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Lymph Node

- Introductory Lecture
Objectives
This lecture is designed to provide general
histopathology of lymph node. By the end of the learning,
you should:
Know the normal histology of lymph node
Know how to assess the lymph node under microscope
Be able to distinguish malignancy from reactive or benign
disorders
Be able to make diagnosis or narrow down the diagnoses based
on morphology
Know what other tests needed to make a definite diagnosis
Know the markers for common pediatric lymphomas
Normal lymph node architectures
Normal lymph node histology

Capsule
Subcapsular sinus
Trabeculum
Follicles of cortex
Paracortex
Medullary sinus

Medullary cords
Lymphocyte homing
The site of T cell homing is the
After initial maturation in the primary
paracortex
immune organs, "virgin" B and T
The separation of B and T lymphocytes
lymphocytes --> peripheral blood -->
not absolute,
home to specific sites within the lymph
Both cell types present throughout
node (and the other secondary organs),
lymph node, necessary for coordinated
The sites of B cell homing include: lymphoid immune response.
The primary and secondary follicles
of cortex-the sites of
Antigen presentation
Consequent lymphocyte
proliferation and differentiation
The medullary cords -->plasma
cells aggregate--> release their
immunoglobulins into the efferent
lymph
Lymph node variation
Lymph node histology
is dynamic: follicles
In the absence of
immune stimulation,
primary follicles (no
germinal centers)

In the presence of
immune stimulation,
secondary follicles and
germinal centers
2nd
follicle
( GC)

Ki67
Normal IHC pattern

A: HE

B- CD20: B cells,
concentrated in folicles

C- IgD: Mantle cells

D- CD23: Folicular
dendritic cells and B
cells

E- CD10: germinal
center cells

F- Bcl6 (nuclear stain):


germinal center cells
Normal IHC pattern

G-Bcl2: absent in
germinal center (GC)
B cells
H-CD3: T cells,
concentrated in
paracortical area,
I-CD57: Scattered
follicular regulatory T
cells
J-PD1: GC regulatory
T cells
K-Ki67: GC
proliferating cells
(polarity)
L-CD21: Follicular
dendritic cells
Where to begin?

Architecture (low power, preserved or


effaced)
Recognizing lymph node patterns (low
power)
Overall growth pattern: Nodular(Follicular)/
Diffuse/Paracortex/Sinus
Capsule (intact/thickened, invasion)
Necrosis
Granuloma (necrotic?)
Benign LN pathology

Architecture preserved or mostly preserved


Four growth patterns
Follicular Pattern Sinus Pattern Diffuse Pattern Mixed Pattern
Nonspecific Sinus histiocytosis Postvaccinial Toxoplamosis
lymphadenitis lymphadenitis
Rheumatoid Lymphangiographic Infectious Dermatopathic
arthritis changes mononucleosis lymphadenitis

Syphilis Rosai-Dorfman Herpes zoster SLE


disease lymphoadenitis
AIDS -realated Whipples disease Diphenylhydantoin Granulomatous
hypersensitivity histiocytic
necrotizing
lymphadenitis
PTGC Monocytoid B-cell Angioimmunoblastic Granulomatous
hyperplasia lymphadenopathy lymphadenitis
Castlemans Infection-associated CMV lymphadenitis Kawasakis disease
disease hemophagocytic
syndrome
Kaposis sarcoma
Vascular
Transformation of
sinuses
Non-specific Reactive Follicular
Hyperplasia
Children and adolescents
Often seen in nodes draining infected sites
Commonly fail to identify a specific
etiologic agent
Increased in both of size and number of
follicles in the cortex
MZ

LZ

DZ
Feature Reactive Neoplastic(FL)
Shape of follicles Variable, fused, dumbbell regular, similar sized
Location of follicles Predominantly cortex Throughout
Interfollicular areas Gen. preserved Scant, back-to-back fol.
GC cells heterogeneous monotonous
Tingible Body Macroph present absent
Mitoses frequent Very rare
Mantle zones Present, sharply Often obliterated
demarcated
polarity present absent
Fol. in perinodal tis. absent May present
BCL-2 in GC negative Positive (90%)
IG gene rearrangement poly mono
CD10/BCL-6 GC only Outside GC
Syphilitic lymphadenoapthy
Generalized lymphadenopathy----- feature of 2
syphilis
Follicular hyperplasia
Plasma cell expands medullary cords
Epithelial cell clusters in paracortex
Naked giant cells
Capsular fibrosis
Arteritis and phlebitis of capsular vessels
Perivascular lymphoplasmacytic cuffing
Silver stains ----Spirochetes
Vascular proliferation and plasmacytosis in the interfollicular
region

pericapsular inflammation and fibrosis vasculitis


HIV-related lymphadenopathy

Generalized lymphadenopathy
Florid Follicular HyperplasiaFollicular.
Involution (PRGC) Lymcyte Depletion
HIV Lymphadenitis (acute stage)
Florid FH, large, irregular
May coalesce to form giant, geographic
structures
Thin mantle zones---naked GC
Follicle lysis (MZ invagination)
Paracortex monocytoid B-cell
hyperplasia
Warthin-Finkeldey giant cells
Follicular lysis

Monocytoid B cell hyperplasia polykaryocytes


HIV-related lymphadenopathy
Follicular involution Lymphocyte depletion
(subacute/chronic stage) (Burnout)

Follicular effacement Atrophic or absent


GC with hyaline material follicles
Lymph. depl. In Hyalinized GC with
paracortex prominent thick vessels
and PAS-postive deposits
Plasma cell accumulation
and vascular proliferation Lymph. depl. In
in paracortex paracortex
Paracortex: extensive
vascular proliferation and
fibrosis
Effacement of lymph node architecture and excessive
proliferation of blood vessels in the paracortex.

Lymphoid follicle depopulated of lymphocytes and largely fibrosed


PTGC
Young males
May recurrent
Single, asymptomatic, enlarged node
Expanded follicles (3 x) with thick mantle cells
which may infiltrate GC (inwards and
outwards)
In a background of FH
NLPHL: relationship, differential?
High power of PTGC: many
mantle B cells with residual GC
cells
Castleman disease
Hyaline vascular type

Young adults
Common location: mediastinum or neck
Microscopic:
Concentric layering of lymphocytes
Atrophic germinal center (GC), multiple GCs
Small hyaline vessels radially penetrating the
GC (lollipop)
Vascular interfollicular tissue
Reactive process, curable by surgical resection
Monoclonality shown in a recent study
Chang KC, et al. Modern Path (2014) 27, 823-
831
Castlemans disease of plasma cell type
Wide age range
Systemic symptoms
Anemia, hyperglobulinemia,
ESR
Increased plasma cells in
BM
Abdominal nodes
FH with narrow mantle
zones; dense interfollicular
plasma cells obscuring
sinus; 1/3 light chain
restriction!
Multicentric CD
Old age
Primary or associated with HIV/AIDS, KS
Histopathology similar to PCD
Assosiated with HHV-8, IL-6-----
systemic symptoms
60% POEMS syndrome
Poor prognosis
Sinus histocytosis
Common in nodes draining the limbs,
mesentery
Nodes draining carcinoma (breast ca, etc.)
Histocytes originate from the sinus lining
cells, which are derived from blood
monocytes
Rosai-Dorfman disease
Childhood and young adult
Fever, night sweats, weight loss, elevated ESR
Bilateral non-tender cervical lymphadenopathy
1/3 extranodal (skin, upper airways, bone)
Marked dilated sinus with histiocytes
Striking emperiopolesis
: S100+, CD1a-, CD207-
Whipples disease
Non-caseating
granulomas
Foamy macrophages
contain bacilli,
Tropheryma whippelli,
and characteristically
stain with PASD.

cystic spaces, sheets of macrophages replace


most of lymphoid tissue
Macrophages filled with PAS-positive bacilli PAS stain.
Vascular transformation of sinuses
Also called nodal
angiomatosis
Usually found incidentally
after resection of a nearby
tumor
Benign; all ages
Due to vascular obstruction
Sinus transformed into
vascular channels
DDx: KS
Infectious mononucleosis
lymphadenitis
Teenagers and young adults
FH, Paracortical expansion
Numerous B- and T-immunoblasts in
paracotex with mottled appearance
Atypical Hodgkin/RS-like cells, more
common in tonsils
EBER
Autoimmune lymphoproliferative syndrome (ALPS)

Due to mutations of genes in the Fas apoptosis pathway. Relatives may


carry mutations without overt evidence of disease

Disease usually presents in childhood and may ameliorate with age

Patients present with lymphadenopathy often accompanied by


hepatosplenomegaly

Patients usually have autoimmune disease at presentation. Autoimmune


cytopenias are the most common

Increased levels of double negative T-cells (CD4 CD8) are found in the
blood and tissues

Lymph nodes show marked paracortical expansion with T-cells/blasts and


polytypic plasma cells

Germinal centres usually prominent, may show progressive transformation

Increased incidence of T- and B-cell lymphomas and Hodgkin lymphoma in


relatives
CD3:T cells

CD20: B cells CD79a: B cells and plasma cells


Drug hypersensitivity
Most commonly seen in hypersensitivity
to anticonvulsant drugs (dilantin,
phenytoin, carbamazepine)
Fever, skin rashes, and
lymphadenopathy
PB eosinophilia
Paracortical expansion with mixed
immunoblast cells and eos.
Necrosis may present
Regress after drug withdrwal
Eosi abscess Immunoblasts and eosi
Toxoplasmosis lymphadenitis
Posterior cervical lymph node unilaterally
Triad:
a.Follicular Hyperplasia
b.small aggregates of epithelioid
histiocytes at the periphery of FC, often
encroach FC
c. monocytoid B-cell hyperplasia
subcapsular and trabecular sinuses
Typical Triad
Dermatopathic lymphadenitis
Superficial lymph nodes draining chronic
dermatoses
Cut surface of node may show subcapsular
rim of pigment
Paracortical expansion with aggregates of
interdigitating reticulum cells and
Langerhans cells
Scattered macrophages containing lipid
and melanin
Kikuchi Disease (histiocytic necrotizing
lymphadenitis)
Young female, asia
Fever and
painful cervical
LN
Widespread apoptosis and necrosis,
no neutrophils
Paracortical small lymphocytes,
immunoblasts, plasmacytoid
monocytes, histocytes, and plasma
cells
Phagocytic histiocyte---cresentic
nuclei
SLE
Non specific change
Follicular hyperplasia
Increased vasculartiy
Immunoblasts and plasma cells
DNA containing basophillic material
deposit in the stroma and wall of blood
vessel (hematoxylin body, DDx with
Kikuchis )
SLE
Cat scratch disease
Suppurative granulomas with stellate
microabscesses surround by pallisading
histiocytes
Background of FH---- early stage
Bartonella henselae----G+, Warthin-starry
silver stain (seen in early stage)
Lymphogranuloma venereum: similar
histology, by CT
area of stellate necrosis in a proven High power view: palisaded epithelioid
case of cat-scratch disease. histiocytes around an area of necrosis
Sarcoidosis
Non necrotizing granuloma
Asteroid body
Kimura Disease
Common in Asians, male
Neck and periauricular LN, may be matted
Blood eosinophlia
Florid follicular and GC hyperplasia with
proteinaceous precipitate (amorphous eosino.
material)
FDC IgE deposition
Paracortical: plasma cells, SL, and mast cells
Marked Eos. Infil. of GC, paracortex, and
medulla with microabscess
Warthin-Finkeldy type giant cells
There is follicular hyperplasia and massive perinodal infiltration, which is
predominantly composed of eosinophils.
Malignant LN pathology

Effacement of normal nodal architecture


Atypical cytology
Monoclonality
B cell lymphoma
Large (> histiocyte nucleus): high grade
Small (< histiocyte nucleus): low grade
Exceptions
T cell lymphoma
Size not useful for grading
Commonly variable size
Increased eosinophils, vasculatures
Clonality detected by molecular study (PCR or Southern Blot)

B cell Ig heavy chain and light chain gene rearrangement:


Sensitivity
SLL ~ 100 %, MCL ~ 100 %, DLBCL ~ 60 %, FL ~ 50 %
False negative?
o Chromosomal translocations into the IgH locus (in FLor DLBCL)
o Somatic hypermutation (in FL and DLBCL)
o Others

False positive? Limited amount of DNA, etc


Reactive clonal proliferation
T cell TCR gene rearrangement:
False positive or negative
Lineage infidelity of Ig and TCR gene rearrangements
Always interpreted in the context of other clinicopathologic information
Clonality detected by flow cytometry
Monotypic--Monoclonal
For mature B lymphoma: surface light chain

Examples:
Lymphoma: lambda restricted - Reactive, K/L: 0.9 ~ 3.7(?)

For mature T-cell lymphoma: TCR Vb subtypes ( 24 subtypes?


Not an easy test)
Loss of pan-T markers indicating malignancy
Nodular Pattern Sinus Pattern Diffuse Pattern Paracortical
Pattern
Follicular lymphoma LCH DLBCL (large cells) granulocytic
sarcoma
CHL, NS type Anaplastic Lymphoblastic lymphoma Anaplastic large
(Nodular pattern with large cell (medium size, starry sky) cell lymphoma,
fibrous bands, scattered lymphoma
large multilobated cells)
NLP HL (Vague nodular Metastatic Burkitts(medium size, NK-cell leukemia/
pattern with rare large cells lymphoma
with popcorn cells/LP cells)
tumors starry sky)
Small lymphocytic Kaposis CHL, MC (Diffuse infiltrate by CHL
lymphoma sarcoma a mixed inflammatory
(psedofollicular pattern) background)

Lymphoblastic rare DLBCL Anaplastic large cell peripheral T-cell


lymphoma lymphoma, lymphoma, NOS
(hallmark cells)
Marginal zone peripheral T- peripheral T-cell DLBCL
lymphoma cell lymphoma lymphoma (large cells or
variable size)
Some MC lymphoma non-hematopoietic metastatic tumors
tumors
How many faces, living creatures can you see?
A: diffuse infiltrate of large cells, seen in DLBCL, PTCL; B: diffuse lymphoid infiltrate
with numerous histiocytes, starrysky, Burkitt lymphoma, lymphoblastic lymphoma;
C: pseudofollicular pattern with small cells background, CLL/SLL; D: nodular pattern,
follicular lymphoma; E: nodular pattern with fibrous bands and scattered large
multilobated cells, NS classical Hodgkin lymphoma (HL); F: vague nodular pattern with
rare large cells with vesicular nuclei (popcorn cells, LP cells), NLPHL; G: paracortical
(interfollicular) infiltrate, PTCL, NOS, granulocytic sarcoma, CHL, anaplastic large cell
lymphoma, occasional DLBCL, metastatic tumors; H: expansion of the marginal zone with
prominent monocytoid B-cells, in marginal zone B-cell lymphoma; I: mantle zone pattern
mantle cell lymphoma (MCL), MCL can present also diffuse and nodular patterns;
J: onionskin mantle cells with more than one germinal center, Castlemans disease
(hyaline-vascular type); K: large expanded follicles composed of small lymphocytes with
disruption of the follicular dendritic meshwork, progressively transformed germinal
centers (PTGC); L: intrasinusoidal pattern, LCH, anaplastic large cell lymphoma,
metastatic non-hematopoietic tumors, rare DLBCL and variants PTCL; M: eosinophils,
increased vascularity, angioimmunoblastic T cell lymphoma; N: diffuse pleomorphic
infiltrate composed of a mixed population of lymphocytes, eosinophils, plasma cells and
histiocytes (inflammatory background) and large multilobated cells, CHL;
O: large mononuclear highly atypical cells predominate, anaplastic large cell lymphoma
should be considered;
Langerhans Cell Histiocytosis

Common in children
M>F(3.7:1)
Birbeck granules on
Electron microscopy
Single site or single system
multisysyem
Langerhans histiocytosis
Solitary or multiple lesions (papules, nodules, plaques) containining
Langerhans cells
Grooved histiocytes in the sinus
Multinucleated giant cells
Increased eosinophils
+: S100, CD1a, langerin / CD207
Common lymphomas in pediatric population
Lymphoblastic lymphoma
Hodgkin lymphoma
Burkitt lymphoma
Diffuse large B cell lymphoma
Anaplastic large cell lymphoma
Lymphoblastic lymphoma
One of the most common lymphomas in children
lymphoblastic lymphoma and Acute Lymphoblastic Leukemia (ALL)
represent the same disease entity based on morphologic, genetic,
and immunophenotypic features, the WHO classification has unified
these entities as B or T lymphoblastic leukemia/lymphoma.
Most institutes use >=25% blasts in PB or BM as the diagnostic
criterion for ALL though the distinction is not clearcut
Immature T in 85-90% of cases and immature B in the remainder.
No difference on morphologies of T or B origin.
Immunophenotyping and cytogenetics studies for classification and
subclassification
Typical flow cytometric findings for B-lymphoblastic lymphoma:
CD19+ CD10 bright, CD20+/, CD22+/, TdT+, HLA-DR+, CD34+/, slg;
T-lymphoblastic lymphoma: sCD3, but cCD3+, CD4+ CD8+ or CD4-
CD8, CD1a+/-, CD2+/, CD5+/, CD7+/, TdT+, CD34+/, CD10+/.
Lymphoblastic lymphoma

Infiltrates lymph node


leaving reticulin architecture
partially intact
Residual reactive
germinal centres may be
present
Infiltration of capsule and
around blood vessels
often shows Indian file
pattern
Smooth or dust-like
nuclear chromatin
Inconspicuous nucleoli or
one nucleolus
Cytoplasm inconspicuous
Nuclei may be convoluted

Mitotic figures frequent, numerous macrophages, starry- sky pattern


Burkitt Lymphoma

3 CLINICAL VARIANTS

ENDEMIC
SPORADIC
IMMUNOSUPPRESSED
ENDEMIC BURKITT LYMPHOMA
Africa
Children 4-7 y/o
Male
Malaria
Jaw/facial bones
95% EBV

Sporadic Burkitt lymphoma


adult median 30 y.o.
30-50% of childhood lymphomas
EBV positive cells in 30% of cases
Touch imprint. A Classical BL. The deeply basophilic cytoplasm can be appreciated as well
as abundant lipid vacuoles in the cytoplasm. B Atypical BL. The cells are relatively similar to

classical BL but have more irregular nuclei .


Immunophenotype and Molecular

Immuno
-Positive for CD20, CD10 & bcl-6
-Ki-67 100% of cells
-Neg for bcl-2, or weakly+ in 20%
Molecular
-T(8;14) IgH/myc
-T(2;8) myc/kappa
-T(8;22) myc/lambda
Diffuse Large B cell lymphoma
Common morphologic variant Other lymphomas of large B cells
-Centroblastic -Primary mediastinal (thymic)
-Immunoblastic
large B cell lymphoma
-Anaplastic
-Intravascular large B cell
Molecular subgroups lymphoma
-Germinal centre B cell like -DLBCL associated w chronic
-Activated B cell like inflammation
-Lymphomatoid granulomatosis
IHC subgroups -ALK-positive LBCL
-CD5+ DLBCL
-Plasmablastic lymphoma
-Germinal centre B cell like
-LBCL arising in HHV8+
-Non germinal centre B cell
like multicentric Castlemans
-Primary effusion lymphoma
Subtypes
-T cell/histiocyte-rich large B
cell lymphoma Borderline cases
-Primary DLBCL of the CNS
-Primary cutaneous DLBCL, leg type
-EBV + DLBCL of the elderly
Score 10 if the arrow hits center Germinal center type: CD10+
Score 5 if it hits Para-center zone Burkitt
No scores if it hits marginal zone Follicular lymphoma
Some DLBCL
AITL (GC T cells)

B Lymphoblastic Lymphoma

CD5+:
Mantle cell lymphoma
CLL/SLL
10 Rare DLBCL
5

CD10- CD5-:
0 Marginal zone lymphoma
HCL
others
Immunoblastic variant

Centrablast variant

Anaplastic variant
Lung, brain, liver, kidney skin
Grading based on # of EBV+ cells
Grade 1 <5 EBER+ per hpf
Grade 2 5-20 EBER+ per hpf
Grade 3 >50 EBER+ per hp

Immunodeficient Children or Adult


M:F>= 2:1
Hodgkin lymphoma

WHO classification:
- Nodular lymphocyte predominant
- Classical
Nodular sclerosis
Mixed cellularity
Lymphocyte-rich
Lymphocyte-depleted
Nodular Lymphocyte Predominant Hodgkin
lymphoma

Nodular, LP cells (popcorn cells)


Immunophenotype
CD45+, CD20+, J-chain and EMA+

CD3+ and CD57+ T-cells in background


ring malignant cells

Nearly all cases are CD15 & CD30 neg

Oct2 and BOB.1 consistently present


whereas in classic HL one or both will be
absent

5% HL
Common in young middle age male (30-50yo)
Classic Hodgkin lymphoma
-- 95% of HL with bimodal age with
15-35 year peak and 2nd peak late life
-- Mediastinal
Nodular Sclerosis Hodgkin lymphoma
Nodular pattern with fibrous bands and scattered large multilobated cells: nodular
sclerosis type of classical Hodgkin lymphoma (HL).

CD30+, CD15+ (75-85%); CD45 neg, LMP-1 and EBER variable, BSAP(PAX5)+
Mixed cellularity Hodgkin lymphoma (MCHL)

Interfollicular growth pattern may be seen


May have interstitial fibrosis but no capsular thickening or
broad bands of collagen fibrosis
EBV-LMP- highest frequently-75%
Mediastinal involvement uncommon
Lymphocyte rich Hodgkin lymphoma

5% of all HL
nodular growth pattern
Regressed germinal centers
RS cells in mantle zone
No eos + PMNs in background
Lymphocyte depleted Hodgkin lymphoma (LDHL)

Variable appearance with RS cells predominating over background cells


May resemble mixed cellularity with increased RS cells
May have a sarcomatoid appearance similar to anaplastic large cell lymphoma
May have diffuse fibrosis with few RS cells
ANAPLASTIC LARGE CELL LYMPHOMA (ALCL), ALK+
Definition: T-cell lymphoma consists of lymphoid cells with large
abundant cytoplasm and polymorphic, often horse-shoe-shaped nuclei.
These cells are CD30+ and most cases express cytotoxic granule-
associated proteins. ALK+

clinically:
-First three decades of life, M:F =1.5:1
-maybe nodal or extranodal
-B symptom
-aggressive, but excellent response to
chemo
pathologically:
- broad morphologic spectrum
- typically sinusoidal/subcapsular
-hallmark cells: eccentric, embryo-like,
reniform, wreath-like nuclei, eosinophilic
Golgi zone in cytoplasm, multiple nucleoli
-numerous variants:
common; small cell; monomorphic;
lymphohistiocytic; giant; sarcomatoid
ALCL, ALK+ common type

A: nodal architecture is obliterated by malignant cells and intrasinusoidal cells. B.


predominant large cells, hallmark cells; C. CD30, D. EMA, F. Granzyme B
Lymphohistiocytic variant
ALCL, ALK+
10%.
Tumor cells
admixed with a
large number of
histiocytes.
The histiocytes may
mask the malignant
cells which are
often smaller than
in the common type.
The neoplastic cell
clusters around
blood vessels and
can be highlighted
by CD30, ALK,
and/or cytotoxic
molecules.

Left: The neoplastic cells are difficult to identify: they are medium-sized to large, and possess distinct
nucleoli. The background is rich in small lymphocytes, histiocytes and plasma cells. Right:
Immunostaining for CD30 reveals a surprising number of neoplastic cells not appreciated on routine
microscopy.
ALCL, ALK+ Small cell type

5-10%.
Small to
medium-sized
neoplastic
cells with
irregular
nuclei.
Hallmark cells
are present
and often
around blood
vessels.
ALCL, ALK+

immunophenotypically:
-variable T-cell marker: CD3- (75%),
CD4+, CD2+, CD5+, CD8-, CD43+,
CD25+
-Cytotoxic associated antigens: TIA1,
granzyme B, perforin
- null-cell type: negative T- and B-
markers
- CD30+, EMA+

genetically:
- t(2;5)(p23;q35) by karyotype
-NPM (nucleophosmin):ALK fusion
- ALK on 2p23
Prognosis
- ~ 15% have partners other than
- Better than ALCLALK-
NPM: cytoplasmic and/or nuclear
ALCL, ALK-
Definition: CD30+ T-cell neoplasm, indistinguishable from
ALCL, ALK+ based on morphology. ALK-
Clinical:
Adults (40-65 yo), M:F =1.5:1
LN and extranodal involvement
Advanced stage, Lymphadenopathy, B symptoms
Morphology: similar to ALCL, ALK+
Immunophenotype:
CD30 strong positive, ALK-
Null T-cell type
CD43+; CD2+, CD3+; CD5+; CD4+
Cytotoxic associated markers: TIA1, granzyme B and/or perforin
Postulated normal counterpart:
Activated mature cytotoxic T-cell
Genetics: TCR rearrangement, chromosome abnormalities deffer from
ALCL, ALK+
Questions?
Email: pedhemepath@gmail.com