I Had a Blast

Hi again everyone!

Welcome back. Last month I talked about a colleague of mine, a fellow student who’s pursuing a career in pathology. The month before that I wrote a bit about Just Culture and how those of us in laboratory medicine ought to act as leaders for patient advocacy—especially when it comes to putting the needs of patients first. And in the spirit of progressing career timelines and fortuitous transitions, this month I want to talk about a place where Just Culture is tangible, where “patient come first” is a mission statement, and where I just spent the last month rotating in their Department of Laboratory Medicine and Pathology: The Mayo Clinic.

Image 1. Commemorative statue of the Mayo brothers in a park in front of the main building of the downtown campus at Mayo Clinic in Rochester, MN.

Before I go any further, if you haven’t seen the PBS Ken Burns’ documentary, I highly suggest you do; it’s fantastic. There are also a few excellent books on the hospital’s history and vision here and here. But back to the rotation: I can’t express how lucky I feel having spent time there or convey how much of a privilege it was to see pathology in a uniquely Mayo way. What I can do is try to talk a little bit about my experience and what that translates to regarding a culture of advocacy and collaboration; and I’ll share a case conference I presented on my last day in a topic I find fascinating.

Image 2. Ken Burns presents The Mayo Clinic: Faith, Hope, and Science on PBS, which aired September 2018.

Mission, Vision, and Values

As with any hospital, academic center, clinic, etc., you’re always going to have a driving philosophy that anchors the values of that particular institution. Some of my experiences in larger academic centers tout their strides at the forefront of medicine and translational research, others advertise that they treat the whole person body and spirit. Community hospitals sometimes lean into their integral part of, well, their communities as a center for trust and health. Sometimes institutions have specific populations to cater to or work intensely with industry and boast strong contributions to medical science. At the Mayo Clinic you’d be hard pressed to miss the message (in various forms) that “The Patients Come First”—in fact that line from many years ago comes from Dr. William Mayo delivering a commencement speech at a Rush Medical College graduation. (I was so happy to see so many Chicago-Mayo Clinic connections!)

Image 3. Dr. W. Mayo articulated the concept of patients’ “needs come first” in a graduation speech at Rush Medical College in Chicago on June 15, 1910.

It becomes very obvious that this culture of advocacy permeates into the daily proceedings there. The hospital makes a strong point to celebrate outreach, education, and research; and clinicians are given a cultivated environment in which to flex muscles of compassion for patient outcomes. It makes you a better clinician, and I argue, person. Everyone at this hospital has a voice and a seat at the table. I was continuously encouraged to interact with staff, clinicians, residents, fellows, and patients and contribute what I thought would benefit patient care. A unique perspective as a visiting medical student with previous MLS experience was both noted and celebrated.

Leadership in Pathology

In many of my pieces on this blog, I frequently discuss how we should champion active roles in testing stewardship, policy advocacy, and promoting positive patient outcomes. Granted, when you find yourself in larger, resource-rich, tertiary academic centers you can really push the envelope for progress. But generally, those of us on the ‘scopes operate in this margin between clinical medicine and translational research. Where does our leadership come in? What does it look like? I think it comes in the form of prolific contributions to societal guidelines and interdisciplinary work. Nowhere have I seen this more than my month in Rochester.

So many of their residents contributed abstracts and presentations at this year’s USCAP conference, some winning awards. The academic cycle of producing something great requires strong support from your home institution and that’s exactly what I saw. Not only were folks supported for their trips to conferences per usual, they were celebrated—hallway handshakes, accolades at morning conference, discussions post-meeting, and social media shares. Which, by the way, social media is now a leadership staple. You can’t go far in the present day without utilizing technology both inside and out of your practice. The Pathologist recently celebrated their first #TwitterPathAward for residents like Dr. Tiffany Graham at UAB for contributions to medical education and advocacy in pathology. Mayo clinicians, including residents, consultants, pathologist’s assistants, and more share case studies, educational material, and cutting-edge pathology news in terabytes! I now find myself increasingly active on social media representing pathology and interests within our field.

Image 4. A spring 2015 issue of The Pathologist discussed the increasing presence of pathology in social media and the trends of utilization for medical laboratorians abound.

Side note: I’ve followed a number of these social media pages about cases in pathology for a while, and when I was fortunate enough to be part of ASCP’s Top 40 Under Forty 2017, I connected with lots of awesome laboratorians. Some of which I got to meet this month! Including a fellow blogger on this site, some celebrated path assistants, and a prolific parasite-discussing clinical microbiologist.

Case Conference

So, my presentation was intense! I’ve given plenty of case reports and conference discussions before, but this was an opportunity for me to explore quite a rare case in genetics and connect it with my interests in hematopathology. This was a case of a patient with Li-Fraumeni Syndrome (LFS) who developed therapy-related Acute Myeloid Leukemia. It’s not a current case and has since been signed-out and closed, but I’ll only be talking about the pathologic entities involved.

Image 5. Remember that power of social media I mentioned earlier? Well, what better way to share information for other medical students interested in pathology and interested in visiting Mayo Clinic! Having my presentation grab an honorable mention amidst their productive and busy residents was great! #path2path #hemepath #lablogatory

Essentially, this patient was found to have Li-Fraumeni after the second manifestation of an acute sarcoma—the first being osteosarcoma in her teenage years and the second breast cancer in her 30s. Both cancer diagnoses were treated accordingly, and this patient was going through routine work-up for anemia before being referred to the Mayo Clinic. By the time the patient reached there, the clinical investigation included a battery of testing for causes of anemia—all within normal limits—so a bone marrow examination was performed which revealed a significant, though not acute (<20% blasts), myelodysplastic process. A follow-up in-house bone marrow collection revealed hypercellular marrow, now in acute myeloid proliferation, with abnormal myeloid cell maturation and very complex cytogenetics. She had a very complex karyotype and several detectable mutations which were consistent with the WHO’s classification and description of therapy-related myeloid neoplasm as a sequale to the treatments she received for her prior cancers. In the setting of a patient with LFS, it is almost impossible to avoid malignancy. The following slides are a (very abridged) summary taken from my presentation of this patient’s case:

Figure 1. Official LFS and AML discussion. As mentioned, this is the case of a patient with a history of osteosarcoma and breast carcinoma, both treated, now presenting status-post initial work-up for evaluating possible causes for anemia. Ultimately, when reaching a bone marrow examination, certain myelodysplastic features were discovered, referring this case for close investigation and expanding the differential to include various hematologic malignancies.
Figure 2. This bone marrow biopsy was evaluated at an outside institution and was reported to this patient’s case at Mayo Clinic. Note the presence of myeloid lineage blasts cells in the peripheral blood (PB) and bone marrow (BM) evaluations, however, at less than 20% this would not immediately indicate any acute myeloid crisis. There is a definitive left-shift in maturity with myeloid dysplasia.
Figure 3. This bone marrow evaluation was done about a month after the previous reported one. Note the significant increase in myeloid blasts present in both peripheral and bone marrow specimens. This time, there was significant dysplasia noted in multiple lineages as well as particular changes in granulocytic lines including left-shift and pseudo Pelger-Huet cells present. This diagnosis was upgraded from myeloid dysplasia to acute myeloid leukemia in the setting of myelodysplasia. The blast count has now crossed the 20% threshold and there are marked changes to morphology in several cell lines. Hypercellularity and cytogenetic testing were also highly contributory in this diagnosis. Not included in this slide but CD34+ cells that previously expressed CD15, CD33, and CD38 were now negative for those three markers. This indicates decrease in maturity and a poorer prognostic and clinical assessment of this malignancy.
Figure 4. A peripheral blood smear at the time of the second bone marrow specimen. In almost every field photographed, there were myeloid blast cells present. No Auer rods were seen, but many blasts had granules. There was left shift, and some immature granulocytes were present. Erythroid immaturity was demonstrated with morphology and circulating nucleated RBCs. Abnormalities in granulocytic lineages were present with hypogranular neutrophils and pseudo Pelger-Huet morphology.
Figure 5. At nearly any age, this bone marrow needle core biopsy on H&E stain would qualify as hypercellular. At low to medium power this is clearly evident. At higher powers, note the presence of predominantly immature granulocytes (with very few, if any, mature PMNs) as well as numerous blasts—on H&E blasts appear differently, but appreciate the increased number of cells with active nuclei, condensing chromatin, and prominent nucleoli.
Figure 6. Back to traditional hematology staining, you can still appreciate this bone marrow aspirate’s hypercellularity. There is a labeled megakaryocyte (which appears slightly abnormal) to scale against the numerous, immature and left-shifted granulocytes which overrun the fields. Myeloid blasts are seen in high numbers, with granules and prominent nucleoli. Increased levels of mitotic activity, abundant (and some abnormal) myeloid precursors, and a highly proliferative picture is appreciated.
Figure 7. Li-Fraumeni Syndrome (LFS) is a rare genetic predisposition to soft-tissue sarcomas. It is a germline mutation of either TP53 or CHECK2, more often the former. The mutation usually has an autosomal dominant inheritance pattern and has very high penetrance, more so in females (possibly due to the fact that the most common presentation of tumor formation in LFS is breast cancer). Note that this patient had a clinical history significant for both breast carcinoma and osteosarcoma which were treated with chemotherapy and radiation.
Figure 8a. Patients with LFS often have a germline mutation in p53, a very significant tumor suppressor gene, which is implicated in a wide host of cellular functions. Located on the short arm of Chromosome 17, when mutated this gene affects a myriad of pathways including cell senescence, growth cycle response, proliferation, DNA damage repair from mutations, epigenetic, or exogenous causes, and programmed cell death. If this downstream protection against severe DNA compromise is lost, this becomes a highly pre-cancerous environment for Knudsen’s “second hit” to negatively affect cells and ultimately lead to a vast array of malignancies.
Figure 8b. I mean just look! P53 is a serious player in cell survival and DNA damage recovery. It is the archetype example of a tumor suppressor gene and is implicated in an ever-growing number of cell survival and growth cycle pathways—of course a loss of p53 function would set the stage for high-risk.
Figure 9a. The World Health Organization (WHO) and its updated guidelines for diagnosing and addressing hematologic malignancies now includes a lot of new data regarding the molecular biology of cancer. Its applications to diagnostics in hematopathology are growing daily. In these guidelines, the WHO classify AML into seven general categories. For reasons relating to her clinical history of cancers and treatment, as well as the timeline she presented with, t-MN or therapy-related myeloid neoplasm would be an appropriate diagnosis.
Figure 9b. The American Society of Hematology (ASH) and the College of American Pathologists (CAP) co-wrote guidelines for the diagnosis of AML and published a number of recommendations in The Hematologist in 2017-2018. Essentially, proper laboratory test utilization and incorporation with significant clinical history is crucial. Staying organized and operating within WHO guidelines for hematologic malignancy diagnosis is just as important. The ASH/CAP guidelines tell diagnosticians to think about several key questions when approaching AML which further underscores the values of consistency, efficiency, and appropriate utilization.
Figure 10a. The reason for establishing a diagnosis of therapy-related AML is a significant one. The use of Topoisomerase II inhibitors, alkylating agents, antimetabolites, and radiation therapy all affect the genetic components relating to this particular leukemia. To correlate further, the patient had a 5q deletion, a complex karyotype, a history of receiving all treatments related to this entity, and a presentation of myelodysplasia which rapidly progressed to AML.
Figure 10b. LFS can cause leukemia on its own, AML can present as a hematologic malignancy on its own too; but this patient’s clinical history and treatment history lean the diagnosis away from de novo cancer to a myeloid process in response to a latent treatment effect.

Why All of This Matters

There are two main reasons why all of this is important enough to discuss in a case conference. First, as clinicians from the bench to the bedside we should all strive to talk through the toughest diagnoses and share with each other what best practices, lessons, and goals we can reach together. In the setting of Li-Fraumeni Syndrome it becomes critical to evaluate new onset (especially myeloid) neoplasms. TP53 mutations are associated with the lowest survival rates in acute myeloid leukemia, which has its own diagnostic and prognostic classifications set forth by the World Health Organization. Furthermore, understanding appropriate patient history, clinical information, and what appropriate lab investigation means is crucial. It not only keeps the needs and interests of the patient first, but also translates to the proper utilization of resources for the best results in the best timelines. Potential future implications of concurrent ongoing work in hematopathology and molecular genetics may yield therapeutic and diagnostic benefits we are not yet aware of—we must constantly include updates as we practice.

Second, this was an opportunity to share insights into the diagnosis and discussion of AML that came from my clinical experiences before rotating there. I previously mentioned the demonstrated value of including clinical viewpoints for the benefit of patient care outcomes, so appropriately I incorporated these topics into this case conference and included the following points to consider:

  • Hematologic premetastatic niches

When I was in graduate school at Rush University in Chicago, I did some research in hematopoietic responses to various therapies in the context of proliferation and understanding mobilization for transplant and engraftment. In this work, I became familiar with the concept of a reactive stroma and a “pre-metastatic niche.” There are small microenvironments in which hematopoietic, mesenchymal, and endothelial cell lines in the bone marrow thrive and develop which are full of cytokines and cell-cell interactions. My work focused on mobilizing all three lines with a CXCR4 target, but the concept holds true when considering germline and somatic mutability. In effect, those cells with pre-malignant mutations can cluster and affect the environment of other cells maturing in the same setting. The same way invasive cells can break through barriers to metastasize and spread past their in situ conditions, the same mobilizing spread can grow from pre-metastatic clusters. This, again, opens the discussion for treatment targets in future LFS and/or AML patients as molecular pathology expands.

  • Acute Myeloid Leukemia and Myeloid Sarcoma

In a recently published paper in Histopathology, I was part of a team at the UAB hospital’s department of pathology which discussed their experience with patients diagnosed with myeloid sarcomas (MS). The point was to look for correlations with MS to connect the entity with age, sex, location of tumor, AML status, genetics, etc. Ultimately, what became the highest predictor of disease was a complex karyotype, consistent with other concurrent literature. With respect to this patient, what if there was another soft tissue (or other location) sarcoma alongside her myelodysplastic picture. What if she had a low blast count, or hypocellular bone marrow, or necrosis/fibrosis, or had received G-CSF? Would AML with myeloid sarcoma be considered in this diagnostic setting, would myeloid sarcoma be something to worry about in her future or in her clinical history as a misdiagnosis? The take-home message would be to pay close attention to patient clinical history and stay both focused on the current diagnostic work-up but also open enough to avoid pitfalls in diagnostic challenges.

  • Misdiagnosis in clinical settings

In a case report from 2017 I discussed a patient who had bilateral lung nodules several years after being treated for breast carcinoma. It was initially thought to be relapse but was later correctly diagnosed as de novo peripheral T-cell lymphoma (PTCL). This could have very well been the same clinical scenario, with a different cell lineage. The lesson gleaned here is the same as those ASH/CAP guidelines: stay organized, consistent, and purposeful with your testing and investigation. What came down to a few immunohistochemical markers in this PTCL case could make all the difference in another case. Missing the clinical history and specific genetic mutations present in this LFS/AML patient could have led to a diagnosis of a myelodysplasia related AML instead of a therapy-related one, especially in the setting of such a severe germline pre-disposition.

  • Future plans for this patient

I thought it was ultimately important to discuss the patient’s future plans with the audience. In pathology we often sign-off after we sign-out. So, in order to make sure we emphasize the patient’s best interests moving forward from a poor prognostic diagnosis, we discussed her enrollment in a trial aimed at improving bone marrow donor matching based on HLA and KIR combination typing. This a relatively new and promising concept in the literature which I hold high hopes for.

If anything, this was something I learned last month: in order for you to call the quality of care the highest possible, you have to uphold many standards, both clinical and non-clinical. Clinically we all have to share with each other the latest and greatest in modern literature and advances in interdisciplinary or translational research. Aside from this, however, we have to keep each other human and connected to our patients. I never like to hear the stereotypes in pathology that place us in lab medicine miles away from patient care; instead, we do things every day that impact our patients’ lives greatly. And when we keep ourselves connected to that fact, like the philosophy at the Mayo Clinic, then we can boast our quality of care—from small community hospital to academic trauma center. Because its not the size of the lens on the scope, it’s the vast scope of impact we look through in a lens of compassion.

There you have it. That’s my month at Mayo and a case conference in a nutshell. It was a fantastic experience and I have to say it—I had a blast!

Thanks for reading, I’ll see you next time!

And have a Happy Lab Week 2019!

–Constantine E. Kanakis MSc, MLS (ASCP)CM graduated from Loyola University Chicago with a BS in Molecular Biology and Bioethics and then Rush University with an MS in Medical Laboratory Science. He is currently a medical student actively involved in public health and laboratory medicine, conducting clinicals at Bronx-Care Hospital Center in New York City.

Gastric Cancer: A Multidisciplinary Approach

Maryam Zenali1*, Dmitriy Akselrod2, Eric Ganguly3, Eswar Tipirneni4 and Christopher J. Anker5*

1 Department of Pathology, 2 Department of Radiology, 3 Division of Gastroenterology, and 5 Division of Radiation Oncology, The University of Vermont Medical Center (UVMMC), Burlington, VT and 4 Department of Hematology Oncology, Central Vermont Medical Center (CVMC), The University Of Vermont Health Network, Adult Primary Care, Berlin, VT

*corresponding authors

A 57 year old woman with a personal and family history of breast cancer presented with early satiety and dysphagia for 5 months. Her abdominal computed tomography (CT) scan (Image 1 A) showed marked thickening of an apparently featureless gastric wall (A, blue arrows indicating the mucosal [rightward pointing] and serosal [leftward pointing] aspects of the gastric wall). Prominent gastrohepatic lymph nodes were noted as well. Her fluoroscopic upper GI study (Image1 B), following administration of barium and effervescent crystals (a double contrast effect to allow for mucosal evaluation), showed thickened rugal folds (B red arrow) and pooling of barium within an antral ulcer (B blue arrow). A subsequent CT scan (Image 1 C) after administration of intravenous and enteric contrast, confirmed marked diffuse gastric wall thickening (C blue arrows again indicating the mucosal [rightward pointing] and serosal [leftward pointing] aspects of the gastric wall) (Image 1, composite radiographs A-C).

The gastric body distended poorly with insufflation and demonstrated thickened, erythematous, edematous folds with erosions (Image 2, endoscopy image). On endoscopic ultrasound, the total thickness of the stomach was 12 mm with expanded wall layers in the proximal stomach to the antrum and a thickness of 3.5 mm in spared areas. Biopsies were obtained; the corresponding H&E and keratin stains are provided (Image 3, composite photomicrographs A-B).

Image 1. Composite radiographs.
Image 2. Endoscopy image.
Image 3. Composite photomicrographs.

Based on the original radiographic imaging that led to the biopsy, what are the differential diagnoses?

Surgical Pathology Case Study: A 42 Year Old Woman with an Enlarging Mass of the Forearm

Case History

A 42 year old female with a history of neurofibromatosis, hypertension and Hashimoto’s thyroiditis had noted a mass on her forearm approximately 15 years ago. According to the patient, the mass did not change in size and did not cause her any discomfort during that time. Approximately 6 months prior to presenting to her primary physician, the mass began to increase in size and caused discomfort and pain. Upon examination with the Orthopedic Surgery department, a 20 x 20 cm firm, smooth mass on her forearm with mild pain on palpation was noted (Image 1). On MRI, the mass appeared to partially surround the radius and ulna, and encased the median, radial and ulnar nerves. A needle core biopsy was subsequently performed on the mass revealing a high grade malignant peripheral nerve sheath tumor (MPNST). A CT scan of the chest showed no evidence of metastatic disease. During her clinical visit, the use of neoadjuvant chemotherapy and chemoradiotherapy were discussed, but based on the large size of the mass, tumor response would have to be significant in order to allow for limb conserving surgery. At the time that the patient was seen, MPNSTs were not known to be chemosensitive and the chances of significant tumor response was very low (clinical drug trials have since shown some improvements in this area). In light of the poor response to systemic therapy of these tumors and the potentially toxic side effects of chemotherapy, the decision was made to proceed with amputation of the arm through the humerus.


Frozen sections were sent from all the major peripheral nerves, including the ulnar, radial and median nerves. There was no evidence of any tumor consistent with a high-grade MPNST, although there was evidence of neurofibromas. There were atypical cells with hyperchromasia in the ulnar nerve margin, however, this was not considered to be consistent with a high grade MPNST. Received in the surgical pathology lab was an above elbow amputation consisting of a 30.0 cm long distal arm, an attached hand measuring 17.0 cm in maximum length., and a 4.5 cm long exposed humerus. The specimen is covered by grossly unremarkable skin, with a palpable mass in the mid-portion of the forearm. Sectioning reveals an 18.0 x 12.0 x 11.0 cm well-circumscribed mass composed of bulging, myxoid, white-tan tissue with central areas of hemorrhagic degeneration and yellow-tan friable tissue (Image 2). The bulging white-tan tissue is mainly found peripherally and encompasses approximately two-thirds of the mass. The mass is confined to a thin translucent lining and does not grossly invade neighboring soft tissue or overlying skin. The radial, median and ulnar nerves are adjacent to but not invaded by the mass, although the distal aspect of the mass shares a translucent, myxoid-like tissue with the peripheral nerve sheath of the ulnar and median nerves.

In addition to the standard bone and soft tissue margins that are taken, representative sections of the mass with the closest approach to the overlying skin are submitted. Sections demonstrating the relationship of the distal mass to the radial, median and ulnar nerves are submitted in separate cassettes. Lastly, representative sections sampled from various areas of the mass are submitted in an additional 15 blocks.

Histologically, the tumor consisted of spindle cells arranged in a fascicular pattern with intermittent whorled areas. The cells contained pleomorphic, hyperchromatic nuclei and intervening myxoid hypocellular areas. Mitotic figures were observed with sparse areas of necrosis and hemorrhage. S-100 was ordered on the prior biopsy of the mass, which was weakly positive. Based on these findings, the specimen was signed out as a malignant peripheral nerve sheath tumor.

Image 1. Above elbow amputation with a large forearm mass.
Image 2. Longitudinal cross section of arm demonstrating a bulging, white-tan mass with areas of hemorrhage and necrosis.


Malignant peripheral nerve sheath tumors (MPNST) are locally invasive tumors that are associated with medium to large nerves (as opposed to cranial or distal small verves) and commonly recur with eventual metastatic spread. Common sites for metastatic spread include lung, liver, brain, bones and adrenals. They are usually found in adults between the second and fifth decades of life, and account for only 5% of malignant soft tissue tumors. Approximately half of MPNSTs will occur sporadically, with the other half generally arising in the setting of neurofibromatosis type 1 (such as in this case). There is a high clinical suspicion for MPNST if the patient has a history of neurofibromatosis type 1 or if the tumor arises within a major nerve component.

Grossly, MPNST will present as a large, poorly defined, fleshy tumor that runs along a nerve and involves adjacent soft tissue. Often, these tumors will have areas of hemorrhage or necrosis and can track along the length of a nerve. Histologically, the tumors are composed of monomorphic spindle cells arranged in fascicles, palisades and whorls, with compact comma-shaped, wavy or buckled hyperchromatic nuclei with alternating hypocellular foci. (Image 3 and 4). Mitotic figures and necrosis are common, and although S-100 is considered the best marker for MPNST, there is a lack of specificity and sensitivity for immunohistochemical markers. Due to the lack of immunohistochemical markers and molecular findings, as well as the variability associated with the cells, it has traditionally been difficult to diagnose MPNST. The differential diagnosis includes fibrosarcoma, monophasic synovial sarcoma, desmoplastic melanoma, and pleomorphic liposarcoma. Goldblum et al put forth the idea that a diagnosis of MPNST can be made if the tumor falls into any one of the following three categories:

  1. The tumor arises along a peripheral nerve
  2. The tumor arises from a pre-existing benign nerve sheath tumor, such as a neurofibroma
  3. The histologic features are consistent with a malignant Schwann cell tumor

Unfortunately, due to the aggressiveness of the tumor and high recurrence rate, MPNST has a poor prognosis with a 2 year overall survival rate of around 57% and a 5 year survival rate around 39%.

Image 3. Low power photomicrograph showing a spindle cell neoplasm arranged in a fascicular pattern.
Image 4. High power photomicrograph demonstrating spindle cells with hypercellular nuclei in a whorled arrangement and adjacent myxoid hypocellular areas.


  1. Case of the week #443. Pathology Outlines. http://www.pathologyoutlines.com/caseofweek/case443.htm. Published November 15, 2017. Accessed March 10, 2019.
  2. Frosch MP, Anthony DC, De Girolami U. Malignant Peripheral Nerve Sheath Tumor. In: Kumar V, Abbas AK, Fausto N, Aster JC. Robbins and Cotran Pathologic Basis of Disease, 8th edition. Philadelphia, PA: Elsevier, Inc. 2010: 1341-1342
  3. Guo A, Liu A, Wei L, Song X. Malignant Peripheral Nerve Sheath Tumors: Differentiation Patterns and Immunohistochemical Features – A Mini-Review and Our New Findings. J Cancer. 2012; 3:303-309. http://www.jcancer.org/v03p0303.html. Accessed March 9, 2019.
  4. Hirbe AC, Cosper PF, Dahiya S, Van Tine BA. Neoadjuvant Ifosfamide and Epirubicin in the Treatment of Malignant Peripheral Nerve Sheath Tumors. Sarcoma. https://www.hindawi.com/journals/sarcoma/2017/3761292/cta/. Accessed March 10, 2019.
  5. Ramnani, DM. Malignant Peripheral Nerve Sheath Tumor. WebPathology. https://www.webpathology.com/case.asp?case=499. Accessed March 9, 2019.
  6. Shankar V. Malignant peripheral nerve sheath tumor (MPNST). Pathology Outlines. http://www.pathologyoutlines.com/topic/softtissuempnst.html. Revised September 12, 2018. Accessed March 9, 2019.

-Cory Nash is a board certified Pathologists’ Assistant, specializing in surgical and gross pathology. He currently works as a Pathologists’ Assistant at the University of Chicago Medical Center. His job involves the macroscopic examination, dissection and tissue submission of surgical specimens, ranging from biopsies to multi-organ resections. Cory has a special interest in head and neck pathology, as well as bone and soft tissue pathology. Cory can be followed on twitter at @iplaywithorgans.

Hematopathology Case Study: A 39 Year Old Woman Presenting with Persistent Cough and Pericardial Effusion

Case history

The patient is a 39 year old woman presenting with a persistent cough. Upon work up, a pericardial effusion is noted. Pericardiocentesis is performed and a smear made from the pericardial fluid reveals atypical lymphoid cells.

Cytology of the Pericardial Fluid

Image 1. Pericardial fluid cytology showing reactive mesothelial cells surrounded by benign small lymphocytes and atypical large lymphocytes.

Additional imaging reveals an anterior mediastinal mass measuring 12.6 cm. Excision of the mediastinal mass is performed. Sections of mediastinal mass show a variable population of lymphoid cells ranging from small to medium lymphocytes and some atypical large lymphocytes. These atypical large lymphocytes have irregular nuclear contours with abundant cytoplasm, vesicular chromatin and prominent nucleoli. These atypical large lymphoid cells are consistent with Hodgkin Reed-Sternberg cells. Abundant eosinophilic and scattered neutrophilic infiltration are noted within the nodules. These nodules are surrounded by dense collagen bands.

Image 2. H&E sections showing small to medium sized lymphoid cells with scattered large Hodgkin Reed-Sternberg cells infiltrating through fibrosis (frozen section A) and inflammatory cells predominantly eosinophilic infiltration (B) Fascin (C) and CD30 (D) are positive for atypical lymphoid cells.

Immunohistochemistry studies are performed, atypical large lymphoid cells are positive for CD30, Fascin and PAX5, while rare small to medium sized lymphocytes are positive for CD20, however, large atypical lymphoma cells are negative for CD20. Tumor cells are negative for CD3, CD5, CD15, LCA, ALK and EBER ISH. CD3 and CD5 highlight the reactive T cells in the background.

Image 3. PAX5 is positive in some tumor cells.

Overall, the case is consistent with nodular sclerosis classic Hodgkin lymphoma.  The presence of sheets of large lymphoma cells is suggestive of the syncytial variant.


Nodular sclerosis classic Hodgkin’s lymphoma (NSCHL) subtype has a distinct epidemiology, clinical presentation and histology. NSCHL is more common in females with peak aged between 15 and 34 years. The risk is higher in high socioeconomic status. The patients are presenting with particularly mediastinal mass and 40% B symptoms.

NSCHL can be distinguished from the other subtypes of Hodgkin’s lymphoma (HL) with characteristic histologic features. There is a nodular growth pattern and the nodules are surrounded by collagen bands representing nodular sclerosis.  The lymphoma is composed of variable number of Hodgkin Reed-Sternberg (HRS) cells, small to medium sized lymphoid cells and non-neoplastic inflammatory cells, predominantly eosinophils, neutrophils and histiocytes. HRS cells have multinucleated or binucleated with irregular nuclear contours and prominent nucleoli. HRS cells induce fibroblastic activity by expressing IL-13 and the fibrosis begins in the lymph node by invaginating into the lymph node along vascular septa.

Immunophenotypically, the lymphoma cells are mostly positive for CD30 and 75-85% positive for CD15. Association with EBV can be demonstrated with EBER in-situ hybridization.  The malignant lymphocytes in NSCHL are variably expressing CD20, PAX5 and CD79a, however, T cell antigen markers, particularly CD4 and CD2 are aberrantly expressed in NSCHL.

NSCHL is classified mostly as grade 2 and the prognosis is better than the other subtypes of HL.  Doxorubicin, bleomycin, vinblastine and dacarbazine (ABVD) is the most frequent induction regimen for NSCHL patients with over 70% response rate.

Patients with Syncytial Variant Nodular Sclerosis Classic Hodgkin Lymphoma experience a lower than expected rate of complete therapeutic response with shorter progression-free than non-SV NSCHL treated with standard therapy. Syncytial Variant NSCHL should therefore be recognized as a high-risk subgroup within the otherwise traditionally docile NSCHL classification. This case fits the classic presentation for syncytial variant with presentation as bulky (mediastinal) disease.


  1. Eberle FC, Mani H, Jaffe ES. Histopathology of Hodgkin’s Lymphoma. Cancer J. 2009 Mar-Apr;15(2):129-37.
  2. Swerdlow SH, Campo E, Harris NL et al. WHO Classification of Tumors of Haematopoietic and Lymphoid Tissues (Revised 4th Edition). IARC: Lyon 2017.
  3. Sethi T, Nguyen V, Li S, Morgan D, Greer J. Differences in outcome of patients with syncytial variant Hodgkin Lymphoma compared with typical nodular sclerosis Hodgkin Lymphoma. Ther Adv Hematol 2017, Vol. 8(1):13-20.

Ayse Irem Kilic is a 2nd year AP/CP pathology resident at Loyola University Medical Center. Follow Dr. Kilic on twitter @iremessa.

Kamran M. Mirza, MD, PhD, MLS(ASCP)CM is an Assistant Professor of Pathology and Medical Education at Loyola University Health System. A past top 5 honoree in ASCP’s Forty Under 40, Dr. Mirza was named to The Pathologist’s Power List of 2018. Follow him on twitter @kmirza

Just Say Know! From Mentoring to High Performance: A Resident Perspective

As pathologists, we are responsible for increasingly intricate anatomic pathology and clinical laboratory services in a continually changing healthcare landscape that requires us to integrate emerging technologies for improved quality of medical care while also being hypervigilant to cost control and efficiency. Hospital systems working under managed care business models seek to expand their coverage networks and boost the number of patients served, and as such, it is going to be very critical for the next generation of pathologists to develop and implement the management skills and techniques necessary to effectively advocate for investment in their departments and meet such goals.

The problem, however, is that we are largely shielded from these issues during our undergraduate and even graduate medical education experiences. We focus, of course, on the basic sciences and clinical skills, which are undeniably important; however, we get significantly less instruction or discussion on functioning within our health care system, addressing quality issues, or general leadership training that is indispensable and highly valuable for practicing physicians.

Earlier in the summer, I saw a number of pathology folks on Twitter promoting and strongly encouraging residents to apply for the two-day “Just Say Know! From Mentoring to High Performance” program, formed through collaboration between ASCP and USCAP, on an approach to leadership, management, and business for pathology. I was highly intrigued and had a feeling this program was the sort of experience for which I had been looking. Traveling to Palm Springs in the middle of the Chicago winter was not a bad deal either!

Drs. Blair Holladay and David Kaminsky assembled an impressive collection of speakers for the weekend, which was divided into four focus areas: leadership, management, business and policy, and change. After an engaging introduction by Drs. Holladay and Kaminsky, current trainees Drs. Kabeer Shah and Melissa Hogan set the stage by highlighting the increasing importance of “management” and “leadership” as reflected in the ACGME milestones as well as recent literature suggesting expectations for newly-trained pathologists include these very skills (Post et al. Arch Pathol Lab Med 2017;141: 193-202).Above all, they encouraged all of the thirty residents and fellows in attendance to “be honest, be open, and be vulnerable,” and ask the tough questions of themselves to gain the most from the weekend.

Lotte Mulder from ASCP led an enlightening discussion on the differences between emotional intelligence (EI) and conventional IQ, as well as the critical need to be self-aware of how our emotions can affect our performance and to understand the extent of our own abilities, strengths, and weaknesses. Dr. Karen Kaul followed with a very timely overview of strategies for identifying mentors. She discussed how our mentorship needs will evolve over the course of our careers and that fulfilling the mentor role for another junior individual while having your own mentors is key to the professional development necessary in leadership positions.

 After lunch, Dr. Dan Milner from ASCP took us through some very interesting global health case studies that forced our group to think critically about the role of pathology and the clinical laboratory in underserved settings as well as the major obstacles and economic disparities that must be considered. There were a number of important teaching points from Dr. Milner’s international cases that will be equally helpful for understanding the disparities we encounter right here in our backyard.

Dr .Yael Heher led off the afternoon management focus series with a really comprehensive look into how she has championed quality improvement and patient safety reviews at her institution to address root causes for laboratory errors, followed by a well-timed interactive session in which we divided into groups to use the six sigma methodology to work in concrete steps through a real-life laboratory error. It was a great opportunity to see people from different institutions and backgrounds bring unique perspectives to a common problem. The first day of the program concluded with a very unique session on art and leadership in which Dr. Kaminsky led us into Downtown Palm Springs to view the Palm Springs Babies art installation set up by David Cerny. Our powers of observation as pathologists were put to the test as we were asked to describe and interpret the meanings behind the exhibit in the same way that we often use visual evidence in our day-to-day work.

The second day of the program focused on business and policy with talks by Dr. Gary Procop on how pathologists can help integrate interventions into the laboratory to improve system-level metrics and by Khosrow Shotorbani on how laboratory data can be used to optimize laboratory services in the model of the rideshare service, Uber. The morning also included an interactive session on negotiation skills, in which each of us assumed the roles of departmental chair and owner of a private practice group negotiating with newly-hired pathologists. The weekend concluded with Dr. Nathan Johnson’s 18 steps to make change a part of an organizational culture, which was based on his experiences in academic research, military operational theory, and real-life lab experiences.

The weekend provided an incredibly impactful and high-yield array of discussions, so much so that I am already finding myself applying many of the strategies and techniques described over the weekend in my role as chief resident as well as to some of the changes and initiatives that I am hoping to bring to our department. Most important, though, were the opportunities to interact with my peers from around the country. We all face similar challenges as residents, and the opportunity to learn each other’s perspectives and approaches to similar issues was just as illuminating as the structured portions of the program. I hope that the ASCP and USCAP continue to offer the Just Say Know! Program and enthusiastically join all those pathology folks on social media promoting the program last summer with my own strong recommendation to challenge yourself and be open to new ways of learning by considering participating in this event!

From Twitter, @Blair_Holladay, December 12, 2018
Photo by Imran Uraizee

-Imran Uraizee, MD, is currently chief resident and a third-year anatomic and clinical pathology resident at the University of Chicago. He also manages the Department of Pathology Twitter account, @UChicagoPath. He majored in Biology at Duke University before earning his MD at the University of Rochester School of Medicine and Dentistry. Dr. Uraizee can be followed on Twitter at @IUraizee3MD.

Dead Wrong About Forensic Pathology

(•_•)         ( •_•)>⌐■-■       (⌐■_■)

[Puts my sunglasses on dramatically]

[Won’t Get Fooled Again by The Who plays]

Image 1. Looks like this medical lab science blogger made quite the … shady… joke. CSI: Miami’s Lt. Horatio Caine (played by David Caruso) donned his shades at pivotal plot times. (Source: CBS)

Okay-okay, I couldn’t resist that. How many times have you just wanted a CSI-style joke on here? No? Just me? That’s fine…

Hello again everybody! Welcome back! Last month I talked a bit about “Just Culture,” a sort of bridge between the values we tout as clinical leaders in our laboratories and the medical culture’s evolving and value-informed paradigm shift. There was a little in there about the lessons paralleled in LMU and the benefits of interdisciplinary teamwork. This month, on the subject of interdisciplinary collaboration, I’d like to talk about our colleagues who often are secluded or in more remote areas in our hospitals, offices, and academic centers. Not here to stereotype; I’m talking about our friends in forensic pathology!

Before I get there, let me go back a bit. I’ve already written several times about the stereotypes that surround our field of lab medicine and there are two times when that is glaringly present: when you’re a medical student or when you’re in forensics. I got the chance to meet someone who falls into both categories.

I’ve just finished up my OB/GYN rotation. But before my last day, I went to the lab at our hospital and followed up on some pending biopsy results. Okay, I can’t lie to you guys: they wanted me to see if I could rush “my lab friends” to expedite the process of fixing, setting, cutting, staining, and reading/reporting—because that’s possible. So, I went to the lab and had a pleasant chat with the staff explaining the situation and they were happy to help. While I was there, however, I happened to see another short white coat (ironically from my same school) who was helping some lab personnel with some grossing. Turns out she wants to match into a pathology residency—just like me—and specifically was interested in forensic path, a field which I don’t know much about. After talking more, I asked if she’d like to share some information. Here’s my conversation with Kyla Jorgenson, a 3rd year medical student at AUC-SOM from Toronto, Canada:

I get lots of hassle when I say I want to become a pathologist. People often ask me, “what’s your back up choice” or “don’t you like patients?” It can be a challenge. What’s your experience been like?

You want to do autopsies, so you want to be a mortician, right? Not quite. Many times, I’ve been faced with blank stares when I say I want to be a forensic pathologist. Other times I get the other end of the spectrum, that’s so cool! Clearly, they’ve seen a few crime-shows and think that I’ll get to go to crime scenes in stiletto high heeled shoes with a song by The Who playing in the background as I arrive. Even today when talking with a dermatopathologist I got a, “well when you realize that hanging out with dead bodies every day isn’t the greatest, you might consider surg path.” Then after hearing my experience as an autopsy assistant and that I’m sure this is what I want to do it was the resigned sigh signalling that I was a lost cause already.

A “lost cause,” that’s frustrating. A lot of specialities rag on other ones, it seems to be part of the culture of medicine—hopefully not forever, but still can’t we all just get along?

So, my background leading to pathology involved me working for several years between college, graduate school, and medical school; in hospitals of various sizes. I have personal experiences in these fields and sort of feel “at home” when I’m dealing with hematopathology, transfusion medicine, cell therapy—that sort of thing. What piqued your interest in forensics?

I started my undergraduate degree in forensic biology at the University of Toronto in the fall of 2008 just as a major review of pediatric forensic pathology in Ontario was being released. After numerous issues came to light, the inquiry looked at policies, procedures, practices, accountability and oversight mechanisms, quality control measures and institutional arrangements within the field in Ontario from 1981 to 2001. Ontario Court of Appeal’s Honourable Justice Stephen T. Goudge developed 169 recommendations on how pediatric forensic pathology in Ontario needed to address and correct its systemic failings to restore public confidence.

(Read more about these inquiries here: https://www.attorneygeneral.jus.gov.on.ca/inquiries/goudge/index.html)

After studying the cases that prompted the inquiry and its recommendations in class, what left the greatest impression was the importance of having medicolegal autopsies performed by those trained in not just pathology, but specifically, forensic pathology. What I took away from the cases of accidental deaths falsely attributed as homicides due to lack of experience on behalf of the pathologist and other such issues, is that forensic pathology isn’t something to be dabbled in. While our patients are no longer alive, there are lives that can be affected by the work we do. In Ontario, false convictions not only stemmed from “junk science” but also from inadequacies in the training of pathologists working in a forensic capacity and also a general shortage of forensic pathologists.

Seems like a lot of us (of the few of us) who enter medical school knowing we want to go into pathology have to sort of wait their turn, as it were, collecting experiences which help make us competitive for residency matching—what keeps your “commitment algorithm” going?

Since discovering that forensic medicine is a career path as a high school student, I’ve geared my education towards training in forensics. First my undergraduate degree and then a side trip for my master’s degree in Forensic Death Scene Investigation and a job as a pathology technician at the Medical Examiner’s office on my way to medical school. I have in each step along the way, confirmed that both medicine and forensics fascinate me. Scroll through my Netflix account and you’ll find crime dramas (with the British shows being my favourite) or my podcast app filled with true crime shows; I am enraptured using science to figure out what happened.

Sidebar: at this point Kyla showed me a first-author published piece in the Journal of Forensic Sciences from 2017 that talked about law enforcement-involved firearm related deaths in Oklahoma, where she worked at the time. Basically, it showed through metadata analysis that gun-related deaths were on the rise. Not just over time, but number of times being shot. Remember when we talked about pathology’s role in the #StayInYourLane/#ThisIsOurLane discussion? Well which pathology speciality do you think works with this stuff directly? Chemistry? Cytology? Last time I checked GSWs don’t get screened for lead poisoning and you can’t FNA a bullet. Forensic pathology has often been tasked with seeing trends in morbidity and mortality and translating that to effective social and public health change: think seatbelts, stents, and maybe someday gun-related legislation changes.

Image 2a. Monthly aggregates of gun-related deaths over a 16-year period in OK. (Source: Jorgenson, K et al (2017) Trends in Officer-Involved Firearm Deaths in Oklahoma from 2000-2015, Journal of Forensic Sciences, doi: 10.1111/1556-4029.13499)
Image 2b. Number of gun shot wounds per victim over time. (Source: Jorgenson, K et al (2017) Trends in Officer-Involved Firearm Deaths in Oklahoma from 2000-2015, Journal of Forensic Sciences, doi: 10.1111/1556-4029.13499)

I was interested when I shadowed at the Cook County ME’s office a few years ago—I saw some cool things. I also remember learning a lot from the first real autopsy I saw in a hospital, ultimately it seems like a totally different field that maybe gets underappreciated even within the pathology umbrella. AP/CP residents have to do a certain number of autopsies to graduate, but the attitude I’ve noticed around the topic is a “necessary evil” and most are working towards not having to do that. So let me ask you definitively, why forensic pathology?

Medicine is science being applied to find out what happened in the body and how we can change or manipulate those variables to diagnose, prevent, treat and manage disease. Each diagnosis is solving a crime occurring within the cells in the body, if you will. In forensic medicine, not only do you get to do all that but add in the crime solving element and you get to be “Dr. Nancy Drew.” While medicolegal systems are different all over the US and Canada, chances are that as a forensic pathologist you won’t only be working on your stereotypical “forensics” cases, the gunshot wounds, stab wounds and other nefarious causes of deaths many associate with that term. You could get the generic, “cause of death atherosclerotic cardiovascular disease, manner of death natural,” for a large proportion of cases.

It’s not glamorous, you could spend your day with a two-week-old decomposing decedent that has a pulsating maggot mass devouring its torso or documenting 51 stab wounds or signing out your cases after reviewing your histology and toxicology reports or testifying on a homicide case you worked on. But for me, those all sound like pretty interesting ways to spend the day, sign me up. As a pathology technician assisting with the autopsies and external exams, I was never required to think about what was happening in the body, but I wanted to understand it all. Now as I progress through medical school and look towards residency and fellowship, I eagerly await the chance to perform my first autopsy as a physician, to put all the knowledge and experience I’ve gained towards helping move Ontario and forensic pathology forward.

Image 3. Kyla M. Jorgenson is a 3rd year medical student at the American University of the Caribbean School of Medicine with prior undergraduate and graduate studies in the field of forensic pathology, professional experience as an autopsy technician, as well as a vested interest in pursuing a career in the field moving forward in residency and fellowship. (Source: Kyla M. Jorgenson)

I’d like to thank Kyla for her time in talking with me and her willingness to share her insights with all of you. I wish her all the best of luck as she continues through her training with electives and core rotations both in the UK and state-side. If you have any questions to relay to her, please feel free to comment below and I will forward appropriately. And as always, don’t forget to share with your colleagues across every discipline!

Thanks for reading, I’ll see you next time where I’ll be writing from the Mayo Clinic Hospital in Rochester, Minnesota, conducting a formal rotation in Anatomic and Clinical Pathology! Don’t miss it, I’ll have lots to share while learning at one of the nation’s top institutions!

Until next time!

–Constantine E. Kanakis MSc, MLS (ASCP)CM graduated from Loyola University Chicago with a BS in Molecular Biology and Bioethics and then Rush University with an MS in Medical Laboratory Science. He is currently a medical student actively involved in public health and laboratory medicine, conducting clinicals at Bronx-Care Hospital Center in New York City.

Surgical Pathology Case Study: A 64 Year Old Man with History of Loose Stools and Abdominal Pain

Case History

A 64 year old male presented with a one year history of loose stools, lower abdominal crampy/gassy pain that improved with defection, and an unclear history of melena. A colonoscopy revealed a circumferential, villous, carpet-like lesion extending from 15 cm to the anal verge, with biopsies demonstrating fragments of a villous adenoma. A follow-up CT scan was negative for metastatic disease. The decision was then made to proceed with a low anterior resection with hand-sewn colo-anal anastomosis and diverting loop ileostomy.


Upon opening the rectum, a 13.8 cm long circumferential, carpet-like lesion is identified, extending to the distal margin (Image 1). Sectioning demonstrated a lesion with a maximum thickness of 1.0 cm, which grossly appears to be confined to the mucosa. Due to the prior biopsy history of a villous adenoma, the entire lesion was completely submitted. This required 116 blocks to be submitted, which were then mapped out to show where each block would have been taken from (Image 2). Although there were many foci of intramucosal carcinoma present, clear cut submucosal invasion was not identified, and the specimen was signed out as a villous adenoma (Image 3).

Image 1. Opened rectum demonstrating the 13.8 cm-long carpet-like lesion.
Image 2. Mapping the lesion to show from where each block is taken.
Image 3. Photomicrograph showing the transition from normal mucosa (black arrow) to villous adenomatous tissue (red arrow).


Polyps are an abnormal tissue growth that is a common occurrence within the colon, although they can also be found throughout the small intestine, stomach and esophagus. Polyps can be further classified as being neoplastic or non-neoplastic based on the histological pattern of the cells. The most common types of neoplastic polyps found within the GI tract are colonic adenomas, which are benign polyps that serve as precursors to the majority of colorectal cancers. Nearly half of adults in the Western world will develop adenomas by the age of 50, and there is no gender predilection. It is because of this that it is recommended that all adults get a colonoscopy by the age of 50 (even earlier when there is a family history of developing colorectal cancer).

Most polyps are small, measuring 0.5 cm or less, but can grow to be over 10 cm in size (as seen in this case). When a colonoscopy is performed, these polyps can appear as sessile, meaning flat, or pedunculated, meaning on a stalk. Due to the abnormal epithelial growth of the mucosa, the surface of an adenoma can have a velvety appearance, resembling that of a raspberry. Most patients will not demonstrate any symptoms from their polyps, with the exception of occult bleeding and anemia which are associated with larger polyps.

Dysplasia, which literally means “disordered growth”, occurs when the individual cells lose their uniformity and architecture, often resulting in cells with a hyperchromatic nuclei and a high nuclear to cytoplasmic ratio. The presence of dysplasia contained within the epithelium of a polyp is what classifies the polyp as an adenoma (Image 4). Based on their epithelial growth pattern, adenomas can be classified as either tubular adenomas or villous adenomas. Tubular adenomas tend to be smaller polyps, with a smoother surface and rounded glands on histologic examination. Villous adenomas, in contrast, tend to be larger polyps with long, slender villi noted on histology (Image 5). If an adenoma contains a mixture of tubular and villous elements, they are classified as tubulovillous adenomas. When a dysplastic cell is no longer contained within the epithelium, and instead breaches the basement membrane which separates the epithelium from the underlying tissue, it is termed invasive.

Image 4. Photomicrograph of the villous adenoma, demonstrating the dysplasia that is confined to the mucosa and not extending to the deeper tissue.
Image 5. Photomicrograph of the long, slender villi that are commonly seen in villous adenomas.

What makes this case so interesting is that there is a direct correlation between the size of an adenoma, and the risk of developing colorectal cancer. This is not true with most other cancers, however, as size plays no part in determining whether the tumor is cancerous or not. With colon polyps, the larger the polyp, the greater the chance of developing invasive carcinoma (i.e. cancer). This is why screening colonoscopies are so important. Studies have shown that regular colonoscopies, combined with the removal of the polyps found on the exam, reduce the incidence of colorectal cancer. Why this case is so interesting is that you could assume based on the size of this polypoid lesion, you would find some invasive component. However, after reviewing 116 blocks, not a single focus of invasion could be identified.

It should be stated that although there is a correlation between an adenomas size and the risk of developing cancer, the majority of adenomas will not progress to cancer, and in fact, there are no tools currently available that help to determine why one patient’s adenoma will progress to cancer, while another patient’s adenoma will not.


  1. Association of Directors of Anatomic and Surgical Pathology, adapted with permission by the American Cancer Society. Understanding Your Pathology Report: Colon Polyps (Sessile or Traditional Serrated Adenomas). cancer.org. https://www.cancer.org/treatment/understanding-your-diagnosis/tests/understanding-your-pathology-report/colon-pathology/colon-polyps-sessile-or-traditional-serrated-adenomas.html. Accessed February 14, 2019.
  2. Colon Polyps. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/colon-polyps/symptoms-causes/syc-20352875. Accessed February 14, 2019.
  3. Turner JR. Polyps. In: Kumar V, Abbas AK, Fausto N, Aster JC. Robbins and Cotran Pathologic Basis of Disease, 8th edition. Philadelphia, PA: Elsevier, Inc; 2010: 815-820

-Cory Nash is a board certified Pathologists’ Assistant, specializing in surgical and gross pathology. He currently works as a Pathologists’ Assistant at the University of Chicago Medical Center. His job involves the macroscopic examination, dissection and tissue submission of surgical specimens, ranging from biopsies to multi-organ resections. Cory has a special interest in head and neck pathology, as well as bone and soft tissue pathology. Cory can be followed on twitter at @iplaywithorgans.