My Journey in Pathology
As a pathologist, our life revolves around the microscope. Every slide we examine holds a story—sometimes subtle, sometimes dramatic—but always meaningful. Each specimen represents a patient, a family, and a clinical journey, and it is our responsibility to interpret that story with accuracy and integrity.
Over the past 30 years, primarily in the field of histopathology, I have learned that no two diseases are ever truly identical. Every case presents with unique clinical features and distinct histomorphology. Disease does not arrive after reading a textbook; rather, textbooks are written after observing disease. This understanding has kept me humble and continuously motivated to learn.
The essence of pathology is constant study and adaptation. Our goal as pathologists is not only to diagnose but to evolve with advancing science and technology. During my career, I have witnessed a complete paradigm shift in the way tumors are diagnosed and treated.
Up until the year 2000, diagnosis was largely morphology-driven. Histological patterns formed the cornerstone of tumor classification. Then came the era of immunohistochemistry, which added specificity and refined our diagnostic accuracy. This was followed by the advent of molecular pathology, where each tumor began to be understood through its unique molecular signature—fundamentally changing therapeutic strategies and ushering in the era of targeted therapy and personalized medicine.
I have also witnessed the evolution of the WHO classification of tumors—from earlier editions such as 1976, through 2000, 2007, 2016, and now the most recent 2021 and 2022 updates. Each revision reflects not only scientific progress but also a deeper understanding of tumor biology.
Today, we are entering yet another transformative phase with the integration of Artificial Intelligence in pathology. Digital pathology and AI-assisted diagnostics are expanding our capabilities and efficiency. However, I say with confidence that morphology will always remain the foundation of our discipline. Technology can assist, but it cannot replace the trained eye, clinical judgment, and experience of a pathologist.
Pathologists are the backbone of medical science. Behind every clinical decision, every surgical intervention, and every targeted therapy, there is a diagnosis made at the microscope.
This journey has been one of continuous learning, adaptation, and dedication—and I remain as passionate today as I was when I first looked through the microscope three decades ago.
AbstractWe present a case of uterine torsion caused by a large 7.0x8.0 cm subserosal myoma in a gravid uterus. This is an uncommon disorder where the prospective diagnosis is difficult thus raises challenges in management. Uterine torsion in gravid uterus is found to carry a substantial degree of risk of perinatal mortality. Leiomyoma is found to be a potential risk factor in these cases. Therefore the diagnosis must not be delayed to prevent complications. Though there are no imaging criteria, CT or MRI can produce a preoperative diagnosis. Uterine torsion can be asymptomatic and in most cases is an accidental finding during cesarian section. Thereby many times cesarian section yields the most certain diagnosis. Posterior low transverse incision is an accessible and effective approach in uterine torsion cases. High degree of suspicion along with swift management is essential factors contributing to favorable outcome.
Keywords: Gravid uterus, Uterine torsion, Cesarian section.
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AbstractMultiple synchronous primary carcinoma involving gall bladder, liver and common bile duct are rare and difficult to differentiate with hepatic and extrahepatic bile duct metastasis from single primary. Radiological features, molecular landscape, and even integrated mutational profiling are not of much help. We describe a case of 48-year-old male who presented with jaundice and follow up CT scan raised the suspicion of gall bladder carcinoma with hepatic metastasis. Peroperative frozen section examination revealed adenocarcinoma with involvement of cystic duct margin; however revised common duct margin was free from tumor invasion. Final histopathology on resected gall bladder revealed multifocal adenocarcinoma, while histomorphology of hepatic nodule was consistent with cholangiocarcinoma. Common bile duct a one focus had also revealed adenocarcinoma while cut margins were negative form malignancy. In view of different morphology of gall bladder and hepatic tumor, no continuity of three tumors and single large, firm, non umblicated hepatic nodule, diagnosis of multiple synchronous carcinoma was suggested.
Keywords: Multiple synchronous
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AbstractCD99 is a transmembrane protein, a product of the MIC2 gene with various functions and limited diagnostic utility, routinely used in laboratories for the differential diagnosis of small blue cell tumors. It is used in establishing the diagnosis of Ewing's sarcoma/PNET where it consistently shows strong membranous staining on immunohistochemistry. However, CD99 has high negative and low positive predictive values. Therefore, if CD99 is negative, the likelihood of Ewing's sarcoma/PNET is low. Conversely, if it is positive, it is not specific to the Ewing Sarcoma family of tumors, as this antigen's expression is seen in a wide variety of tumors. Thus for confirmation cytogenetic examination for reciprocal translocation t(11;22)(q24;q12) or t(21;22)(q22;q12) which results in the fusion of EWSR1 gene with FLI1 or ERG genes are essential. Here, I describe two cases where the diagnosis of Ewing's sarcoma was made based on immunohistochemistry. In both cases, the EWSR1-FLI1 fusion was found to be negative. Further molecular testing revealed synovial sarcoma in one case, while total resection of the tumor revealed the morphology of mesenchymal chondrosarcoma in the other case. These cases highlight that strong membranous immunostaining of CD99 with NKX2.2 positivity, which is highly specific for Ewing's sarcoma, is insufficient for diagnosis. Round cell sarcoma cases should be confirmed with molecular testing before starting chemotherapy.
Keywords: CD99, Ewings sarcoma, NKX2.2
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