auer rod-like intracytoplasmic
inclusions in multiple myeloma. A case report and review of the litera-
ture. Int J Lab Hematol. 2009;31:236-240.
38. Mohammadnia Avval M, Kumar PV, Dehghani F. Multiple Auer rods
in fine-needle aspiration smears of medullary thyroid carcinoma: an
unusual finding. Int Med Case Rep J. 2020;13:85-88.
39. Gao Z, Cui F, Liu M, Guo Y, Hu Y, Shi M. Auer rod-like inclusions in
the cytoplasm of B-cell lymphoma cells with bone marrow infiltration.
Exp Hematol. 2019;77:6-11.
40. Juneja HS, Rajaraman S, Alperin JB, Bainton DF. Auer rod-like inclu-
sions in prolymphocytic leukemia. Acta Haematol. 1987;77(2):
115-119.
41. Rahman K, Singh P, Chandra D, Dev Yadav D, Gupta R, Gupta A. Early
T-cell precursor acute lymphoblastic leukemia with Auer rods-a case
report. Int J Lab Hematol. 2020;42(1):e27-e29.
42. Metzgeroth G, Back W, Maywald O, et al. Auer rod-like inclusions in
multiple myeloma. Ann Hematol. 2003;82(1):57-60. https://doi.org/
10.1007/s00277-002-0574-0
43. Bennett JM, Catovsky D, Daniel MT, et al. Proposals for the classifica-
tion of the acute leukaemias. French-American-British (FAB) co-
operative group. Br J Haematol. 1976;33:451-458.
44. Bene MC, Castoldi G, Knapp W, et al. Proposals for the immunologi-
cal classification of acute leukemias. European Group for the Immu-
nological Characterization of Leukemias (EGIL). Leukemia. 1995;9:
1783-1786.
45. van den Ancker W, Westers TM, de Leeuw DC, et al. A threshold of
10% for myeloperoxidase by flow cytometry is valid to classify acute
leukemia of ambiguous and myeloid origin. Cytometry B Clin Cytom.
2013;84:114-118.
46. Guy J, Antony-Debré I, Benayoun E, et al. Flow cytometry thresholds
of myeloperoxidase detection to discriminate between acute lympho-
blastic or myeloblastic leukaemia. Br J Haematol. 2013;161:551-555.
47. Castoldi GL, Liso V, Specchia G, Tomasi P. Acute promyelocytic leuke-
mia: morphological aspects. Leukemia. 1994;8(9):1441-1446.
48. Volkov MV. Filling skeletal defects with thin plates of homogenous
bone by the “faggot” method. Acta Chir Plast. 1966;8(1):32-39.
49. Volkov MV, Berezhnoĭ AP. Printsipy lecheniia distroficheskikh kist
kosteĭ u deteĭ [principles of the treatment of dystrophic bone cysts in
children]. Vestn Khir Im I I Grek. 1983;131(8):68-73.
50. Greenwood B, Kerry PJ. The faggot method: a technique for the sep-
aration of blood lymphocytes. J Physiol. 1972;226(2):37P.
51. Zhang Y, Li S, Zhang L. Aggregation behavior of triple helical polysac-
charide with low molecular weight in diluted aqueous solution. J Phys
Chem B. 2010;114(15):4945-4954.
52. Bhat MS. Chapter 27: urologic surgeries. SRB's Surgical Operations:
Text & Atlas. Jaypee Brothers Medical Publishers (P) Ltd; 2014. doi:
10.5005/jp/books/12221_27

10
53. Choi YW, Park JS, Jung YS, Cho SR. Faggot-like cells observed in
acute myeloid leukemia with myelodysplasia-related changes mimick-
ing acute promyelocytic leukemia. Leuk Lymphoma. 2015;56(6):1906-
1907.
54. Guérin E, Mahon FX, Lippert E. Bundles of Auer rods in blast cells and
mature neutrophils in a non-promyelocytic acute myeloblastic leukae-
mia. Br J Haematol. 2008;141(6):749.
55. Dmitrienko S, Vercauteren S. Auer rods in mature granulocytes
of a patient with mixed lineage leukemia. Blood. 2012;119(19):
4348.
56. Gupta A, Reddy KG, Goyal M. “Faggot neutrophils!” in non-acute pro-
myelocytic leukemia: a rare occurrence. Indian J Hematol Blood Trans-
fus. 2018;34(4):778-780.
57. Sehgal T, Singh P, Kaul E. Stodtmeister cells (polymorphs with
Pelger-Huët anomaly) showing “Faggots” in mixed phenotypic acute
leukemia (T/myeloid). Indian J Hematol Blood Transfus. 2018;34(1):
148-150.
58. Garrastazul-Sánchez MP, Vilches-Moreno M, Fernández-Valle MC,
et al. Neutrophil faggot cells and inv(16): not such a fortuitous associ-
ation? Ann Hematol. 2019;98(5):1293-1295.
59. Yanagisawa H, Mizuta S, Kawabata H, et al. Faggot cells in acute mye-
loid leukemia with t(7;11)(p15;p15) and NUP98-HOXA9 fusion. Ann
Hematol. 2021;100(8):2121-2123.
60. Ohnishi H, Yoshino H, Yoneyama R, Ishii M, Watanabe T, Bessho F.
Faggot formation in mature neutrophils and metamyelocytes in acute
16000609, 0, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/ejh.13872 by CAPES, Wiley Online Library on [28/10/2022]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
SEHGAL AND SHARMA
myeloid leukemia without maturation. Pediatr Hematol Oncol. 2008;
25(3):165-170.
61. Jerez A, del Mar OM, Amigo ML, Ortuño FJ. Faggot cells in an
HIV-positive patient with inv(16)/therapy-related acute myeloid
leukaemia. Br J Haematol. 2010;150(6):646.
62. Ogura H, Inagaki A, Wakita A. A case of myelodysplastic syndrome
presenting with faggot-like cells. Int J Hematol. 2013;97:443-445.
63. Sehgal T, Sharma P, Varma N. Faggot cells in a non-promyelocytic
acute myeloid leukemia. Hematol Oncol Stem Cell Ther. 2014;7(3):
120-122.
64. Kim JA, Shin WY, Kim J, et al. A case of acute myeloid leukemia with
inv(16)(p13.1q22);CBFB-MYH11 presenting with faggot cells. Ann
Lab Med. 2021;41(3):333-335.
65. Kim KJ, Kim IS. Bundles of Auer rods in mature neutrophils in a pedi-
atric acute myeloid leukemia patient with inv(16)(p13.1q22). Int J Lab
Hematol. 2020;42(4):e164-e166.
How to cite this article: Sehgal T, Sharma P. Auer rods and
faggot cells: A review of the history, significance and mimics
of two morphological curiosities of enduring relevance. Eur
J Haematol. 2022;1‐10. doi:10.1111/ejh.13872