An 18 year old
female with no significant past medical history experienced multiple episodes
of gastrointestinal bleeding over the course of a few weeks. The most recent
bout included a bloody episode that filled the toilet, for which she provided a
picture for the clinician. She denies any other associated symptoms including epigastric
pain, nausea, vomiting, fever, or chills. Her travel history is unknown.
her history reveals an unremarkable family and social history. She has never
had an incident similar to this in the past and no other family members have ever
complained of similar symptoms. Review of systems was unremarkable and within
normal limits. Physical exam was unremarkable. A rectal exam was performed and
was noted to have brown stool that was guaiac (occult blood) positive. Non
bleeding internal hemorrhoids were noted. There were no external hemorrhoids
Labs drawn including
CBC were within normal ranges with the exception of absolute eosinophils which
were at the upper limit of normal range at 0.6 x 103/µL [normal
range= 0.0 – 0.6 103/µL].
The patient had
an esophagogastroduodenoscopy (EGD) to further investigate the gastrointestinal
bleed. The exam was otherwise normal with exception of the ascending colon
where they noted a worm on the surface of the mucosa (Image 1-2). The worm was
collected and transported to microbiology for examination (Image 3-4).
the worm and eggs revealed morphology consistent with Trichuris trichiura, or whipworm.
T. trichiura is most prevalent in warm, moist
regions. The worldwide prevalence of infection is estimated to be roughly 800
million, mostly among poorer populations. Infection from T. trichiura is spread via fecal-oral route and caused by ingesting
embryonated eggs. This occurs when contaminated dirt is ingested or by consumption
of vegetables or fruits that have not been carefully cooked, washed or peeled.
The male and
female worms both have the long whip-like structures at the anterior end. T. trichiura worms are 30-50 mm in
length and the average life span is 1 year but they can live up to 10 years. The
females have a straight and thick head while the males have a curly ended head.
The males are typically longer the females. The eggs classically have barreled
shaped, brown eggs with thick shells that measure 50-55 µm long by 22-24 µm
wide. At each pole is lucent mucoid plug. The can also vary in size as noted in
female T. trichiura produces
1,000-7,000 eggs per day. The life cycle begins as unembryonated eggs passed in
feces into soil (Figure 1). It takes approximately 21 days in the soil for an
unembryonated egg to go through the process of embryonation to become the
infective form of the parasite. Once ingested, the embryonated eggs hatch in
the human intestine.
symptoms vary depending on the worm biomass present with most infections being asymptomatic.
Symptoms include cramping, weight loss, growth restriction in children, bloody
stool, and anemia. It can also result in Trichuris dysentery syndrome, which is
more common in children. Recurrent rectal prolapse has also been reported. Lab
findings include peripheral eosinophilia. T.
trichiura is treated with Albendazole for 5-7 days +/- Ivermectin. Our
patient was then prescribed albendazole and is being followed in GI clinic.
Procop, G. W.,
Church, D. L., Hall, G. S., Janda, W. M., Koneman, E. W., Schreckenberger, P.
C., & Woods, G. L. (2017). Koneman’s color atlas and textbook of diagnostic
microbiology (Seventh edition.). Philadelphia: Wolters Kluwer Health.
-Sharif Nasr, MD, 4th year anatomic
and clinical pathology resident at University of Chicago (NorthShore). Dr. Nasr
has an interest in GI pathology.
-Erin McElvania, PhD, D(ABMM), is the Director of Clinical
Microbiology NorthShore University Health System in Evanston, Illinois.
Follow Dr. McElvania on twitter @E-McElvania.
In 1939, the first issue of Marvel Comics introduced the original Human Torch, an android named
Jim Hammond who would burst into flames when exposed to oxygen. Fourteen years
before that, President Calvin Coolidge proclaimed the first National Fire
Prevention Week to commemorate the Chicago fire of 1871 which killed over 300
people 54 years earlier. In that entire span of 68 years, from 1871 to 1939,
over 17,000 people died in fires in the United States. Because of fire
awareness campaigns over the years, the number of home and work place deaths have
greatly decreased, and the risk of fire in your lab goes down when fire safety
awareness increases as well.
In the laboratory, fire safety begins with a look at the
physical environment. It is important to make sure the department is set up to
prevent a fire from starting and to keep one from spreading if a fire ignites.
The electrical wiring in the lab plays a large part in fire safety. Frayed
cords are the number one cause of laboratory fires, and daisy-chained extension
cords or multi-plug adaptors are fire hazards as well. Damaged outlets can also
present danger. Because equipment may move often in the environment, it is a
good idea to check for safety in the lab electrical set up regularly. In audits
I have performed this year alone, I have discovered three damaged electrical
cords just waiting to cause a fire. Things change rapidly in the lab physical
environment, so looking for these potential safety issues is vital.
The next aspect of the lab physical layout that needs
attention is flammable chemical storage. There are complicated regulations
about that, and multiple classes of flammable liquids, but you can simplify
storage rules to make it easy to understand. In general, there should be no
more than one gallon of a flammable liquid out in the lab per every 100 square
feet. If there are automatic sprinklers in the department, that amount can go
up to two gallons. If safety cans are used, the amount can be doubled again.
Any excess volume of flammable liquids should be stored inside of a flammable safety
cabinet with self-closing doors. Remember, the point of these storage limits is
so that if a fire occurs, there is not a large amount of flammable material in
one location. That slows the spread of the fire and allows automatic fire
extinguishing systems to be able to perform their job effectively.
Fire-fighting equipment should be available as well, and
staff are required to have training to use that equipment if it is available in
the department. The best training includes a regular hands-on return
demonstration and periodic fire drills. Making sure staff can use fire
extinguishers and know how to respond to a fire situation may be the one of the
most important safety training policies you can implement. Fire blankets are
typically not required per local fire code, but if they are in place, be sure
staff is aware of how to use them should the need arise.
The last actions in a departmental fire situation include
evacuating and preventing the spread of the fire. To that end, it is important
to keep aisles clear and wide for safe travel, and all exit routes and
stairwells should be checked to make sure no obstructions exist. Staff should
be aware of their primary and secondary evacuation routes, and all exits should
be adequately marked. Make sure employees know to close fire and smoke doors
during a fire situation.
Even in modern times there are structure fires in the work place, and unfortunately, laboratories are not excluded from that list. The Human Torch could catch fire and not get burned, but we all know that is science fiction, and burns from a fire are no joke. The best practice is to be prepared for a fire-provide training, conduct physical environment rounds, and run drills often. That will protect your staff and make you a true safety super hero.
–Dan Scungio, MT(ASCP), SLS, CQA (ASQ) has over 25 years experience as a certified medical technologist. Today he is the Laboratory Safety Officer for Sentara Healthcare, a system of seven hospitals and over 20 laboratories and draw sites in the Tidewater area of Virginia. He is also known as Dan the Lab Safety Man, a lab safety consultant, educator, and trainer.
When a patient gets their “testosterone test” at the doctor to assess their
libido, do they really know what they’re getting? Does your lab test for
testosterone, and are you confused about which of these confusingly-named tests
are in-house versus send-out? Do you need a refresher on the types of
testosterone tests out there and the clinical significance of each?
A Primer on Testosterone
Testosterone, being a fairly hydrophobic member of the steroid-ring family,
is the major androgen in males. Apart from its well-known function in promoting
the development of primary male reproductive organs and secondary male sex
characteristics, it also has important anabolic effects in maintaining muscle
mass, bone maturation, regulation of the hypothalamic-pituitary-adrenal axis
under stress, and even in promoting platelet aggregation through enhancing
platelet thromboxane A2 expression.1 In females, testosterone increases sexual arousal, and is in fact used
clinically as treatment for female sexual arousal disorders. So, clearly an
important member of the steroid family.
Being hydrophobic, much of the testosterone in the human body is not freely
available, but rather bound. Total testosterone signifies the total pool
of testosterone available in the human body, and is largely encompassed by the
majority of bound testosterone with a small (usually 1.5-2.0%)
proportion of free testosterone, which is biologically active. The bound
testosterone can further be subdivided into testosterone bound to sex-hormone
binding globulin (SHBG), a small glycoprotein that strongly binds various
androgens and estrogens, and testosterone bound toalbumin, which is a
relatively weak interaction.
Recently, the concept of bioavailabletestosterone has been
defined,2 based on the understanding that testosterone bound to SHBG (around 2/3rd
of the bound proportion) is relatively inaccessible, while testosterone bound
to albumin is weakly interacting, and thus potentially bioactive. Therefore,
the definition of bioavailable testosteroneincludes both free and
albumin-bound testosterone, which comprise the non-SHBG bound proportion.
How is testosterone measured?
Conventionally, total testosterone is measured through either immunoassays
(both radioimmunoassays, or more commonly, chemiluminescent immunoassays) or
mass spectrometry coupled with gas chromatography (GC/MS) or liquid
chromatography (LC-MS/MS). Isotope dilution mass spectrometry (IDMS) is the
reference method for testosterone measurement,3 but due to cost and convenience, most labs utilize immunoassays. Sex
hormone binding globulin (SHBG) is commonly measured through chemiluminescent
immunoassays, and also available for many platforms.4
There are two main approaches to the measurement of free testosterone,
which is significantly more challenging. The gold standard for free
testosterone measurement is equilibrium dialysis (see inset), a time consuming,
expensive, and laborious assay that uses semi-permeable membranes to measure
antibody-bound fractions of testosterone. Moreover, results can vary with pH,
temperature, and methods of dilution.5 Due to these complications, calculated free testosterone is an attractive
alternative used by many laboratories.
What is equilibrium
Equilibrium dialysis and ultrafiltration are reference methods used to
determine true free testosterone calculation. Briefly, a relatively large
quantity of serum (500 to 1000 uL) is placed in one chamber of an equilibrium
dialysis apparatus, which is comprised of two fluid chambers separated by a
semi-permeable membrane. Free-labeled testosterone passes through the
membrane, while testosterone bound to SHBG does not. The radioactivity in the
free chamber is quantified as a proportion of the total testosterone level,
as measured by another assay, such as LC/MS-MS.
What is calculated free testosterone, and how is it calculated?
Recognizing the difficulty of performing equilibrium dialysis on large volumes of testosterone specimens, several researchers have looked into devising good approximations of free testosterone through mathematical expressions modeling the distribution of testosterone among its various compartments. One of the most popular approximations, the Vermeulen equation developed by Dr. Alex Vermeulen,6 models the distribution of testosterone among the SHBG-bound, albumin-bound, and free component through association constants of testosterone among these compartments, and can be modeled by the equation in Figure 1, which depends on the total testosterone, SHBG concentration, and concentration of albumin (although this will be discussed below). The overall concordance of this method with apparent free testosterone obtained through equilibrium dialysis (AFTC), the reference method, is very good, with a correlation coefficient of 0.987 and mean values well within the SEM between the two methods.6
In studies of the variation of calculated free testosterone values to the
albumin concentration, Vermeulen et al. demonstrated that between “normal”
albumin concentrations ranging from 5.8–7.2 × 10−4 mol/L (40
to 50 g/L), the mean calculated free testosterone varied from 340 ± 40.9 pmol/L
assuming an albumin concentration of 40 g/L, to 303 ± 35.4 pmol/L assuming a
concentration of 50 g/L albumin. Moreover, the concordance of calculated FT
results to AFTC concentrations remained very good (correlation coefficient of
0.992) when an intermediate fixed albumin concentration (43 g/L) was used in
this calculation, compared to actual albumin levels. Overall, these
calculations suggest that for healthy individuals without marked abnormalities
in plasma protein composition, such as in nephrotic syndrome or cirrhosis of
the liver, or pregnant patients, a fixed albumin concentration could be used
without significantly affecting calculated FT results. Of course, in
individuals with marked changes in plasma proteins, the actual albumin
concentration should be accounted for.
Willem de Ronde et al5 compared five different algorithms for calculating free or
bioavailable, which includes the Vermeulen and Sodergard method (which use
similar parameters), as well as methods by Emadi-Konjin et al, Morris et
al, and Ly et al. In general, there was high concordance between the Vermeulen
and Sodergard methods (r=0.98) for measuring free testosterone, and lower, but
still reasonable (r=0.88) concordance between Vermeulen and other methods.
Fundamentally, the Vermeulen and Sodergard equations were derived from
experimentally derived association constants from the law of mass action, as
opposed to the other algorithms, which rely on experimentally derived free and
bioavailable testosterone measurements that was modeled by regression
equations, and thus depends on the accuracy of these measurements. Though the
experimental basis underlying the Vermeulen and Sodergard equations is
stronger, it is known that supraphysiologic concentrations of other steroid
hormones (estradiol or dihydrotestosterone), in competition for binding
sites to SHBG, can significantly underestimate free testosterone by any
of these methods. Of course, inaccuracies in the measurement of total
testosterone or SHBG can significantly affect results, as well as significant
perturbations in total serum protein concentrations (as mentioned above).
Since the publication of the above work, additional
calculations for free testosterone accounting for other modes of interaction of
SHBG such as allostery and dimerization have been published that may further
improve concordance with AFTC;7,8 however, further study is
needed to determine if these methods actually result in superior calculated FT
measurement for clinical decision making, as well as changes in sensitivity to
Why do accurate free testosterone measurements matter?
Testosterone bound to serum albumin is essentially inactive; therefore, the
only testosterone that is biologically relevant is free (and to a lesser
extent, bound to SHBG). Current consensus guidelines still support the use of
total testosterone for defining hypogonadism in men,9,10 although emerging studies and newer task-force consensus groups11,12 highlight an emerging role for both calculated and free testosterone
measurements in addition to total testosterone. The role of direct free
testosterone measurement is still hotly debated; a recent analysis of CAP
proficiency data indicates considerable heterogeneity among laboratories using
the reference methods described above, and suggests considerable cost savings
without significant loss of reliability can be achieved by using calculated or
FT bioavailable T over direct FT measurement.13 Further standardization of these assays is needed to better understand the
Ajayi A a. L, Halushka PV. Castration reduces platelet thromboxane A2
receptor density and aggregability. QJM. 2005;98(5):349-356.
Shea JL, Wong P-Y,
Chen Y. Free testosterone: clinical utility and important analytical aspects of
measurement. Adv Clin Chem. 2014;63:59-84.
Shacklady C, Cooper HC, et al. Isotope-Dilution Liquid Chromatography–Tandem
Mass Spectrometry Candidate Reference Method for Total Testosterone in Human
Serum. Clinical Chemistry. 2013;59(2):372-380.
Dittadi R, Fabricio
ASC, Michilin S, Gion M. Evaluation of a sex hormone-binding globulin automated
chemiluminescent assay. Scand J Clin Lab Invest. 2013;73(6):480-484.
Ronde W de, Schouw
YT van der, Pols HAP, et al. Calculation of Bioavailable and Free Testosterone
in Men: A Comparison of 5 Published Algorithms. Clinical Chemistry.
Verdonck L, Kaufman JM. A Critical Evaluation of Simple Methods for the
Estimation of Free Testosterone in Serum. None. 1999;84(10):3666-3672.
Zeinyeh W, Déchaud H, et al. Inverse relationship between hSHBG affinity for
testosterone and hSHBG concentration revealed by surface plasmon resonance. Molecular
and Cellular Endocrinology. 2015;399:201-207. doi:10.1016/j.mce.2014.10.002
Zakharov MN, Bhasin
S, Travison TG, et al. A multi-step, dynamic allosteric model of testosterone’s
binding to sex hormone binding globulin. Mol Cell Endocrinol.
Margo KL, Winn R.
Testosterone Treatments: Why, When, and How? AFP. 2006;73(9):1591-1598.
Association of Clinical Endocrinologists Medical Guidelines for Clinical
Practice for the Evaluation and Treatment of Hypogonadism in Adult Male Patients—2002
Update. Endocrine Practice. 2002;8(6):439-456. doi:10.4158/EP.8.6.439
Cunningham GR, Hayes FJ, et al. Testosterone therapy in men with androgen
deficiency syndromes: an Endocrine Society clinical practice guideline. J
Clin Endocrinol Metab. 2010;95(6):2536-2559. doi:10.1210/jc.2009-2354
Liu Z, Liu J, Shi
X, et al. Comparing calculated free testosterone with total testosterone for
screening and diagnosing late-onset hypogonadism in aged males: A
cross-sectional study. J Clin Lab Anal. 2017;31(5).
Morales A, Collier
CP, Clark AF. A critical appraisal of accuracy and cost of laboratory
methodologies for the diagnosis of hypogonadism: the role of free testosterone assays. Can
J Urol. 2012;19(3):6314-6318.
-Dr. Jim Hsu is a 2nd year pathology resident currently in training at Houston Methodist Hospital. After completing a M.D./Ph.D at the University of Texas Medical Branch in Galveston, he realized his passions remained in the lab, but wanted to bring that passion into patient care, and soon realized that pathology was the key to achieving both. His love for all things data drew him to pathology informatics, and with the suggestion of his mentor Dr. Wesley Long, to API. In particular, he is interested in the transformative power of data analysis in improving best practices, reducing error, and combating bias. Outside of the lab, he is interested in financial markets, algorithms, neuroscience, reading, and traveling (for the food, of course).
I first started in my
current lab back in 2008. At that time, we did not have a separate section for
testing solid tumors in our lab. The small amount of testing we did have were
for three different types of sarcomas, and we still used a thermal cycler that
didn’t have a heated lid, so we had to put mineral oil over the top of the
Fast forward eleven
years and we now have a “bench” dedicated to solid tumor testing with next
generation sequencing as a major part of this testing. We have been running our
current solid tumor assay, a hotspot panel of fifty genes, for almost five years
now and it has served us well. However, many of our oncologists have been
starting to ask for more. We have begun the search for a larger panel to
fulfill the needs of our oncologists and our patient population. As a smaller
lab, we are somewhat limited in resources and are not quite ready to go
completely custom, so we are left with kitted options from major vendors. As we
research and evaluate these options, though, certain questions come to light. These
panels have more than 150 genes and upwards of 500 genes in order to cover the
most relevant genes in a number of different cancers. The areas tested in these
genes are important for therapy and/or prognosis, but with the sheer number of
bases we are looking at, we are bound to find many variants that do not have a
So, question one, how
do the pathologists deal with trying to interpret the large number of variants
of unknown significance (VUS’s)? Currently, with our very limited 50 gene
panel, we may get one or two VUS’s, so it doesn’t take much time to assign
significance and sign out the report. Our myeloid panel, which is a larger
panel of 40 genes, some with full gene coverage, though, can sometimes result
in reports with eight to ten VUS’s. These reports take a lot of time to
research the potential impact each of these variants will have in the disease. I
have seen reports from some of these large gene panels that have upwards of 25
or more VUS’s detected in a single specimen. How are these handled in the pathologists’
workflow? Can time be taken to investigate each of these, or are they just
placed in a list in the report?
Question two, how do
the oncologists feel when they receive a report with few, if any, variants with
known significance, and many variants with unknown significance? Does this help
at all, or make it more difficult and frustrating? I’d be interested if anyone
has feedback in this area. In our internal tumor boards, when we review testing
done at other locations, a great deal of time is spent trying to filter through
the results to see how they can help point to the best possible treatment for
the patient. If the variants do not point to therapy or clinical trials, those
variants are not currently helpful.
Lastly, if and when we bring up a larger panel, do we keep running our smaller 50 gene panel? We believe the answer to this one is easy – yes. The amount of DNA needed for some of these larger panels is more than what we can get sometimes from the smaller biopsies. Also, insurance may not always cover the larger panels. The information we get from the 50 gene panel is still very useful and can point the oncologists to therapy options, as well as clinical trials, so we believe the smaller panel will still have a place in our lab.
-Sharleen Rapp, BS, MB (ASCP)CM is a Molecular Diagnostics Coordinator in the Molecular Diagnostics Laboratory at Nebraska Medicine.
An 80 year old man presented with rapid onset of cervical adenopathy over a period of few months. The largest lymph node measuring 6 cm was biopsied and sent for histopathological evaluation.
from the lymph node showed effacement of the lymph node architecture by a
fairly monotonous population of medium to large sized lymphoid cells arranged
in vague nodular pattern. Focally, a starry sky pattern was observed. The cells
were 1.5-2 times the size of an RBC, with high N:C ratio, irregular angulated
nuclei and small nucleoli. A high mitotic rate of 2-3 mitoses/hpf was seen.
stains showed that the lymphoma cells were positive for CD20, CD5, SOX-11, and
negative for Cyclin D1, CD10, CD23, CD30, BCL-1, and BCL-6. Ki67 index was
of Mantle cell lymphoma, pleomorphic variant was made.
lymphoma is a peripheral B cell lymphoma, occurring in middle aged or older
adults, with a male: female ratio of 7:1. Although Cyclin D1 expression is
considered a hallmark of mantle cell lymphoma, yet about 7% cases are known to
be Cyclin D1 negative. In these cases, morphological features and SOX-11
positivity helps in establishing a definitive diagnosis.
assessment of morphological features of lymphoma, the cell size is an important
starting point. In this case, the lymphoma cells ranged from medium to large
sized. The following differential diagnoses were considered:
This case showed a “starry sky” pattern focally. A medium sized
population of cells, high mitotic rate and a high Ki67 index (70%) favoured a
Burkitt lymphoma. However, although commonly seen in Burkitt lymphoma, a
“starry sky” pattern is not specific for this type of lymphoma. Also, the lack
of typical “squaring off” of nuclei, basophilic cytoplasmic rim were against
the diagnosis of Burkitt lymphoma. The nuclei in this case showed 0-1 small
nucleoli, unlike the typical basophilic 2-3 prominent nucleoli of Burkitt
lymphoma. Moreover, Ki67 index, even though high was not enough for Burkitt
lymphoma where it approaches 100%. The cells were negative for CD10 and Bcl-6, which
are almost always found in a Burkitt lymphoma. Hence, a diagnosis of Burkitt
lymphoma was ruled out.
Diffuse Large B cell Lymphoma
The presence of interspersed large cells with nucleoli, irregular
nuclei, high mitotic rate, and a high Ki67 index with a history of very rapid
enlargement of lymph node suggested a diagnosis of Diffuse Large B cell
lymphoma. However, the scant cytoplasm, lack of bizarre cells, and absence of
CD10, BCl-2, BCl-6 were against a diagnosis of DLBCL.
A diagnosis of lymphoblastic lymphoma was favoured by the irregularly
angulated nuclei, and presence of nucleoli. However, the cells of lymphoblastic
lymphoma have a more delicate nuclear chromatin, higher mitotic rate as against
the relatively condensed chromatin and the low to high variable mitotic rate of
Mantle cell lymphoma. Also, lymphoblastic lymphomas are more commonly of the T
cell subtype and occur commonly in younger individuals. In this case, B cell
markers were positive (CD 20), and the patient was 80 year old, disfavouring a
lymphoblastic lymphoma. The blastoid variant of mantle cell lymphoma is
practically indistinguishable from lymphoblastic lymphoma, except that it is
D1 negativity in Mantle cell lymphoma
cases of Cyclin D1 negative mantle cell lymphomas, morphology plays a critical
role in coming to a diagnosis of mantle cell lymphomas. In this case, points
that favoured the diagnosis of mantle cell lymphoma were clinical features such
as older age (80 years), and male gender, and morphological features such as a
vaguely nodular pattern of growth, irregular nuclei, and 0-1 small nucleoli.
Due to the presence of variably sized cells with distinct nucleoli, a
pleomorphic variant was considered. Even though Cyclin D1 was found to be
negative, the cells were positive for SOX-11.
SOX-11 is a
transcription factor that is not normally expressed in B cells, but is
sensitive and fairly specific for mantle cell lymphomas. It is important to
note that SOX-11 is also positive in 25% Burkitt lymphoma, 100% lymphoblastic
lymphoma, and 66% T-prolymphocytic leukemia. Herein lies the importance of
recognising morphological features, as all of these lymphomas that may express
SOX-11 were ruled on the basis of morphology. A more specific antibody, MRQ-58
may be used for greater specificity. The presence of SOX-11 is considered a
specific biomarker for Cyclin-D1 negative mantle cell lymphomas. In these
cases, there is upregulation of Cyclin D2 or D3 that may substitute for Cyclin
D1 upregulation. But, immunohistochemical detection of Cyclin D2 or D3 is not
helpful for establishing a diagnosis, as other lymphomas are commonly positive
for these markers. Hence, it is important to perform SOX-11
immunohistochemistry to diagnose the Cyclin D1 negative variant of mantle cell
be used not just for the diagnosis, but also for determining prognosis of
mantle cell lymphoma. Indolent MCL usually lack SOX-11 expression. The pattern
of SOX-11 staining has also been used a marker of prognosis. Cytoplasmic
expression of MCl, seen in only a few cases was associated with a shorter
survival as compared to the more common nuclear staining of SOX-11.
age, lymphoma diagnosis relies heavily on the use of immunohistochemical
markers. However, this case highlights the importance of morphological features
in diagnosing lymphomas with unusual immunohistochemical marker profile.
Although, this case was negative for Cyclin D1, considered a hallmark of Mantle
cell lymphoma, yet, the combination of morphological features with SOX-11
staining helped in clinching the diagnosis. To avoid a misdiagnosis, it would
be prudent to perform SOX-11 staining in all lymphoma cases morphologically
resembling MCL, but lacking Cyclin-D1.
-Swati Bhardwaj, MD has a special interest in surgical pathology and hematopathology. Follow her on Twitter at @Bhardwaj_swat.
–Kamran M. Mirza, MD, PhD, MLS(ASCP)CM is an Assistant Professor of Pathology and Laboratory Medicine, Medical Education and Applied Health Sciences at Loyola University Chicago Stritch School of Medicine and Parkinson School for Health Sciences and Public Health. A past top 5 honoree in ASCP’s Forty Under 40, Dr. Mirza was named to The Pathologist’s Power List of 2018 and placed #5 in the #PathPower List 2019. Follow him on twitter @kmirza.