Challenges and Opportunities in Pathology
Manan Christian
Department of Pathology, Maimonides Medical Center, 4802 10th Ave, Brooklyn, NY 11219
Jeremy Minkowitz, Elmer Gabutan, Eric Steimetz,Juan Coca-Guzman & Matthew R. Pincus
Department of Pathology, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203
Martin Bluth
Department of Pathology, Maimonides Medical Center, 4802 10th Ave, Brooklyn, NY 11219; Department of Pathology, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203
Abstract
We have performed stability studies on thyroid function tests, i.e., T4, T3, free T4, free T3 and thyroid stimulating hormone (TSH), over a five-day period on the sera of ten patients. We find that the levels for each analyte were stable; the mean coefficients of variation (CV) ranged from 3.2 % for TSH to 8.7% for T4. ANOVA statistical analysis of group means for each analyte over the five-day period indicated that there was no statistically significant difference in these means, confirming the reproducibility of values. On the other hand, the CVs are significantly larger than those found in our prior stability studies for other critical analytes such as electrolytes (sodium, potassium, chloride, calcium). In addition, significant variations in values over the five-day period occurred for T4 which showed the largest variations in values of the five analytes studied. In one patient, the values ranged from a low of <10 ug/dL to over 14 ug/dL over the five-day period. A two-tailed t test comparing the mean CV for TSH with the mean CVs of the other four analytes showed that the mean CV for TSH was statistically significantly lower than that for the other four analytes indicating that the assay for TSH yield the most precise results. These results parallel those obtained in our prior electrolyte study that showed very low CVs for sodium, potassium and chloride and a significantly higher CV for calcium. Since approximately half of total serum calcium is bound to albumin and since very high percentages of T4 and T3 (≥99%) are bound to thyroid binding globulin and albumin, protein binding of these analytes may introduce a possible source of assay imprecision.
Bernardica Jurić
Clinical Department of Pathology and Cytology “Ljudevit Jurak”, University Hospital Center “Sestre milosrdnice”, Zagreb, Croatia.
Monika Ulamec
Clinical Department of Pathology and Cytology “Ljudevit Jurak”, University Hospital Center “Sestre milosrdnice”, Zagreb, Croatia./ Department of Pathology and Center of Excellence for Reproductive and Regenerative Medicine, School of Medicine, University of Zagreb, Zagreb, Croatia.
Božo Krušlin
Clinical Department of Pathology and Cytology “Ljudevit Jurak”, University Hospital Center “Sestre milosrdnice”, Zagreb, Croatia./ Department of Pathology and Center of Excellence for Reproductive and Regenerative Medicine, School of Medicine, University of Zagreb, Zagreb, Croatia.
Melita Perić Balja
Department of Pathology and Center of Excellence for Reproductive and Regenerative Medicine, School of Medicine, University of Zagreb, Zagreb, Croatia./ Clinical Department of Pathology and Cytology “Ljudevit Jurak”, Tumor Oncology Clinic, University Hospital Center “Sestre milosrdnice”, Zagreb, Croatia.
Abstract
Breast cancer is the most common malignancy in women worldwide, and one of the leading causes of cancer death. This disease shows a significant heterogeneity due to its genomic and histological diversity. Breast cancer is classified by pathologic features (i.e. histological subtype, tumor grade) and gene expression profiles (i.e. molecular subtypes). There are complex mechanisms implicated in its progression and the development of chemotherapy resistance. In recent times, tumor stroma is increasingly being recognized as an important factor which influences tumor pathogenesis and progression. Tumor-stromal cells interactions are involved in many phases of tumor growth, by modulating different cellular processes. Tumor-infiltrating lymphocytes are proven to be clinically significant as they correlate with good prognosis, especially in triple-negative and HER2-positive breast cancer patients. However, tumor-infiltrating lymphocytes are just one of the many components of the tumor microenvironment, which includes fibroblasts, macrophages, adipocytes, vascular cells etc., but also non-cellular components. One of the main cellular components of the tumor microenvironment are the fibroblasts which are activated and differentiated into breast cancer associated fibroblasts. They secrete many growth factors, cytokines, and chemokines which influence tumor growth and dissemination. Tumor microenvironment could be a source of new biomarkers with a potential predictive and prognostic significance. This review highlights the tumor microenvironment as an important contributor to the process of cancer development with an overview of the main components and the potential impact on the prognosis of breast cancer. It’s important to expand our understanding and knowledge of tumor-stromal signalling processes which may lead to the development of more successful and individualized therapeutic strategies.
Natalia Zubieta-DeUrioste
Christian Arias-Reyes
Lida Sanchez
Nestor Freddy Armijo-Subieta
Alfredo Merino-Luna
Ivan Solarte
Raffo Escalante-Kanashiro
Jose Antonio Carmona-Suazo
Enrique Maravi Poma
Rosalinda Jimenez-Aguilar
Jose M. Calle-Aracena
Alberto Lopez-Bascope
Roberto Vera
Rafaela Zubieta-DeUrioste
Ninoska Rossel
Yeshua Peña-Y-Lilio
Gary Chambi-Quilla
Luis Herrera-Leon
Santiago Garrido-Salazar
Francisco Ney Villacorta Cordova
Fausto Vinicio Maldonado Coronel
Elisabeth Deindl
Ricki Sheldon
Roberto Alfonso Accinelli
Edith M Schneider-Gasser
Jorge Soliz
Gustavo Zubieta-Calleja
Abstract
The COVID-19 pandemic, caused by the SARS-COV-2 virus, has had devastating consequences worldwide. Remarkably, the incidence, virus transmission capacity, and severity of COVID-19 have been reported to be significantly decreased in high-altitude human populations. The clinical significance of these findings is enormous, as they suggest that permanent inhabitants of high altitudes have developed adaptive protective changes against certain pathologies. However, these observations have been overshadowed by contradictory reports on the COVID-19 mortality rate at high altitude, ascribed to low population densities. These interpretations, however, fail to consider that the environmental conditions of high-altitude regions of the temperate and tropical geographical zones are radically different from each other. Contrary to common thought, the conditions of high-altitude areas of countries within the tropical zone are so benign that they have favored the growth and development of densely populated cities. In this work, we use data from a COVID-19 database covering five Latin American countries in the tropical and subtropical geographic zone that corresponded to the period between the start of the pandemic and the end of 2020, when no vaccine was yet available. Our results reveal that residing above 1,000 m in tropical countries was a protective factor against COVID-19 mortality. Interestingly, this protective effect was independent of population size. The findings presented here, and those from other similar studies, substantiate the need for more research to reveal the secrets of the physiology of permanent high-altitude residents. In conclusion, our findings clearly demonstrate that the high-altitude environment in tropical and subtropical geographic zones significantly contributes to the decreased mortality impact of the SARS-COV-2 virus in high-altitude-exposed populations.
Snijders S, Sevenants R & Van Eerdenbrugh S
Dept. of Speech-Language Pathology, Thomas More University College, Belgium
Eggers K
Dept. of Speech-Language Pathology, Thomas More University College, Belgium; Dept. of Rehabilitation Sciences, Ghent University, Belgium; Dept. of Psychology and Speech-Language Pathology, Turku University, Finland
Abstract
Background: For long, a wait-and-see approach was implemented for preschool age children who started to stutter. The last two decades, however, research indicated more and more that this is not the most appropriate action. Speech pathologists specialised in stuttering have gained much knowledge about stuttering near onset the past few years. A previous exploratory study showed that primary care professionals have not yet gained all this knowledge.
Aims: The aim of this systematic review was to fill the knowledge gaps of primary care professionals by formulating evidence-based information and to provide them to the primary care professionals.
Methods: To find evidence-based information for the knowledge that the respondents lack, a systematic literature search was conducted on 24 October 2022 in Cochrane, PubMed and Evidence Maps (American Speech-Language-Hearing Association). Systematic reviews and guidelines of the past decade about stuttering in preschool age children were consulted. Relevant information was selected. Resources were developed and fine-tuned by a focus group. Quality assessments were conducted on all included studies by using the Joanna Briggs Institute tools for systematic reviews and the Appraisal of Guidelines for Research and Evaluation (AGREE II) for guidelines. Findings are presented on a poster, flyer, website and video.
Results: Eight systematic reviews and one guideline met the inclusion criteria and were used to create information materials. Findings are that the cause of stuttering is very complex and influenced by multiple factors. Characteristics of stuttering include repetitions, prolongations, and blocks, but stuttering can also affect social and emotional functioning. It is clear that a wait-and-see approach is not the desired approach anymore.
Conclusions: The resources developed in this study can help primary care professionals in identifying stuttering and referring families of young children to a stuttering specialist, to maximize the chance on recovery for the child. A stuttering specialist will decide based on the stuttering characteristics and its development if a family needs advice and active follow-up or if treatment needs to be initiated.
Gang Zhou
1. Ostrom QT, Gittleman H, Farah P, et al. CBTRUS statistical report: Primary brain and central nervous system tumors diagnosed in the United States in 2006-2010. Neuro-oncology 2013; 15 Suppl 2: ii1-56. Doi: 10.1093/neuonc/not151. 2. Thakkar JP, Dolecek TA, Horbinski C, et al. Epidemiologic and molecular prognostic review of glioblastoma. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2014; 23: 1985-1996. DOI: 10.1158/1055-9965.EPI-14-0275. 3. Korja M, Raj R, Seppa K, et al. Glioblastoma survival is improving despite increasing incidence rates: a nationwide study between 2000 and 2013 in Finland. Neuro-oncology 2019; 21: 370-379. Doi: 10.1093/neuonc/noy164. 4. Miranda-Filho A, Pineros M, Soerjomataram I, et al. Cancers of the brain and CNS: global patterns and trends in incidence. Neuro-oncology 2017; 19: 270-280. Doi: 1093/neuonc/now166. 5. Stupp R, Mason WP, van den Bent MJ, et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. The New England journal of medicine 2005; 352: 987-996. Doi: 10.1056/NEJMoa043330. 6. Visser O, Ardanaz E, Botta L, et al. Survival of adults with primary malignant brain tumours in Europe; Results of the EUROCARE-5 study. European journal of cancer 2015; 51: 2231-2241. DOI: 10.1016/j.ejca.2015.07.032. 7. Davis L. Spongioblastoma Multiforme of the Brain. Ann Surg 1928; 87: 8-14. 8. Pasquier B, Pasquier D, N’Golet A, et al. Extraneural metastases of astrocytomas and glioblastomas: clinicopathological study of two cases and review of literature. Cancer 1980; 45: 112-125. 9. Anzil AP. Glioblastoma multiforme with extracranial metastases in the absence of previous craniotomy. Case report. Journal of neurosurgery 1970; 33: 88-94. Doi: 10.3171/jns.1970.33.1.0088. 10. Anghileri E, Castiglione M, Nunziata R, et al. Extraneural metastases in glioblastoma patients: two cases with YKL-40-positive glioblastomas and a meta-analysis of the literature. Neurosurgical review 2016; 39: 37-45; discussion 45-36. Doi: 10.1007/s10143-015-0656-9. 11. Schweitzer T, Vince GH, Herbold C, et al. Extraneural metastases of primary brain tumors. Journal of neuro-oncology 2001; 53: 107-114. DOI: 10.1023/a:1012245115209. 12. Hoffman HJ and Duffner PK. Extraneural metastases of central nervous system tumors. Cancer 1985; 56: 1778-1782. DOI: 10.1002/1097-0142(19851001)56:7+<1778::aid-cncr2820561309>3.0.co;2-i. 13. Figueroa P, Lupton JR, Remington T, et al. Cutaneous metastasis from an intracranial glioblastoma multiforme. Journal of the American Academy of Dermatology 2002; 46: 297-300. DOI: 10.1067/mjd.2002.104966. 14. Lun M, Lok E, Gautam S, et al. The natural history of extracranial metastasis from glioblastoma multiforme. Journal of neuro-oncology 2011; 105: 261-273. DOI: 10.1007/s11060-011-0575-8. 15. Han SR, Yoon SW, Yee GT, et al. Extraneural metastases of anaplastic oligodendroglioma. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 2008; 15: 946-949. Doi: 10.1016/j.jocn.2006.09.013. 16. Piccirilli M, Brunetto GM, Rocchi G, et al. Extra central nervous system metastases from cerebral glioblastoma multiforme in elderly patients. Clinico-pathological remarks on our series of seven cases and critical review of the literature. Tumori 2008; 94: 40-51. Doi: 10.1177/030089160809400109. 17. Romero-Rojas AE, Diaz-Perez JA, Amaro D, et al. Glioblastoma metastasis to parotid gland and neck lymph nodes: fine-needle aspiration cytology with histopathologic correlation. Head and neck pathology 2013; 7: 409-415. Doi: 10.1007/s12105-013-0448-x. 18. Huang P, Allam A, Taghian A, et al. Growth and metastatic behavior of five human glioblastomas compared with nine other histological types of human tumor xenografts in SCID mice. Journal of neurosurgery 1995; 83: 308-315. Doi: 10.3171/jns.1995.83.2.0308. 19. Zustovich F, Della Puppa A, Scienza R, et al. Metastatic oligodendrogliomas: a review of the literature and case report. Acta neurochirurgica 2008; 150: 699-702; discussion 702-693. DOI: 10.1007/s00701-008-1507-z. 20. Tuettenberg J, Grobholz R, Korn T, et al. Continuous low-dose chemotherapy plus inhibition of cyclooxygenase-2 as an antiangiogenic therapy of glioblastoma multiforme. Journal of cancer research and clinical oncology 2005; 131: 31-40. Doi: 10.1007/s00432-004-0620-5. 21. Taha M, Ahmad A, Wharton S, et al. Extra-cranial metastasis of glioblastoma multiforme presenting as acute parotitis. British journal of neurosurgery 2005; 19: 348-351. DOI: 10.1080/02688690500305506. 22. Kraft M, Lang F, Braunschweig R, et al. Parotid gland metastasis from glioblastoma multiforme: a case report and review of the literature. European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies 2008; 265: 709-711. DOI: 10.1007/s00405-007-0499-2. 23. Frank S, Kuhn SA, Brodhun M, et al. Metastatic glioblastoma cells use common pathways via blood and lymphatic vessels. Neurologia i neurochirurgia polska 2009; 43: 183-190. 24. Mentrikoski M, Johnson MD, Korones DN, et al. Glioblastoma multiforme in skin: a report of 2 cases and review of the literature. The American Journal of dermatopathology 2008; 30: 381-384. Doi: 10.1097/DAD.0b013e31817532c4. 25. Gururangan S, McLaughlin CA, Brashears J, et al. Incidence and patterns of neuraxis metastases in children with diffuse pontine glioma. Journal of neuro-oncology 2006; 77: 207-212. DOI: 10.1007/s11060-005-9029-5. 26. Nager GT. Gliomas involving the temporal bone clinical and pathological aspects. The Laryngoscope 1967; 77: 454-488. Doi: 10.1288/lary.1967.000770403. 27. M T, Stephenson, Corinne, Y, Shan, Bui, Marilyn. Cytological Diagnosis of Extracranial Extension of Glioblastoma to Scalp. ASCP Case Reports 2013; 41: 13140. DOI: 2.1.3466.3041. 28. McGovern PC, Lautenbach E, Brennan PJ, et al. Risk factors for postcraniotomy surgical site infection after 1,3-bis (2-chloroethyl)-1-nitrosourea (Gliadel) wafer placement. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2003; 36: 759-765. Doi: 10.1086/368082. 29. Shi M and Sanche L. Convection-Enhanced Delivery in Malignant Gliomas: A Review of Toxicity and Efficacy. Journal of oncology 2019; 2019: 9342796. Doi: 10.1155/2019/9342796. 30. Duffy PE, Graf L and Rapport MM. Identification of glial fibrillary acidic protein by the immunoperoxidase method in human brain tumors. Journal of neuropathology and experimental neurology 1977; 36: 645-652. Doi: 10.1097/00005072-197707000-00001. 31. Stoyanov GS, Petkova L, Iliev B, et al. Extracranial Glioblastoma Metastasis: A Neuropathological Case Report. Cureus 2023; 15: e35803. Doi: 10.7759/cureus.35803. 32. Ogungbo BI, Perry RH, Bozzino J, et al. Report of GBM metastasis to the parotid gland. Journal of neuro-oncology 2005; 74: 337-338. DOI: 10.1007/s11060-005-1480-9. 33. Alhoulaiby S, Abdulrahman A, Alouni G, et al. Extra-CNS metastasis of glioblastoma multiforme to cervical lymph nodes and parotid gland: A case report. Clinical case reports 2020; 8: 1672-1677. Doi: 10.1002/ccr3.2985. 34. Swinnen J, Gelin G, Fransis S, et al. Glioblastoma with extracranial parotid, lymph node, and pulmonary metastases: a case report. Radiology case reports 2019; 14: 1334-1347. Doi: 10.1016/j.radcr.2019.08.011. 35. Schwock J, Mirham L and Ghorab Z. Cytology of Extraneural Metastases of Nonhematolymphoid Primary Central Nervous System Tumors: Six Cases with Histopathological Correlation and Literature Update. Acta cytologica 2021; 65: 529-540. Doi: 10.1159/000517480.
Tao L Wan
1. Ostrom QT, Gittleman H, Farah P, et al. CBTRUS statistical report: Primary brain and central nervous system tumors diagnosed in the United States in 2006-2010. Neuro-oncology 2013; 15 Suppl 2: ii1-56. Doi: 10.1093/neuonc/not151. 2. Thakkar JP, Dolecek TA, Horbinski C, et al. Epidemiologic and molecular prognostic review of glioblastoma. Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2014; 23: 1985-1996. DOI: 10.1158/1055-9965.EPI-14-0275. 3. Korja M, Raj R, Seppa K, et al. Glioblastoma survival is improving despite increasing incidence rates: a nationwide study between 2000 and 2013 in Finland. Neuro-oncology 2019; 21: 370-379. Doi: 10.1093/neuonc/noy164. 4. Miranda-Filho A, Pineros M, Soerjomataram I, et al. Cancers of the brain and CNS: global patterns and trends in incidence. Neuro-oncology 2017; 19: 270-280. Doi: 1093/neuonc/now166. 5. Stupp R, Mason WP, van den Bent MJ, et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. The New England journal of medicine 2005; 352: 987-996. Doi: 10.1056/NEJMoa043330. 6. Visser O, Ardanaz E, Botta L, et al. Survival of adults with primary malignant brain tumours in Europe; Results of the EUROCARE-5 study. European journal of cancer 2015; 51: 2231-2241. DOI: 10.1016/j.ejca.2015.07.032. 7. Davis L. Spongioblastoma Multiforme of the Brain. Ann Surg 1928; 87: 8-14. 8. Pasquier B, Pasquier D, N’Golet A, et al. Extraneural metastases of astrocytomas and glioblastomas: clinicopathological study of two cases and review of literature. Cancer 1980; 45: 112-125. 9. Anzil AP. Glioblastoma multiforme with extracranial metastases in the absence of previous craniotomy. Case report. Journal of neurosurgery 1970; 33: 88-94. Doi: 10.3171/jns.1970.33.1.0088. 10. Anghileri E, Castiglione M, Nunziata R, et al. Extraneural metastases in glioblastoma patients: two cases with YKL-40-positive glioblastomas and a meta-analysis of the literature. Neurosurgical review 2016; 39: 37-45; discussion 45-36. Doi: 10.1007/s10143-015-0656-9. 11. Schweitzer T, Vince GH, Herbold C, et al. Extraneural metastases of primary brain tumors. Journal of neuro-oncology 2001; 53: 107-114. DOI: 10.1023/a:1012245115209. 12. Hoffman HJ and Duffner PK. Extraneural metastases of central nervous system tumors. Cancer 1985; 56: 1778-1782. DOI: 10.1002/1097-0142(19851001)56:7+<1778::aid-cncr2820561309>3.0.co;2-i. 13. Figueroa P, Lupton JR, Remington T, et al. Cutaneous metastasis from an intracranial glioblastoma multiforme. Journal of the American Academy of Dermatology 2002; 46: 297-300. DOI: 10.1067/mjd.2002.104966. 14. Lun M, Lok E, Gautam S, et al. The natural history of extracranial metastasis from glioblastoma multiforme. Journal of neuro-oncology 2011; 105: 261-273. DOI: 10.1007/s11060-011-0575-8. 15. Han SR, Yoon SW, Yee GT, et al. Extraneural metastases of anaplastic oligodendroglioma. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia 2008; 15: 946-949. Doi: 10.1016/j.jocn.2006.09.013. 16. Piccirilli M, Brunetto GM, Rocchi G, et al. Extra central nervous system metastases from cerebral glioblastoma multiforme in elderly patients. Clinico-pathological remarks on our series of seven cases and critical review of the literature. Tumori 2008; 94: 40-51. Doi: 10.1177/030089160809400109. 17. Romero-Rojas AE, Diaz-Perez JA, Amaro D, et al. Glioblastoma metastasis to parotid gland and neck lymph nodes: fine-needle aspiration cytology with histopathologic correlation. Head and neck pathology 2013; 7: 409-415. Doi: 10.1007/s12105-013-0448-x. 18. Huang P, Allam A, Taghian A, et al. Growth and metastatic behavior of five human glioblastomas compared with nine other histological types of human tumor xenografts in SCID mice. Journal of neurosurgery 1995; 83: 308-315. Doi: 10.3171/jns.1995.83.2.0308. 19. Zustovich F, Della Puppa A, Scienza R, et al. Metastatic oligodendrogliomas: a review of the literature and case report. Acta neurochirurgica 2008; 150: 699-702; discussion 702-693. DOI: 10.1007/s00701-008-1507-z. 20. Tuettenberg J, Grobholz R, Korn T, et al. Continuous low-dose chemotherapy plus inhibition of cyclooxygenase-2 as an antiangiogenic therapy of glioblastoma multiforme. Journal of cancer research and clinical oncology 2005; 131: 31-40. Doi: 10.1007/s00432-004-0620-5. 21. Taha M, Ahmad A, Wharton S, et al. Extra-cranial metastasis of glioblastoma multiforme presenting as acute parotitis. British journal of neurosurgery 2005; 19: 348-351. DOI: 10.1080/02688690500305506. 22. Kraft M, Lang F, Braunschweig R, et al. Parotid gland metastasis from glioblastoma multiforme: a case report and review of the literature. European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies 2008; 265: 709-711. DOI: 10.1007/s00405-007-0499-2. 23. Frank S, Kuhn SA, Brodhun M, et al. Metastatic glioblastoma cells use common pathways via blood and lymphatic vessels. Neurologia i neurochirurgia polska 2009; 43: 183-190. 24. Mentrikoski M, Johnson MD, Korones DN, et al. Glioblastoma multiforme in skin: a report of 2 cases and review of the literature. The American Journal of dermatopathology 2008; 30: 381-384. Doi: 10.1097/DAD.0b013e31817532c4. 25. Gururangan S, McLaughlin CA, Brashears J, et al. Incidence and patterns of neuraxis metastases in children with diffuse pontine glioma. Journal of neuro-oncology 2006; 77: 207-212. DOI: 10.1007/s11060-005-9029-5. 26. Nager GT. Gliomas involving the temporal bone clinical and pathological aspects. The Laryngoscope 1967; 77: 454-488. Doi: 10.1288/lary.1967.000770403. 27. M T, Stephenson, Corinne, Y, Shan, Bui, Marilyn. Cytological Diagnosis of Extracranial Extension of Glioblastoma to Scalp. ASCP Case Reports 2013; 41: 13140. DOI: 2.1.3466.3041. 28. McGovern PC, Lautenbach E, Brennan PJ, et al. Risk factors for postcraniotomy surgical site infection after 1,3-bis (2-chloroethyl)-1-nitrosourea (Gliadel) wafer placement. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2003; 36: 759-765. Doi: 10.1086/368082. 29. Shi M and Sanche L. Convection-Enhanced Delivery in Malignant Gliomas: A Review of Toxicity and Efficacy. Journal of oncology 2019; 2019: 9342796. Doi: 10.1155/2019/9342796. 30. Duffy PE, Graf L and Rapport MM. Identification of glial fibrillary acidic protein by the immunoperoxidase method in human brain tumors. Journal of neuropathology and experimental neurology 1977; 36: 645-652. Doi: 10.1097/00005072-197707000-00001. 31. Stoyanov GS, Petkova L, Iliev B, et al. Extracranial Glioblastoma Metastasis: A Neuropathological Case Report. Cureus 2023; 15: e35803. Doi: 10.7759/cureus.35803. 32. Ogungbo BI, Perry RH, Bozzino J, et al. Report of GBM metastasis to the parotid gland. Journal of neuro-oncology 2005; 74: 337-338. DOI: 10.1007/s11060-005-1480-9. 33. Alhoulaiby S, Abdulrahman A, Alouni G, et al. Extra-CNS metastasis of glioblastoma multiforme to cervical lymph nodes and parotid gland: A case report. Clinical case reports 2020; 8: 1672-1677. Doi: 10.1002/ccr3.2985. 34. Swinnen J, Gelin G, Fransis S, et al. Glioblastoma with extracranial parotid, lymph node, and pulmonary metastases: a case report. Radiology case reports 2019; 14: 1334-1347. Doi: 10.1016/j.radcr.2019.08.011. 35. Schwock J, Mirham L and Ghorab Z. Cytology of Extraneural Metastases of Nonhematolymphoid Primary Central Nervous System Tumors: Six Cases with Histopathological Correlation and Literature Update. Acta cytologica 2021; 65: 529-540. Doi: 10.1159/000517480.
Bing Leng
Department of Pathology, Baylor Scott & White Health, 2401 S. 31st. St. MS-01-266 Temple, TX 76508
Frank Yuan Shan
Department of Pathology, Baylor Scott & White Health, 2401 S. 31st. St. MS-01-266 Temple, TX 76508
Abstract
Glioblastoma multiforme (GBM) is a WHO grade 4 primary brain tumor with a recalcitrant and dismal prognosis and a 14-month-median survival time. The extracranial spread of GBM is so rare that historically it was not believed to spread outside of the central nervous system (CNS). Since the first extracranial spread of GBM was described in 1928, more cases have been reported. However, the mechanisms have yet to be elucidated due to the rareness of well-documented cases. Here, we reported two cases of GBM with postoperative extracranial spread and reviewed related literature.
Shabnam Seydafkan
Department of Pathology, SUNY Downstate Medical Center, 450 Clarkson, Brooklyn, NY 11203.
Hagar Atia
Department of Pathology, SUNY Downstate Medical Center, 450 Clarkson, Brooklyn, NY 11203.
Bo Lin
AdventHealth, Department of Pathology, 301 Memorial Medical Pkwy, Daytona Beach, FL 32117, USA.
Matthew R. Pincus
Department of Pathology, SUNY Downstate Medical Center, 450 Clarkson, Brooklyn, NY 11203.
Abstract
In a prior study of the occurrence of prostate cancer in a unique population of African American patients many of whom have West Indian ancestry, we found that seventy percent of patients screened for prostate were found to have this disease and that, of the seventy percent diagnosed with prostate cancer, 70 percent were found to have high-grade (Gleason score ≥ 7) disease. Overall, therefore, high-grade prostate cancer was found in over 50 percent of all cancers diagnosed, a rate of occurrence that was significantly higher than the corresponding ones for other demographic populations. Since the average age for screening was 65, the same as in other demographic groups, we conjectured that earlier screening of our patients might eliminate many of these high-grade tumors. To validate this hypothesis, we have now examined the rates of occurrence of high-grade prostate cancers in successive age groups, i.e., 40-<50, 50-<60, 60-<70, 70-<80 and >80. Surprisingly, we found that, already in the 50-<60 age group, the frequency of occurrence of high-grade cancers is >50%. (The number of patients in the 40-<50, i.e.,12 and >80, i.e., 6, were too small to be accurately evaluated.) Since the high rate of high-grade cancer occurs in the 50-<60-year group, we conclude that screening for prostate cancer should be performed on our patients at significantly earlier ages such as 40-<50. Also, in view of the expectation that high-grade tumors would increase with increasing age, a second unexpected finding was that the percentage of high-grade tumors was statistically the same at >50 percent in the 50-<60, 60-<70 and 70-<80 age groups. This result could be explained if there was a concurrent increase in low-grade tumors occurring in older patients suggesting that continued, persistent screening is necessary even in advanced age groups. We further found that the mean Gleason score of the 50-<60 and 60-<70 age groups is statistically the same, suggesting that the high-grade tumors are “stable”. However, there is a statistically significant increase in Gleason scores between the 70-<80 age group and the two lower age groups which is associated with a large increase in Gleason 9 cancers in the 70-<80 age group and a concurrent, marked decrease in Gleason 7 cancers, suggesting significant recurrent progression of high-grade tumors in this age group.
Teodonno Francesca
Department of Orthopaedic Surgery, Hospital Universitario Fundación Jiménez Díaz, Madrid.
García Maya Beatriz
Department of Orthopaedic Surgery, La Paz University Hospital, Madrid. Spain. Bone and Soft Tissue Sarcoma Unit.
Moriel-Garceso Diego
Department of Orthopaedic Surgery, La Paz University Hospital, Madrid. Spain. Bone and Soft Tissue Sarcoma Unit.
Peleteiro-Pensado Manuel
Department of Orthopaedic Surgery, La Paz University Hospital, Madrid. Spain. Bone and Soft Tissue Sarcoma Unit.
Barrientos-Ruiz Irene
Department of Orthopaedic Surgery, La Paz University Hospital, Madrid. Spain. Bone and Soft Tissue Sarcoma Unit.
Pozo- Kreilinger Jose J
Department of Pathology and Histology, La Paz University Hospital, Madrid. Spain.
Dominguez Franjo Purificación
Department of Pathology and Histology, Hospital Ruber Intenacional, Madrid. Spain.
Ortiz-Cruz Eduardo J
Department of Orthopaedic Surgery, Hospital Universitario Fundación Jiménez Díaz, Madrid. ; Department of Pathology and Histology, La Paz University Hospital, Madrid. Spain. ; Department of Pathology and Histology, Hospital Ruber Intenacional, Madrid. Spain.
Abstract
Mazabraud’s syndrome is a condition that combines fibrous dysplasia with of single or multiple intramuscular myxomas, which etiology remains relatively unknown.
We present three cases of this uncommon disease. All patients received marginal resection of their symptomatic myxomas, with histopathological confirmation of the lesions after surgery and follow-ups of more than one year.
Mazabraud’s syndrome corresponds to a very rare disease. The management of these patients should be focused on the treatment of symptoms and avoidance of complications. Fracture risk is to be studied and treated if necessary.
Conclusions:
This disease is probably underestimated. It’s important to report cases in order to advance in the knowledge of this syndrome.
Hanan M Garalla, MBChB, MSc, PhD
Department of Pathology, Fac-ulty of Medicine, Benghazi University, Libya
Ahmed G.Y. Elsayed
Cosultant of pathology, Tobruk Medical Center, Tobruk, Libya.
Abstract
Background: Colorectal carcinoma (CRC) is the most common and one of the main causes of mortality and morbidity globally among gastrointestinal tract tumors. A benign polyp is the first step in the multistage pathogenesis of colorectal cancer, which eventually progresses to an adenoma and a carcinoma. Wnt/ βeta-catenin signaling pathway plays an initiating and rate-limiting role in colorectal tumorigenesis.
Aim of the work: To evaluate the association between the immunohistochemistry (expression of E-cadherin, and β-catenin with the histopathological grade, and stage of colorectal cancer.
Materials and Methods: The study was retrospectively collected from the archives of the Department of Pathology in Tobruk Medical Center. Eighty-two histopathologically confirmed cases of adenomas (n = 48) (tubular, villous, and tubulovillous), and colorectal adenocarcinoma (Mucinous, and Non-mucinous) (n = 34) were included in this study over two years (2021-2023). The histopathological diagnosis, grade, and staging of the tumors were obtained. While clinical information was obtained from medical records and pathology reports. immunohistochemical staining was performed for all the cases using E-cadherin and β-catenin antibodies, and the results were analyzed.
Results: A total of 82 patients were studied out of these, 51(62.2%) patients were male, whereas 31 (37.8%) were females with a male: female ratio of 1.6:1. Age ranged from 30 years to 80 years. The mean age was the mean age of 52.9 (SD±15.8). A high prevalence of adenoma cases was observed in the age group 30– 40 years. The peak incidence for both types of colorectal carcinoma was in 61-70 years. By scoring the intensity of β-catenin there are significant correlation of β-catenin expression with tumor grade, stage, lymph node metastasis, and types of adenomas. The intensity of staining of E-cadherin in 48 cases of adenomas was showing high expression in 39 cases (81.3%), and low expression in only 9 cases (18.7%). While, the majority of the patients with CRC (58.8%) had low expression of E-cadherin levels, and (41.2%) had high expression.
Conclusion: Our findings imply that E-cadherin and β-catenin may contribute to the invasion and progression of colorectal cancer, which may serve as prognostic indicators for colorectal carcinoma
PRERNA GHODKE
Private Practitioner
SHARAYU DHANDE
Assistant Professor, Sinhgad Dental College and Hospital, Department Of Periodontology and Oral Implantology
RASHMI HEGDE
Professor M A Rangoonwala College of Dental Sciences and Research Centre, Pune Department of Periodontology and Oral Implantology
AJIT KOSHY
Professor and Head of the Department, Department Of Oral Pathology and Microbiology M A Rangoonwala College of Dental Sciences and Research Centre, Pune
AMISHA SHAH
Professor, Department of Oral Pathology and Microbiology M A Rangoonwala College of Dental Sciences and Research Centre, Pune
PRACHI BALDAWA
Reader, Department of Oral Pathology and Microbiology M A Rangoonwala College of Dental Sciences and Research Centre, Pune.
Abstract
Background: Plasma cell gingivostomatitis belongs to a group of uncommon benign inflammatory conditions characterised by macular lesions that are bright red, velvety, sharply circumscribed, flat to slightly elevated in nature. Intra-oral lesions can manifest as dense band-like gingival enlargements with plasma-cystic infiltrate seen in the histo-pathological sections. The present case report highlights findings of atypical plasma cell gingivostomatitis further managed through clinical, radiological, histopathology, immunohistochemistry, hematological analysis and treated with surgical periodontal therapy.
Method: Intra-oral periodontal parameters were assessed followed by non-surgical periodontal therapy. In the later phase, internal bevel gingivectomy carried out and approximated with interrupted sutures. Furthermore, gingivoplasty with a 810nm diode laser, for better adaptation of gingival margins was performed. The patient was recalled for follow-up visits at regular intervals and results were maintained.
Result: Intra-oral histopathological sections revealed plasma cell gingivitis whereas hematological reports were suggestive of anemia. Gradual follow up showed reduced gingival inflammation. Post-surgical wound healing was satisfactory. Disappearance of extraoral induration was highlighting feature in the post-operative phase.Further patient was recalled for follow-up visits at regular intervals and results were found to be maintained.
Conclusion: The overall gingival condition was seen to be improving at the follow-up visits. The authors thus conclude that the case of plasma cell gingivitis treated by comprehensive periodontal therapy showed satisfactory results at 3 years follow-up and no recurrence in extra-oral findings was noted.
Tommaso Susini, MD, PhD
Head, Breast Unit, Gynecology Section, Department of Health Sciences, University of Florence, Italy.
Irene Renda & Milo Giani
Breast Unit, Gynecology Section, Department of Health Sciences, University of Florence, Italy.
Vania Vezzosi, Gianna Baroni & Simonetta Bianchi
Pathology Unit, Department of Health Sciences, University of Florence, Italy.
Abstract
Background: Collagen type XI, alpha 1 (COL11A1) is a minor component of extracellular matrix and its overexpression is associated with tumoral progression and poorer outcome in several human cancers; data on breast cancer are promising but scarce. FGD3 expression has been shown to be a strong independent prognostic factor in breast cancer. The aim of our study was to investigate whether COL11A1 expression correlates with other classic pathologic prognostic factors including FGD3 expression, as well as with clinical outcome, to evaluate its potential use as prognostic factor in breast cancer patients.
Methods: We evaluated by immunohistochemistry COL11A1 expression and we studied the relationship between this protein expression and traditional breast cancer prognostic factors, FGD3 expression, as well as with patients’ outcome.
Results: We found that higher stromal COL11A1 expression was associated with higher tumour grade (G3) (p = 0.001), higher Ki67 proliferation index (p = 0.006), more advanced AJCC stage (p = 0.031) and lower FGD3 expression (p = 0.039). In a case-control analysis, we observed that patients with high-COL11A1 had a higher risk of recurrence (OR = 2.0) and of dying of the disease (OR = 2.0). Patients with high-COL11A1-expressing tumours had shorter disease-free survival and overall survival (difference not significant). There was a linear positive correlation between COL11A1 expression on epithelial tumoral cells and surrounding stromal cells (r = 0.247, p = 0.04).
Conclusion: Our findings suggest that COL11A1 may represent a marker of aggressiveness in invasive breast cancer and that its detection warrants further study on larger series to evaluate its possible use in clinical practice.
Katsutoshi Miura
Department of Regenerative & Infectious Pathology, Hamamatsu University School of Medicine
Toshihide Iwashita, Dr. Professor
Department of Regenerative & Infectious Pathology, Hamamatsu University School of Medicine
Abstract
Organs with different levels of stiffness support the musculoskeletal system. Light microscopy cannot evaluate organ stiffness, whereas scanning acoustic microscopy (SAM) discriminates stiffness based on speed-of-sound (SOS) because sound waves pass faster in stiffer tissues. This study aimed to evaluate SOS imaging for orthopedic diseases using formalin-fixed paraffin-embedded sections. SOS imaging in SAM uses unstained light microscopic (LM) sections to prevent the bias of staining variation. Digital SOS values are comparable in different organ components and diseases.
Mouse organs with the lowest mean SOS values included the adipose tissue, bone marrow, calcified cartilage, and nucleus pulposus; those with intermediate values included hyaline cartilages, osteoid, skeletal muscles, cortical and trabecular bones, and ligaments; and those with the highest values comprised fibrocartilages of the vertebral disc and meniscus. Water contents and delipidating procedures decreased SOS values. Collagenous density and arrangement affected higher SOS values. The trabecular bones of mice were thinner and showed significantly lower values of SOS than those of humans.
Various orthopedic diseases and disorders displayed the characteristic SOS images. In osteoporosis, the trabecular bone becomes thin with lower SOS, indicating lesser stiffness to cause fractures. Comparison of woven and lamellar bones revealed that woven bones with lower SOS had lesser stiffness to fracture. Changes in SOS values indicated intramembranous bone formation. The trabecular bone develops from the connective tissues with an abrupt increase in SOS values. The regenerating process of bone fractures was monitored using SOS images, in which the granulation tissues transformed into calli in the osteoid to grow a new mineralized bone. The stiffness increased in phases, which appeared in SOS values.
Although several methods have been used to visualize the stiffness of biological tissues, SAM only needs 10-µm unstained slides and can simultaneously compare mechanical stiffness and histology. SOS images provide informative mechanical alterations of the bone, cartilage, and connective tissues to assess the status and diagnose a disorder.
Claire Valburg, MD
Residency, Internal Medicine, George Washington University, Washington, DC, USA
Mamoun Younes, MD
Professor of Pathology and Vice Chair of Pathology Director of Surgical Pathology, George Washington University Hospital, Washington, DC, USA
Farida Izzi, MD
Assistant Professor of Medicine, George Washington University Hospital, Washington, DC, USA
Abstract
Leiomyosarcoma of the inferior vena cava is a rare smooth muscle sarcoma with a variable presentation. We report a case of inferior vena cava leiomyosarcoma with the sole presenting symptom of lower extremity edema, with an initial diagnosis of deep venous thrombosis. Further evaluation with a venogram and computed tomography scan of the patient’s abdomen and pelvis revealed a wall-adherent filling defect and soft tissue mass and subsequent biopsy revealed leiomyosarcoma of her inferior vena cava. Our patient was treated with a thrombectomy and excision of her tumor and was then provided chemotherapy as an outpatient with resolution of her symptoms. Such a case demonstrates a rare underlying etiology of the common presenting symptom of lower extremity edema.
Pamela Causa Andrieu
Radiology Department. Memorial Sloan Kettering Cancer Center, United States.
Refky Nicola
Roswell Park Comprehensive Cancer Center, United States.
Federico Lipsich, Daniel Adri, Mariaangeles Gomez & Carolina Chacon
Radiology Service. Hospital Italiano de Buenos Aires, Argentina.
Melina Pol & Alejandra Wernicke
Pathology Service. Hospital Italiano de Buenos Aires, Argentina.
Gabriel Saraniti
Gynecology Service. Hospital Zonal de Bariloche, Argentina.
Abstract
Purpose: To identify the MRI features that aid in the characterization of ovarian granulosa cell tumors.
Materials and methods: 11 MR pelvis of an adult woman with pathology-proven ovarian granulosa cell tumors with surgical pathology.
We evaluated the patient’s age, Ca-125, size, laterality, and with MRI features such as indirect signs (i.e., thickened endometrium > 0.9 cm), morphology (cystic, solid-cystic, or solid), subacute hemorrhage, T2 signal (low or intermediate-to-high), restricted diffusion (B values: 0, 50, 1000 sec/mm3/ADC), and dynamic enhancement (intense or similar to myometrium). Also, the presence of ascites, peritoneal implants, or adenopathy.
Results: The final cohort included 11 women with a surgical-pathological diagnosis of granulosa cell tumors. The median age was 52.4 years (range, 17-80). The Ca-125 level was with a median within normal limits. The median size was 9.4 cm. Most cases were unilateral (81.8%) and more frequent on the left (54.5%).
MRI Analysis: 36.4% had endometrial thickening. Ovarian granulosa cell tumors were polymorphous: cystic (54.6%), mixed solid-cystic (9.1%), and solid (36.3%). Most GC had intermediate to high signal on T2 (90.9%), restricted diffusion (81.8%), intense enhancement (81.8%), and 36.4% had intraparenchymal bleeding. 9.1% had associated implants/adenopathy/ ascites at diagnosis.
Conclusion: The MRI features characteristic of ovarian granulosa cell tumors were the polymorphous morphology, an intense enhancement to the myometrium, restricted diffusion, and the presence of intraparenchymal hemorrhage.
Amna Ali, MD
Shamsuddin Khwaja, MD
Jeffrey Saavedra, MD
Kamell Eckroth-Bernard, MD
Usman Javed, MD
Chandrasekar Venugopal, MD
Heidi Reich, MD
Habiba Hashimi, MD
Leheb Araim, MD
Robert Stewart, MD
Lisa Wilkins, NP
Navjot Janday, NP
Alex Calkins, NP
John C Lin, MD
Abstract
There have been significant advances in the technique and application of endovascular repair of thoracic aortic pathology over the past 20 years. The Stanford type A and the complicated type B dissection patients require urgent/emergent intervention. In the last decade, earlier intervention has been pursued for uncomplicated type B dissections. The INvestigation of STent-grafts in Aortic Dissection (INSTEAD) Long term (XL) study showed that there was significant crossover from medical management to Thoracic EndoVascular Aortic Repair (TEVAR) at year 3, suggesting TEVAR might benefit this population long term.
Today, the application of TEVAR, which was initially designed to address aneurysmal disease, has become a standard and Food and Drug Administrative (FDA) approved management option in dissections.
Currently there are four FDA approved TEVAR devices in the United States for the treatment of the thoracic dissections, namely Gore, Medtronic, Cook, and Terumo. With each iteration, there are increased opportunities for customization and widespread use in individualized patient’s pathology. As the technology improves and the feasibility of the grafts expands, the complication rates continue to decline cementing the safety and efficacy of these thoracic aortic grafts. Two rare but catastrophic complications in spinal ischemia and retrograde Stanford type A aortic dissection are further discussed. With the success of the TEVAR, a new frontier of hybrid aortic surgery has developed. The debranching of the aortic arch vessels in order to advance the TEVAR proximal landing zones has been aggressively pursued. With the widespread growth of TEVAR technology it is apparent that complex aortic pathology can be safely repaired endovascularly.
Omar Zardain Medlich Ducoulombier
Sofía Teresa Lozano Díaz
Erick Roberto Santaella Sosa
Félix Adolfo Sánchez Chávez
Arnulfo Miramontes Morales
Manuel Torres Nájera
Francisco González Salazar
Abstract
Introduction: Osteoarticular tuberculosis poses a significant diagnostic and therapeutic challenge in developing countries, where the absence of molecular tools demands reliance on clinical suspicion and histopathological findings for diagnoses. Here, we present a compilation of case studies on osteoarticular tuberculosis for academic reference and support to aid primary care physicians in providing the best possible patient care.
Methods: Retrospective analysis of cases diagnosed with osteoarticular tuberculosis through biopsy from 2010 to 2020 at a Mexican Traumatology and Orthopedics Hospital, examined using descriptive statistics.
Results: Thirty-three patients were registered: 23 men (70%) and 10 women (30%). The most affected regions included the spine in 28 cases (84%), the hip in 3 (9%), and the elbow and sternoclavicular joints in 1 case each. The main clinical manifestations were paravertebral abscesses in 16 patients (48%), discitis in 12 (36%) and arthritis in 5 (15%), while the primary associated diseases were immunosuppression in 8 cases (24%), 2 cases with hepatitis (6%) and 3 with hypertension (9%).
Discussion: Tuberculosis is endemic in Mexico, similar to other developing countries, with numerous reported cases of osteoarticular tuberculosis. This study highlights the importance of using alternative diagnostic tools when molecular tests and cultures are not accessible to general practitioners and orthopedic physicians who treat patients with clinical suspicion of osteoarticular tuberculosis.
Fatima Ezzahra Rizkou
Yassine Jaouhari
Youssef Lakhdar
Othmane Benhoummad
Mohammed Chehbouni
Omar Oulghoul
Youssef Rochdi
Abdelaziz Raji
Mohamed Ilias Tazi
Ali Bouddounit
Hanane Rais
Abstract
Aims: Our goal was to obtain comprehensive and accurate information about primary extranodal non-Hodgkin lymphomas of the head and neck region to contribute to the advancement of medical knowledge in this field.
Materiels and methods: We conducted a retrospective study of 341 patients with primary extra-nodal, non-Hodgkin lymphomas of the head and neck, over a period of 7 years from January 2016 to December 2022, in the departments of ENT and Head and Neck Surgery and Hematology, with the help of the department of anatomical pathology of the university hospital Mohammed VI of Marrakech.
Results: 341 patients, with primary extra-nodal, non-Hodgkin lymphomas of the head and neck, was included, with an average age of 57 years, and a sex ratio male/female of 2.21 . in more than half of the cases; Waldeyer’s ring was concerned; especially palatine tonsils. Type B NHL was the most frequent and involved 308 patients. Diffuse large B-cell lymphoma was the commonly observed histological type, found in 214 patients; followed by a Follicular Lymphoma and Extra-Nodal NK/T‑Cell Lymphoma, Nasal Type. Following the extension workup; patients were all staged according to the ANN ARBOR classification; with a 77.8% of them were localized stages I and II, and of the therapeutically evaluable cases, complete remission was achieved in 112 patients.
Conclusion: Our study focused on all extra-nodal localizations of NHL in the head and neck region. Due to the very heterogeneous nature of these tumors, most of the current studies are limited to a specific site of involvement. Nevertheless, our study provides an overall picture; which those specific studies can be based. The management of NHL has evolved considerably in recent years, insisting on the multidisciplinary character to a better management of these patients.
Tianchi Ren, MD
Ilona Lavender, BRADMedImag
Dee Nandurkar, A. Prof., FRANZCR
Steuart Rorke, FRCPA
Ronnie Ptasznik, A. Prof., FRANZCR
Abstract
Objective:To assess efficacy of bedside cytology assessment of thyroid fine needle aspirate samples performed by junior medical staff compared to cytologists.
Methods: Retrospective analysis was performed of 1490 thyroid fine needle aspirates. Samples were divided into three groups: cellular adequacy assessment performed by cytologists, interns, and no onsite adequacy assessment (blind). A 45-minute training session was provided to medical interns with the aim of identifying whether adequate cellular material was demonstrated, as defined by the Bethesda criteria. The primary outcome was the rate of nondiagnostic samples, and the secondary outcome was the number of fine needle aspirate passes required to reach sample adequacy.
Results: The incidence of non-diagnostic samples for the cytologist, blind, and intern groups were 6.90%, 17.1% and 14.0% respectively (p<0.001). There was no statistically significant difference in non-diagnostic rate between the blind and intern groups. Significantly more aspirates required more than two passes in the cytologist group (74.8%) and blind (94.7%) compared to the intern group (58.7%, p<0.001).
Conclusions: On-site adequacy assessment performed by cytopathologists is the gold standard for minimising non-diagnostic thyroid FNAs, however, medical staff with minimal anatomical pathology experience can be trained to perform on-site adequacy assessment and improve outcomes with the implementation of a simple targeted training program.
