1. IHC plays a significant role in the diagnosis of testicular tumors, helping to differentiate between types of germ cell tumors and sex cord-stromal tumors.
2. Common markers used in the diagnosis of germ cell tumors include OCT3/4, SALL4, PLAP, Glypican-3, and AFP. Sex cord-stromal tumors commonly stain positive for Inhibin, Calretinin, and SF1.
3. Pre-analytical errors can lead to false IHC results, so appropriate controls, fixation, and antibody selection are important for accurate diagnosis.
Chronic lymphoproliferative disorders (CLPDs) are a heterogeneous group of malignancies characterized by the proliferation of mature B and rarely T lymphoid cells. They are classified according to the WHO into precursor lymphoid neoplasms, mature B-cell and T-cell neoplasms, and Hodgkin's lymphoma. Common CLPDs include chronic lymphocytic leukemia/small lymphocytic lymphoma, prolymphocytic leukemia, hairy cell leukemia, and various subtypes of non-Hodgkin's lymphoma such as follicular lymphoma and mantle cell lymphoma. Diagnosis involves morphology, immunophenotyping, cytogenetics, and other analyses.
Perivascular epithelioid cell neoplasm (PEComas)Shreya D Prabhu
Perivascular epithelioid cell tumors (PEComas) are mesenchymal neoplasms defined by the presence of distinctive perivascular epithelioid cells. They can arise in various organs. Angiomyolipoma and lymphangioleiomyomatosis are examples of PEComas that arise in the kidney and lung respectively. Angiomyolipoma is a typically benign tumor composed of blood vessels, smooth muscle, and fat cells, while lymphangioleiomyomatosis involves proliferation of perivascular epithelioid cells around lymphatics leading to cyst formation in the lungs. The pathological features, diagnosis, and management of these PEComa subtypes were discussed in
The document discusses minimal residual disease (MRD), which refers to small amounts of malignant cells that remain undetectable by conventional methods but can be detected using highly sensitive techniques like PCR. It provides an overview of techniques used for MRD detection in various hematologic malignancies, including morphology, immunophenotyping, cytogenetics, FISH, and PCR. The sensitivity and limitations of each technique is reviewed. Common genomic targets for MRD detection are discussed for several leukemias and lymphomas. The significance of accurately measuring MRD levels for prognosis, monitoring relapse risk, and guiding treatment is also summarized.
This document discusses the use of immunohistochemistry in breast pathology. It covers several topics:
1. Analyzing prognostic markers like hormone receptors in breast cancer and their predictive value.
2. Using myoepithelial cell markers to help solve diagnostic dilemmas and distinguish lesions.
3. Identifying tumor subtypes and assessing diagnoses using markers like luminal vs basal.
4. Evaluating cell populations in proliferative breast lesions and assessing neoplasia vs hyperplasia.
This document discusses various histological structures and lesions that can mimic prostate carcinoma on biopsy. It describes entities such as atrophy, basal cell hyperplasia, adenosis, non-specific granulomatous prostatitis, and clear cell cribriform hyperplasia that resemble low or high-grade prostate cancer. Distinguishing these mimickers from cancer relies on architectural features, cytology, immunohistochemistry, and the presence of basal cells. While some mimickers can be difficult to differentiate from cancer on limited biopsy sampling, correlation with clinical findings and use of immunohistochemical markers are important to arrive at an accurate diagnosis.
Minimal Residual Disease in Acute lymphoblastic leukemiaDr. Liza Bulsara
This document discusses minimal residual disease (MRD) in acute lymphoblastic leukemia (ALL). It provides information on several key points:
1. MRD refers to small amounts of leukemia cells that can be detected through sensitive laboratory techniques like flow cytometry and PCR, but not through standard morphology.
2. Various methods for detecting MRD are discussed, including immunophenotyping, PCR, FISH, and cytogenetics. PCR can detect a single malignant cell among 100,000 normal cells and is the most sensitive method.
3. MRD levels determined at different time points during treatment have prognostic significance and can be used for risk stratification and determining the need for treatment intensification or reduction. Monitoring
The document discusses Myelodysplastic/Myeloproliferative Neoplasms (MDS/MPN), a group of rare chronic myeloid neoplasms characterized by features of both myelodysplasia and myeloproliferation. It describes the key subtypes including Chronic Myelomonocytic Leukemia (CMML), Juvenile Myelomonocytic Leukemia (JMML), and Atypical Chronic Myeloid Leukemia (aCML). CMML is defined by persistent monocytosis and can be subdivided based on blast percentage. JMML mainly affects children and is characterized by leukocytosis with monocytosis. aCML involves dysplastic neutrophilic
Chronic lymphoproliferative disorders (CLPDs) are a heterogeneous group of malignancies characterized by the proliferation of mature B and rarely T lymphoid cells. They are classified according to the WHO into precursor lymphoid neoplasms, mature B-cell and T-cell neoplasms, and Hodgkin's lymphoma. Common CLPDs include chronic lymphocytic leukemia/small lymphocytic lymphoma, prolymphocytic leukemia, hairy cell leukemia, and various subtypes of non-Hodgkin's lymphoma such as follicular lymphoma and mantle cell lymphoma. Diagnosis involves morphology, immunophenotyping, cytogenetics, and other analyses.
Perivascular epithelioid cell neoplasm (PEComas)Shreya D Prabhu
Perivascular epithelioid cell tumors (PEComas) are mesenchymal neoplasms defined by the presence of distinctive perivascular epithelioid cells. They can arise in various organs. Angiomyolipoma and lymphangioleiomyomatosis are examples of PEComas that arise in the kidney and lung respectively. Angiomyolipoma is a typically benign tumor composed of blood vessels, smooth muscle, and fat cells, while lymphangioleiomyomatosis involves proliferation of perivascular epithelioid cells around lymphatics leading to cyst formation in the lungs. The pathological features, diagnosis, and management of these PEComa subtypes were discussed in
The document discusses minimal residual disease (MRD), which refers to small amounts of malignant cells that remain undetectable by conventional methods but can be detected using highly sensitive techniques like PCR. It provides an overview of techniques used for MRD detection in various hematologic malignancies, including morphology, immunophenotyping, cytogenetics, FISH, and PCR. The sensitivity and limitations of each technique is reviewed. Common genomic targets for MRD detection are discussed for several leukemias and lymphomas. The significance of accurately measuring MRD levels for prognosis, monitoring relapse risk, and guiding treatment is also summarized.
This document discusses the use of immunohistochemistry in breast pathology. It covers several topics:
1. Analyzing prognostic markers like hormone receptors in breast cancer and their predictive value.
2. Using myoepithelial cell markers to help solve diagnostic dilemmas and distinguish lesions.
3. Identifying tumor subtypes and assessing diagnoses using markers like luminal vs basal.
4. Evaluating cell populations in proliferative breast lesions and assessing neoplasia vs hyperplasia.
This document discusses various histological structures and lesions that can mimic prostate carcinoma on biopsy. It describes entities such as atrophy, basal cell hyperplasia, adenosis, non-specific granulomatous prostatitis, and clear cell cribriform hyperplasia that resemble low or high-grade prostate cancer. Distinguishing these mimickers from cancer relies on architectural features, cytology, immunohistochemistry, and the presence of basal cells. While some mimickers can be difficult to differentiate from cancer on limited biopsy sampling, correlation with clinical findings and use of immunohistochemical markers are important to arrive at an accurate diagnosis.
Minimal Residual Disease in Acute lymphoblastic leukemiaDr. Liza Bulsara
This document discusses minimal residual disease (MRD) in acute lymphoblastic leukemia (ALL). It provides information on several key points:
1. MRD refers to small amounts of leukemia cells that can be detected through sensitive laboratory techniques like flow cytometry and PCR, but not through standard morphology.
2. Various methods for detecting MRD are discussed, including immunophenotyping, PCR, FISH, and cytogenetics. PCR can detect a single malignant cell among 100,000 normal cells and is the most sensitive method.
3. MRD levels determined at different time points during treatment have prognostic significance and can be used for risk stratification and determining the need for treatment intensification or reduction. Monitoring
The document discusses Myelodysplastic/Myeloproliferative Neoplasms (MDS/MPN), a group of rare chronic myeloid neoplasms characterized by features of both myelodysplasia and myeloproliferation. It describes the key subtypes including Chronic Myelomonocytic Leukemia (CMML), Juvenile Myelomonocytic Leukemia (JMML), and Atypical Chronic Myeloid Leukemia (aCML). CMML is defined by persistent monocytosis and can be subdivided based on blast percentage. JMML mainly affects children and is characterized by leukocytosis with monocytosis. aCML involves dysplastic neutrophilic
The document discusses immunotherapy and the role of pathologists in assessing tumor samples. It describes how certain tumors express PD-L1 antigens that can be recognized by the immune system, but the tumors also engage immune checkpoint pathways like PD-1 and CTLA-4 to evade the immune response. Immunotherapy drugs target these checkpoint pathways to enhance the immune response. The document outlines the FDA-approved PD-L1 immunohistochemistry assays and biomarkers used to identify cancer patients most likely to respond to immune checkpoint inhibitors for various cancer types including NSCLC, melanoma, bladder cancer, and colorectal cancer.
Bethesda system for reporting thyroid cytologyariva zhagan
The document discusses the Bethesda System for Reporting Thyroid Cytopathology (BSRTC), which provides a standardized classification system for thyroid fine needle aspiration (FNA) results. The BSRTC aims to improve communication between clinicians by establishing uniform diagnostic terminology. It categorizes FNA results as non-diagnostic, benign, atypia of undetermined significance/follicular lesion of undetermined significance, follicular neoplasm/suspicious for follicular neoplasm, suspicious for malignancy, or malignant. The document outlines the criteria for each category and risk of malignancy. It notes recent enhancements in the 2017 version of BSRTC, including recalculated risk of malignancy and the
The document provides an outline and overview of a presentation on cytopathology of the breast. It discusses the normal breast anatomy and cells seen on fine needle aspiration (FNA). It covers patient workup, techniques for FNA, and considerations for interpreting results. Inflammatory conditions, benign and malignant breast tumors are addressed. The accuracy and limitations of FNA are summarized. Reporting categories for breast FNA results are also outlined.
The document provides an overview of thyroid gland embryology, anatomy, common pathologies, and the steps for grossing a thyroid specimen in the laboratory. The thyroid gland develops from an endodermal outpouching in the embryo and normally descends to the anterior neck. Common pathologies include Hashimoto's thyroiditis, Graves' disease, multinodular goiter, and various thyroid cancers. When grossing a thyroid specimen, the pathologist examines, describes, weighs, measures, and sections the gland to identify any lesions for histological analysis.
Papillary lesions of the breast form a spectrum ranging from benign intraductal papillomas to preinvasive and invasive papillary carcinomas. Intraductal papillomas are characterized by arborescent fibrovascular cores lined by epithelial cells and can be central or peripheral in location. Some papillomas may have areas of atypical ductal hyperplasia or ductal carcinoma in situ. Intraductal papillary carcinoma lacks a myoepithelial cell layer. Encapsulated papillary carcinoma and solid papillary carcinoma are rare variants that typically have a good prognosis with local therapy. Invasive papillary carcinoma is exceedingly rare.
Common pitfalls in bone marrow biopsy based diagnostic approachspa718
1. Bone marrow biopsy is the gold standard for diagnosing many hematological diseases but can have pitfalls in interpretation if not done or interpreted properly.
2. Key factors that can limit interpretation include inadequate clinical information, small or distorted specimen, limited staining, and insufficient experience.
3. Specialized ancillary tests like cytogenetics, immunophenotyping, and immunohistochemistry are often needed to make an accurate diagnosis when morphology is inconclusive or to differentiate between possible conditions.
4. A systematic approach incorporating clinical findings and additional test results is important to avoid common pitfalls like misdiagnosing infiltration, fibrosis, or focal lesions.
NEW UPDATES IN KIDNEY TUMOR PATHOLOGY: WHO 5th EDITION.pptxAnjalyNarendran
The WHO 5th Edition updates to kidney tumour pathology include changes to established renal tumors such as papillary renal cell carcinoma and chromophobe RCC, as well as the definition of new molecularly defined renal tumors including TFEB-rearranged RCC, ELOC-mutated RCC, fumarate hydratase-deficient RCC, succinate dehydrogenase-deficient RCC, and ALK-rearranged RCC. Emerging and provisional entities are also discussed such as thyroid-like follicular carcinoma, hybrid oncocytic chromophobe tumor, eosinophilic vacuolated tumor, low-grade oncocytic tumor, and biphasic hyalinizing psam
MPNs are clonal hematopoietic stem cell disorders characterized by overproduction of one or more myeloid cell lineages in the bone marrow and blood. The key subtypes include CML, PV, PMF, and ET. CML is driven by the Philadelphia chromosome and BCR-ABL1 fusion gene. PV is characterized by elevated red blood cell counts and the JAK2 V617F mutation in over 95% of cases. Without treatment, MPNs can progress to more advanced stages including myelofibrosis, leukemia, or transformation. Molecular testing plays an important role in diagnosis and classification.
- Plasma cell neoplasms originate from terminally differentiated B cells and produce monoclonal immunoglobulins. They commonly affect people around age 70 and have a male predominance.
- Risk factors include prior radiation exposure and certain chemical exposures. They are caused by genetic mutations that allow a clonal plasma cell population to proliferate in the bone marrow.
- Presentations depend on the type but commonly include anemia, bone lesions, kidney dysfunction, and infections. Workup involves blood and urine tests and imaging like skeletal surveys and PET scans.
- Treatment involves chemotherapy, radiation, stem cell transplants, surgery, and palliative care. Prognosis depends on the stage and type, ranging from potentially cur
This document provides guidelines for the pathological diagnosis of lymph node biopsy specimens. It discusses the importance of adequate biopsy samples and multidisciplinary evaluation. Common non-neoplastic conditions that can cause lymphadenopathy like infections are reviewed. The key aspects of lymph node anatomy are summarized. The pathological approach involves first determining if the process is non-neoplastic or neoplastic. If non-neoplastic, patterns like follicular hyperplasia or sinus histiocytosis are considered. Specific granulomatous and inflammatory conditions are also discussed. If neoplastic, the document reviews distinguishing features of common lymphoma subtypes. Immunohistochemistry to characterize lymphomas using markers like CD20 and Bcl2 is also mentioned.
This document provides guidance on the pathological assessment of colorectal resection specimens. It describes the different types of colorectal surgery specimens and margins that need assessment. It discusses the total mesorectal excision technique for rectal cancers and how to evaluate the quality of the surgery. Key pathological features that require reporting are described, including tumor staging, lymphovascular invasion, perineural invasion, tumor budding and tumor deposits. The document provides details on lymph node assessment and reporting colorectal cancers using a synoptic format.
Dr shashi bansal approch to bone marrow examinationShashi Bansal
This document provides guidance on performing and interpreting bone marrow examinations. It discusses:
1. The importance of bone marrow examinations for diagnosing blood disorders when other tests are inconclusive.
2. The procedures involved in bone marrow examinations, including aspiration, biopsy, staining, and specialized testing.
3. How to analyze bone marrow samples under the microscope, including identifying cell types, assessing cellularity, iron content, fibrosis, and other features that provide diagnostic information.
This document provides an approach for evaluating undifferentiated tumors. It begins by categorizing undifferentiated tumors into 4 groups based on morphology: small round cell tumors, epithelioid cell tumors, spindle cell tumors, and pleomorphic tumors. It then outlines the diagnostic algorithm which involves determining the main lineage (epithelial, melanocytic, hematopoietic/lymphoid, or mesenchymal), specifying a diagnosis using immunohistochemistry and clinical correlation, and considering the differential diagnoses for each category. A variety of immunohistochemical markers are also described that can help identify the cell or tumor type.
This document discusses the role of immunohistochemistry (IHC) in diagnosing soft tissue tumours. It begins by defining soft tissue and the WHO classification of soft tissue tumours. IHC is an important ancillary technique that can be used to identify discrete tissue components using antigen-antibody binding. The document outlines the IHC protocol and discusses various markers that can help diagnose different types of soft tissue tumours, including markers for fibroblastic, adipocytic, vascular, neural, osseous and cartilaginous tumours. Specific markers and the tumours they are useful for identifying are provided. The document emphasizes that IHC should be used along with other techniques as markers sometimes show cross-reactivity.
1. The combination of SMMHC and p63 is ideal for marking myoepithelial cells and assessing features such as stromal invasion and differentiation of in situ versus invasive lesions.
2. Positive 34βE12 and CK5/6 staining within the proliferative component indicates atypical papilloma rather than papilloma with DCIS.
3. Intracystic papillary carcinoma shows positive staining by Collagen IV around ducts, distinguishing it from solid papillary carcinoma.
- A 55-year-old male presented with peripheral and central lymphadenopathy and splenomegaly but was asymptomatic. A lymph node biopsy was performed.
- Microscopic examination revealed features consistent with follicular lymphoma (FL), a neoplasm composed of follicle center B-cells which usually has at least a partially follicular pattern. FL is characterized by t(14;18) translocation and involves bone marrow in 40-70% of cases.
- FL was further classified based on the number of centroblasts per high power field according to the Mann and Berard grading system into Grade I (0-5 centroblasts/HPF), Grade II (6-15 centroblasts/
This document discusses various non-neoplastic and neoplastic conditions that can cause lymphadenopathy. It focuses on filariasis as a cause of non-neoplastic lymphadenopathy. Filarial parasites can infect the lymphatics and lymph nodes, causing inflammation and blockage. On pathology, the lymph nodes show an intense inflammatory reaction around dead or dying larvae with eosinophils and multinucleated giant cells. Rarely, microfilaria can be seen embedded in the lymph node tissue. The document emphasizes that a diligent search is needed to identify the parasite and make an accurate diagnosis.
Subclassification into type 1 and type 2 is no longer recommended.
PRCC has classic morphology historically in type 1 category.
Criteria of foamy histiocytes and psammoma bodies is not required.
Many tumors previously diagnosed as type 2 PRCC now constitute independent entities
The document discusses immunotherapy and the role of pathologists in assessing tumor samples. It describes how certain tumors express PD-L1 antigens that can be recognized by the immune system, but the tumors also engage immune checkpoint pathways like PD-1 and CTLA-4 to evade the immune response. Immunotherapy drugs target these checkpoint pathways to enhance the immune response. The document outlines the FDA-approved PD-L1 immunohistochemistry assays and biomarkers used to identify cancer patients most likely to respond to immune checkpoint inhibitors for various cancer types including NSCLC, melanoma, bladder cancer, and colorectal cancer.
Bethesda system for reporting thyroid cytologyariva zhagan
The document discusses the Bethesda System for Reporting Thyroid Cytopathology (BSRTC), which provides a standardized classification system for thyroid fine needle aspiration (FNA) results. The BSRTC aims to improve communication between clinicians by establishing uniform diagnostic terminology. It categorizes FNA results as non-diagnostic, benign, atypia of undetermined significance/follicular lesion of undetermined significance, follicular neoplasm/suspicious for follicular neoplasm, suspicious for malignancy, or malignant. The document outlines the criteria for each category and risk of malignancy. It notes recent enhancements in the 2017 version of BSRTC, including recalculated risk of malignancy and the
The document provides an outline and overview of a presentation on cytopathology of the breast. It discusses the normal breast anatomy and cells seen on fine needle aspiration (FNA). It covers patient workup, techniques for FNA, and considerations for interpreting results. Inflammatory conditions, benign and malignant breast tumors are addressed. The accuracy and limitations of FNA are summarized. Reporting categories for breast FNA results are also outlined.
The document provides an overview of thyroid gland embryology, anatomy, common pathologies, and the steps for grossing a thyroid specimen in the laboratory. The thyroid gland develops from an endodermal outpouching in the embryo and normally descends to the anterior neck. Common pathologies include Hashimoto's thyroiditis, Graves' disease, multinodular goiter, and various thyroid cancers. When grossing a thyroid specimen, the pathologist examines, describes, weighs, measures, and sections the gland to identify any lesions for histological analysis.
Papillary lesions of the breast form a spectrum ranging from benign intraductal papillomas to preinvasive and invasive papillary carcinomas. Intraductal papillomas are characterized by arborescent fibrovascular cores lined by epithelial cells and can be central or peripheral in location. Some papillomas may have areas of atypical ductal hyperplasia or ductal carcinoma in situ. Intraductal papillary carcinoma lacks a myoepithelial cell layer. Encapsulated papillary carcinoma and solid papillary carcinoma are rare variants that typically have a good prognosis with local therapy. Invasive papillary carcinoma is exceedingly rare.
Common pitfalls in bone marrow biopsy based diagnostic approachspa718
1. Bone marrow biopsy is the gold standard for diagnosing many hematological diseases but can have pitfalls in interpretation if not done or interpreted properly.
2. Key factors that can limit interpretation include inadequate clinical information, small or distorted specimen, limited staining, and insufficient experience.
3. Specialized ancillary tests like cytogenetics, immunophenotyping, and immunohistochemistry are often needed to make an accurate diagnosis when morphology is inconclusive or to differentiate between possible conditions.
4. A systematic approach incorporating clinical findings and additional test results is important to avoid common pitfalls like misdiagnosing infiltration, fibrosis, or focal lesions.
NEW UPDATES IN KIDNEY TUMOR PATHOLOGY: WHO 5th EDITION.pptxAnjalyNarendran
The WHO 5th Edition updates to kidney tumour pathology include changes to established renal tumors such as papillary renal cell carcinoma and chromophobe RCC, as well as the definition of new molecularly defined renal tumors including TFEB-rearranged RCC, ELOC-mutated RCC, fumarate hydratase-deficient RCC, succinate dehydrogenase-deficient RCC, and ALK-rearranged RCC. Emerging and provisional entities are also discussed such as thyroid-like follicular carcinoma, hybrid oncocytic chromophobe tumor, eosinophilic vacuolated tumor, low-grade oncocytic tumor, and biphasic hyalinizing psam
MPNs are clonal hematopoietic stem cell disorders characterized by overproduction of one or more myeloid cell lineages in the bone marrow and blood. The key subtypes include CML, PV, PMF, and ET. CML is driven by the Philadelphia chromosome and BCR-ABL1 fusion gene. PV is characterized by elevated red blood cell counts and the JAK2 V617F mutation in over 95% of cases. Without treatment, MPNs can progress to more advanced stages including myelofibrosis, leukemia, or transformation. Molecular testing plays an important role in diagnosis and classification.
- Plasma cell neoplasms originate from terminally differentiated B cells and produce monoclonal immunoglobulins. They commonly affect people around age 70 and have a male predominance.
- Risk factors include prior radiation exposure and certain chemical exposures. They are caused by genetic mutations that allow a clonal plasma cell population to proliferate in the bone marrow.
- Presentations depend on the type but commonly include anemia, bone lesions, kidney dysfunction, and infections. Workup involves blood and urine tests and imaging like skeletal surveys and PET scans.
- Treatment involves chemotherapy, radiation, stem cell transplants, surgery, and palliative care. Prognosis depends on the stage and type, ranging from potentially cur
This document provides guidelines for the pathological diagnosis of lymph node biopsy specimens. It discusses the importance of adequate biopsy samples and multidisciplinary evaluation. Common non-neoplastic conditions that can cause lymphadenopathy like infections are reviewed. The key aspects of lymph node anatomy are summarized. The pathological approach involves first determining if the process is non-neoplastic or neoplastic. If non-neoplastic, patterns like follicular hyperplasia or sinus histiocytosis are considered. Specific granulomatous and inflammatory conditions are also discussed. If neoplastic, the document reviews distinguishing features of common lymphoma subtypes. Immunohistochemistry to characterize lymphomas using markers like CD20 and Bcl2 is also mentioned.
This document provides guidance on the pathological assessment of colorectal resection specimens. It describes the different types of colorectal surgery specimens and margins that need assessment. It discusses the total mesorectal excision technique for rectal cancers and how to evaluate the quality of the surgery. Key pathological features that require reporting are described, including tumor staging, lymphovascular invasion, perineural invasion, tumor budding and tumor deposits. The document provides details on lymph node assessment and reporting colorectal cancers using a synoptic format.
Dr shashi bansal approch to bone marrow examinationShashi Bansal
This document provides guidance on performing and interpreting bone marrow examinations. It discusses:
1. The importance of bone marrow examinations for diagnosing blood disorders when other tests are inconclusive.
2. The procedures involved in bone marrow examinations, including aspiration, biopsy, staining, and specialized testing.
3. How to analyze bone marrow samples under the microscope, including identifying cell types, assessing cellularity, iron content, fibrosis, and other features that provide diagnostic information.
This document provides an approach for evaluating undifferentiated tumors. It begins by categorizing undifferentiated tumors into 4 groups based on morphology: small round cell tumors, epithelioid cell tumors, spindle cell tumors, and pleomorphic tumors. It then outlines the diagnostic algorithm which involves determining the main lineage (epithelial, melanocytic, hematopoietic/lymphoid, or mesenchymal), specifying a diagnosis using immunohistochemistry and clinical correlation, and considering the differential diagnoses for each category. A variety of immunohistochemical markers are also described that can help identify the cell or tumor type.
This document discusses the role of immunohistochemistry (IHC) in diagnosing soft tissue tumours. It begins by defining soft tissue and the WHO classification of soft tissue tumours. IHC is an important ancillary technique that can be used to identify discrete tissue components using antigen-antibody binding. The document outlines the IHC protocol and discusses various markers that can help diagnose different types of soft tissue tumours, including markers for fibroblastic, adipocytic, vascular, neural, osseous and cartilaginous tumours. Specific markers and the tumours they are useful for identifying are provided. The document emphasizes that IHC should be used along with other techniques as markers sometimes show cross-reactivity.
1. The combination of SMMHC and p63 is ideal for marking myoepithelial cells and assessing features such as stromal invasion and differentiation of in situ versus invasive lesions.
2. Positive 34βE12 and CK5/6 staining within the proliferative component indicates atypical papilloma rather than papilloma with DCIS.
3. Intracystic papillary carcinoma shows positive staining by Collagen IV around ducts, distinguishing it from solid papillary carcinoma.
- A 55-year-old male presented with peripheral and central lymphadenopathy and splenomegaly but was asymptomatic. A lymph node biopsy was performed.
- Microscopic examination revealed features consistent with follicular lymphoma (FL), a neoplasm composed of follicle center B-cells which usually has at least a partially follicular pattern. FL is characterized by t(14;18) translocation and involves bone marrow in 40-70% of cases.
- FL was further classified based on the number of centroblasts per high power field according to the Mann and Berard grading system into Grade I (0-5 centroblasts/HPF), Grade II (6-15 centroblasts/
This document discusses various non-neoplastic and neoplastic conditions that can cause lymphadenopathy. It focuses on filariasis as a cause of non-neoplastic lymphadenopathy. Filarial parasites can infect the lymphatics and lymph nodes, causing inflammation and blockage. On pathology, the lymph nodes show an intense inflammatory reaction around dead or dying larvae with eosinophils and multinucleated giant cells. Rarely, microfilaria can be seen embedded in the lymph node tissue. The document emphasizes that a diligent search is needed to identify the parasite and make an accurate diagnosis.
Subclassification into type 1 and type 2 is no longer recommended.
PRCC has classic morphology historically in type 1 category.
Criteria of foamy histiocytes and psammoma bodies is not required.
Many tumors previously diagnosed as type 2 PRCC now constitute independent entities
This document provides information on carcinoma of unknown primary (CUP). It defines CUP and discusses the epidemiology, pathology, diagnostic approach, and treatment. Some key points:
- CUP accounts for 2-5% of cancers and has a median survival of 6-9 months. Adenocarcinoma is the most common histology (60%).
- Diagnostic evaluation includes imaging, endoscopy, and immunohistochemistry to identify the primary site. Cytokeratin 7/20 staining patterns provide clues to site of origin.
- Favorable prognostic subsets include isolated axillary adenocarcinoma in women, papillary adenocarcinoma of the peritoneum in women,
1. Carcinoma of the prostate is the second most common cancer in males. It typically occurs in men over 50 and prevalence increases with age.
2. Pathogenesis involves progression from premalignant prostatic intraepithelial neoplasia to invasive adenocarcinoma through genetic and epigenetic changes.
3. Diagnosis is made through digital rectal exam, prostate-specific antigen levels, and transrectal ultrasound-guided biopsy. Treatment involves surgery, radiation therapy, and hormone therapy such as androgen deprivation.
1. Carcinoma of the prostate is the second most common cancer in males. It typically occurs in men over 50 and prevalence increases with age.
2. Pathogenesis involves premalignant prostatic intraepithelial neoplasia progressing to adenocarcinoma through genetic and epigenetic changes.
3. Diagnosis is made through digital rectal exam, prostate-specific antigen levels, and biopsy. Treatment involves surgery, radiation therapy, and hormone deprivation therapy.
Testicular tumours are divided into three main groups: germ cell tumours, sex cord-stromal tumours, and mixed forms. Germ cell tumours account for 95% of cases and are further classified as seminomas and non-seminomas. Seminomas and non-seminomas have distinct characteristics and prognoses. Common germ cell tumour subtypes include embryonal carcinoma, yolk sac tumour, choriocarcinoma, and teratoma. Tumour markers such as HCG and AFP help diagnose and monitor germ cell tumours. Mixed germ cell tumours contain more than one histologic type and typically have a worse prognosis.
- HCC displays a high degree of molecular and histological heterogeneity. Morphological subtypes of hepatocellular carcinoma are strongly associated with tumour subclasses and gene mutations. Development of a morpho-molecular classification could improve precision medicine for patients with this highly aggressive malignancy. Although unlike lung or colorectal cancer, increasing knowledge of HCC subtypes has not yet resulted in biomarker discovery and improved clinical care. Integrative pathological and molecular studies are needed to define a consensus HCC morpho-molecular classification that could guide ongoing therapeutic trials.
TESTICULAR TUMOURS & MALIGNANT TUMOUR OF PENISDr. Roopam Jain
This document provides an overview of male genital system tumours, focusing on testicular tumours. It discusses the classification, histogenesis, clinical features, diagnosis, spread, tumour markers, prognosis, and characteristics of the main types of testicular tumours - germ cell tumours (seminomas, embryonal carcinomas, yolk sac tumours, choriocarcinomas, teratomas), sex cord-stromal tumours (Leydig cell tumours, Sertoli cell tumours), and mixed forms. Key information on etiology, morphology, markers, and treatment approach is provided for each tumour type.
This document provides an overview of male genital system tumours, focusing on testicular tumours. It discusses the classification, histogenesis, clinical features, diagnosis, spread, tumour markers, prognosis, and characteristics of the main types of testicular tumours - germ cell tumours (seminoma, embryonal carcinoma, yolk sac tumour, choriocarcinoma, teratoma), Leydig cell tumours, and Sertoli cell tumours. It describes the gross and microscopic morphological features of each tumour type.
This document summarizes different types of male genital tract tumors, specifically focusing on testicular tumors. It discusses that testicular tumors are divided into germ cell tumors, sex cord-stromal tumors, and mixed forms. The vast majority are germ cell tumors, which are further divided into seminomatous and non-seminomatous types. Various tumor types are described including their etiology, clinical features, spread patterns, tumor markers, prognosis, and morphological features.
1. Testicular tumours are divided into three main types: germ cell tumours, sex cord-stromal tumours, and mixed forms. Germ cell tumours account for 95% of cases.
2. Germ cell tumours are further classified as seminomas and non-seminomas. Seminomas have a better prognosis than non-seminomas.
3. Common germ cell tumours include seminoma, embryonal carcinoma, yolk sac tumour, choriocarcinoma, teratoma, and mixed forms. Tumour markers like HCG and AFP help diagnose and monitor these tumours.
This document defines neoplasia and describes the characteristics and classification of tumors. It discusses the components of tumors, benign and malignant tumor nomenclature, criteria to differentiate benign from malignant neoplasms including clinical features, growth rate, microscopy, invasion and metastasis. It also covers tumor markers, immunohistochemistry and cytology methods.
Thyroid Neoplasms an update based on latest WHOVivekanand A
This document discusses updates to the classification of thyroid neoplasms in the latest WHO classification. It describes the hierarchical classification system used which is based on cell of origin, pathologic features, molecular characteristics, and biological behavior. It provides details on the classification of benign and malignant follicular cell-derived neoplasms. It introduces new entities such as noninvasive encapsulated follicular variant of papillary thyroid carcinoma (NIFTP) and differentiated high-grade thyroid carcinoma (DHGTC). It also discusses criteria for diagnosing poorly differentiated thyroid carcinoma and provides recommendations for management and follow-up of thyroid neoplasms based on risk stratification.
This document discusses ovarian tumors, specifically germ cell tumors. It provides information on the classification, histopathology, immunoprofile, and other characteristics of various types of ovarian germ cell tumors including dysgerminoma, yolk sac tumor, embryonal carcinoma, choriocarcinoma, immature teratoma, and mature cystic teratoma. It also mentions other rare subtypes such as struma ovarii. The document aims to provide pathology residents with comprehensive information on diagnosing and classifying these tumor types.
GROUP 1 Case 967-- A Teenage Female with an Ovarian MassCLI.docxgilbertkpeters11344
GROUP 1: Case 967-- A Teenage Female with an Ovarian Mass
CLINICAL HISTORY
A teenage female presented with secondary amenorrhea (https://www.healthline.com/health/secondary-amenorrhea#causes). The patient had 1 menstrual cycle 3 years ago and has had no menses since. Laboratory work-up was negative for pregnancy test, mildly increased calcium level (11.7 mg/dL, normal range: 8.5-10.2 mg/dL) and CA 125 (43 Units/ml, normal range: 0-20 Units/ml). Prolactin, TSH, AFP, Inhibin A, Inhibin B and CEA were normal. Imaging revealed a 13 x 11.8 x 8.6 cm, predominately cystic left pelvis mass, with multiple internal septations. Her past medical history was not contributory. Patient underwent left salpingo-oophorectomy (https://www.healthline.com/health/salpingo-oophorectomy), omentectomy (https://moffitt.org/cancers/ovarian-cancer/omentectomy/) and tumor debulking (https://en.wikipedia.org/wiki/Debulking) with intraoperative frozen section consultation.
GROSS EXAMINATION
The 930.9 g tubo-ovarian complex consisted of a 20.0 x 16.0 x 8.0 cm large mass, with no recognizable normal ovarian parenchyma grossly and an unremarkable fallopian tube. The cut surface was gray, "fish-flesh", soft with foci of hemorrhage and necrosis.
MICROSCOPIC EXAMINATION
Microscopically, the majority of main tumor was growing in large nests, sheets and cords with focal follicle-like structures and geographic areas of necrosis. It was predominantly composed of small cells with hyperchromatic nuclei, round to oval nucleus with irregular nuclear contour, inconspicuous to occasional conspicuous nucleoli and minimal cytoplasm. This component was variably admixed with a population of larger cells, which as the name implies composed of cells with abundant eosinophilic cytoplasm, with central or eccentric round to oval nuclei, pale chromatin and prominent nuclei. Both, the small and large cell components demonstrated brisk mitotic activity. All staging biopsies and omentectomy were composed of large cell component.
An extensive panel of immunohistochemical stains was performed. Overall, the staining pattern was strong and diffuse in small cell component compared to patchy weak staining pattern in the large cell component.
FINAL DIAGNOSIS
Small cell carcinoma (https://en.wikipedia.org/wiki/Small-cell_carcinoma) of the ovary, hypercalcemic type (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939673/)
DISCUSSION
Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is an aggressive and highly malignant tumor affecting the women under 40. It was first described as a distinct entity by Dickersin et al in 1982 (1). Fewer than 500 cases have been described in the literature and it accounts for less than 1% of all ovarian cancer diagnoses. Due to the initial consideration of epithelial origin, the term of SCCOHT has been used to distinguish this entity from its mimicker, the neuroendocrine or pulmonary type (2). In fact epithelial origin of SCCOHT was recently challenged as new imm.
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Immunohistochemical diagnosis of carcinoma from an unkown primarykrish penugonda
1. The document discusses immunohistochemical diagnosis of carcinoma from an unknown primary site. Certain transcription factors and keratins can help identify the organ of origin for metastatic cancers of unknown primary.
2. Transcription factors like TTF1, CDX2, GATA3, NKX3-1, PAX8 are highly specific markers that can identify lung, colon, breast, prostate, and thyroid primary cancers, respectively.
3. Combinations of markers like CK7+/CK20+ suggest origins in organs like the bladder, pancreas, or upper GI tract. The document reviews expression patterns of various markers to diagnose primary organ site in cancer of unknown primary.
Target Audience: Oncology fellows and Oncologists
Carcinoma of unknown primary is a challenging scenario often encountered in Oncology practice. This slide presentation discusses favorable and unfavorable presentations of CUP and it's management
This document summarizes liver diseases including α1-antitrypsin deficiency, a genetic disorder causing liver and lung disease. It also describes intrahepatic biliary tract diseases like primary and secondary biliary cirrhosis. Benign liver tumors like hemangiomas and adenomas are outlined as well as primary malignant tumors such as hepatoblastoma and angiosarcoma. Hepatocellular carcinoma is discussed in depth, including risk factors, morphology, clinical features, and prognosis. Metastatic liver tumors from other primary cancers are also noted.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
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• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
10 Benefits an EPCR Software should Bring to EMS Organizations Traumasoft LLC
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Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
The skin is the largest organ and its health plays a vital role among the other sense organs. The skin concerns like acne breakout, psoriasis, or anything similar along the lines, finding a qualified and experienced dermatologist becomes paramount.
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
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3. INTRODUCTION
•Testicular cancers are the most common solid malignancy and the second leading
cause of cancer death in young men
•Affecting males between the ages of 15 and 35, although they represent only
approximately 1 percent of all solid tumors in men
•The are classified as per WHO CLASSIFICATION OF TUMORS OF TESTIS 2016
•THE H&E is gold standard for diagnosis, IHC plays a significant role and <5% of tumors
require Immunostaining for accurate interpretation.
•Differential diagnosis can be resolved with IHC
•BUT, few pre-analytical errors to be kept in mind
4.
5. PREANALYTICAL ERRORS
IHC is very important for diagnosis of type of cancer, however there can few errors which give
false results
FALSE NEGATIVE:
Antibody inappropriate, denatured , used at wrong concentration
Loss of antigen through poor fixation/diffusion.
Presence of antigen at a density below level of detection.
FALSE POSITIVES:
Cross- reactivity of antibody with unintended antigens
Nonspecific binding of the antibody to the tissue
Presence of endogenous peroxidase
Entrapment of normal tissues by tumor cells
10. GERM CELL NEOPLASIA IN SITU
•Syn – Intratubular germ cell neoplasia, unclassified;
testicular intraepithelial neoplasia
•Derived from primordial germ cells/gonocytes that failed to
differentiate into spermatogonia
• Adult testis – inside seminiferous tubules, between sertoli
cell and basal membrane;
•infantile testis - GCINS cells detached from basal membrane
•No. tubules affected – few to 100% (variable)
•Gonocyte-like germ cells - clear cytoplasm; angulated nuclei;
coarse chromatin ,base of tubules
•Nuclei - string of beads – separated from the lumen of
tubule – by uniform sertoli cell nuclei
11. IHC – PLAP (cytoplasmic), OCT3/4(NUCLEAR), Podoplanin, NANOG, LIN28 (absent – normal
spermatogonia), SALL4
KIT(CD117) – non specific; normal spermatogonia – may be positive (cytoplasmic
membrane)
Frozen section – Alkaline phosphatase – helpful
EMA, CD30, GLYPICAN 3, SOX2
12. •DD
Vacolization of seminiferous tubule cells (degenerative change)
Maturation arrest in spermatogonia
Metastatic carcinoma- melanoma, lymphoma may colonize seminiferous tubules
OCT ¾ - resolve this matter
13. Marker with normal tissues expressing type dd
Oct ¾ (Octamer-binding transcription
factor 4)
Is not expressed in normal,
differentiated cells
nuclear • Highly sensitive and specific for seminoma
• Poor prognostic factor for esophageal squamous cell
carcinoma
• May be poor prognostic factor for non-small cell lung
cancer
• MAY LOOSE REACTIVITY AFTER CHEMOTHERAPY
PLAP (Placental Alkaline Phosphatase)
placenta
Cytoplasmic • Germ cell tumors(does not stain spermatocytic seminoma)
• Intratubular germ cell neoplasia
• Trophoblastic tumors
• Serum PLAP is increased 10 fold in smokers- so not always
included in diagnostic workup
Podoplanin (D2-40)
Novel marker of mesothelial cells,
germ cells, lymphatic endothelial cells
membranous Seminoma (100%)
Embroyonal carcinoma (30%)
Others: mesothelioma
dermatofibroma
Hemangioblastoma
Primary skin adnexal tumor
14. Marker with normal tissues
expressing
type dd
SALL4
Embryonic stem cells
Nuclear Pan germ cell tumor marker
CD117(stem cell factor receptor)
Germ cells
Cytoplasmic and membranous • Seminoma
• Intratubular germ cell neoplasia
Others: Gist
PEComas
Oncocytomas
CD 30 Membranous and golgi(paranuclear
dot like)
Embryonal carcinoma
15. Specificforms – Intratubulargermcellneoplasia
Intratubular seminoma – complete filling of tubules
by neoplastic cells (identical to seminoma, GCINS),
lymphocytes present
IHC – simillar to seminoma
Intratubular non – seminoma – almost always
embryonal carcinoma
Distortion of tubules , enlarged beyond normal
diameter, necrosis, calcification
IHC – OCT3/4 +, CD 30 +, CD 117 –
(CD 30 is negative in GCNIS)
17. Seminoma
•Malignant germ cell tumour - considered - neoplastic
counterparts of the primordial germ cells /gonocytes present
during early embryonic development
•Syn – geminoma; ovary - dysgerminoma
GROSS MICRO:
23. Marker with normal tissues expressing type dd
Sox 2
Fetal CNS tissue
nuclear Embryonal carcinoma
PNET in teratoma
AE1/AE3 (pan cytokeratin cocktail)
Most epithelial cells
cytoplasmic Used with conjugation with CAM5.2
to screen carcinomas
29. Marker with normal tissues expressing type dd
Glypican – 3
By- embroyonic liver, placenta
(syntiotrophoblast)
Cytoplasmic,
membranous,
canlicular
HCC
Hepatoblastoma
Yolk sac tumor
Choriocarcinoma
Placental ste trophoblastic tumor
AFP
Fetal liver
Cytoplasmic Yolk sac tumor
OTHERS :HCC
HEPATOBLASTOMA
GATA -3
Involved in the luminal differentiation of
breast epithelium, development of
collecting system / urothelium and
trophoblastic differentiation
nuclear renal tumors
Paragangliomas
Choriocarcinomas
Mesotheliomas
yst
30. TROPHOBLASTICTUMOR
Choriocarcinoma
Malignant GCT that differentiates to resemble the
trophoblastic cells of the extraembryonic chorion –
cytotrophoblast, intermediate trophoblast, and
syncytiotrophoblast
Gross - Micro -
32. Non-choriocarcinoma trophoblastic tumors:
•GCTS showing trophoblastic differentiation other than choriocarcinoma and
non-trophoblastic contaning syntiotrophoblasts
• Cystic trophoblastic tumor – post therapy
• Epithelioid trophoblastic tumour
• Placental site trophoblastic tumour,
• Regressing choriocarcinoma,
• Hybrid trophoblastic tumours.
Positive stain - Beta hydroxysteroid dehydrogenase, Inhibin, GATA 3 & CK 18
33. Marker with normal tissues expressing type dd
Hcg (human chrionic gonadotrophin)
syntiotrophoblast
cytoplasmic • Choriocarcinoma
• Syntiotrophoblast gaint cells in
seminoma
Inhibin
Granulosa cell, Sertoli cells, adrenal cortical
cells, trophoblasts
cytoplasmic • Adrenocortical neoplasm
• Sex cord stromal tumors
• Trophoblastic tumors
• Hemangioblastoma
34. Teratoma
postpubertal-type
Malignant GCT composed of several types of tissue
representing one or more of the germinal layers
endoderm, mesoderm & ectoderm
syn – mature teratoma, immature teratoma
Gross
Micro - any epithelial or mesenchymal tissue type can
be seen, as can neural tissue.; cytological atypia
35. • IHC- glandular element- epithelial membrane antigen, HCG (syntiotrophoblast), PLAP
(glandular structures)
Histologically different from prepubertal
Solid appearance
Disordered arrangement of tissues
Atypia and mitosis
Associated to GCNIS (Primary criteria for distinction between pre and postpubertal)
36. TERATOMAS WITH SOMATIC TYPE MALIGNANCY
•Develops a distinct secondary component that resembles somatic-type malignant
neoplasm (eg. Sarcomas and carcinomas)
•GROSS- grey white nodule, with necrosis and haemorrhage
•HISTO : Expansile/infiltrative growth patterns. Organoid admixtures of varied elements
admixed with GCT components.
• PNET another m/c to be found
• Adult type: Neuroendocrine tumors (carcinoids), carcinomas.
• IHC – similar to the counter parts in other organs
PLAP, OCT3/4, ALPHA FETO protein
38. Mixedgermcell tumour
•Contains 2 or more malignant GCT components
•Most frequent combination: Embryonal Ca with teratoma,
seminoma and/or yolk sac
•Combination of prepubertal teratoma and yolk sac tumor is
not considered mixed GCT
•Gross – variegated appearance depending upon the
components present
39. MICRO:
A cystic glands of embryonal carcinoma with a more subtle
microcystic yolk sac tumour component.
B Polyembryoma variant of a mixed germ cell tumour forms
embryo-like bodies with a core of embryonal carcinoma, an
amniotic-like space, and a "ventral" yolk sac tumour component
C Diffuse embryoma. A diffuse embryoma variant of a mixed
germ cell tumour shows a necklace-like arrangement of
columnar embryonal carcinoma cells with a parallel component
of flat yolk sac tumour cells.
46. TERATOMA, PREPUBERTAL- TYPE
Composed of somatic tissues derived from one or more germinal layer.
SIMILAR TO MATURE CYSTIC TERATOMA OF OVARY
Gross and micro:
48. Pre pubertal Yolk Sac tumor
m/c tesisticular GCT in infants and children
Histologically, identical to postpubertal type
SAME IHC PROFILE AS POST-PUBERTAL YST
51. IHC- lnhibin, calretinin, SF1 , melan A, and C D99 are
typically positive. Chromogranin , synaptophysin, and cytokeratins are variably expressed, and
< 10% of tumours are S 1 00 protein-positive
Dd- Congenital adrenal hyperplasia (testicular adrenal rest tumours)
52. SERTOLI CELL, NOS
is a neoplasm composed of sex cord cells that usually shows focal tubular differentiation
but rarely grows diffusely.
GROSS- 2-5cms, well circumscribed with uniform yellow cut surface
HISTO-
IHC- Inhibin (50%) nuclear beta catenin (60-70%) , calretinin, SF1, CD99, melan A, WT1
vimentin, s100, sox9 (few)
53.
54. LARGE CELL CALCIFYING SERTOLI CELL TUMOR
Composed of abundant eosinophilic cytoplasm and focal to massive calcifications.
PRKAR1A germ line mutation (60-70%)
GROSS- 1-15cms, tan to white, gritty, necrosis and haemorrhage
HISTO-
IHC- INHIBIN, s100, SF1, beta-catenin
55. INTRATULAR LARGE CELL HYALINIZING SERTOLI CELL NEOPLASIA
Occurs exclusively in paitents with Peutz – Jeghers syndrome
GROSS- Scattered firm foci measuring few mm in diameters
HISTO-
IHC- Inhibin, aromatase, cytokeratin
56. GRANULOSA CELL TUMOR- ADULT
•Neoplasm composed of sex cord cells that resemble granulosa cells of Graafian follicles of
ovary.
GROSS- well circumscribed, solid,sometimes cyst, c/s- lobulated yellowish tan.
MICRO-
IHC- VIMENTIN, calretinin , CD99, melan A, FOXL2, smooth muscle actin, S100
nuclear beta catenin
57. JUVENILE GRANULOSA CELL TUMOR
Shows solid and follicular patterns with immature nuclei
GROSS- well circumscribed, solid, cystic , yellow to tan-white
MICRO-
IHC- Inhibin, calretinin, CD99, SOX9, VIMENTIN, PANCYTOKERATIN, SMOOTH MUSCLE ACTIN
58.
59.
60. TUMOR CONTAINING BOTH GERM CELL AND
SEX CORD STROMAL TUMOR ELEMENTS
GONADOBLASTOMA
Arise from dysgenetic gonad
Restis-specific protein Y-encoded (TSPY) gene involved
GROSS-granular, gritty c/s- calcifications
HISTO- Spindle cell gonadal stroma , occasional
Leydig like cells lacking reinke crystal.
61. IHC-OCT3/4, FOXL2 (does not stain Sertoli cells of GCNIS THUS DIFFRENTIATE FROM
GCNIS) SEC CORD CELLS ( staing for alpha-inhibin, calretinin, FOXL2) and absence of
infiltrating lymphocytes distingyush from dysgerminoma/seminoma.
The testis is composed of lobules of seminiferous tubules, interlobular septa, the mediastinum testis, rete testis, the tunica albuginea, and tunica vaginalis. Normal seminiferous tubules have a basement membrane and a thin fibrous wall, and contain germ cells in various stages of maturation plus Sertoli cells. Blood vessels and lymphatics, mesenchymal supporting tissue, macrophages, and Leydig cells are contained within the intertubular interstitium.
Lobules are separated from each other by fibrous interlobular septa, which contain blood vessels and lymphatics.
FOR THE ACCURATE RESULT
We will discuss about important ones
So therefor preanytical errors are the first step to keep in mind for avoiding the error further workup.
GCNIS originates from primordial germ cells or gonocyte blocked in its maturation to a prespermatogonia
Polypoidization is an early step initiating GCNIS WHICH remain dormant until puberty, after puberty it progresses to seminoma by default pathway or reprogrammed to non-seminoma consisting of------
This is due to gain or loss in specific chromosome mentioned……. KIT mutation is recurrent finding
GCNIS UNRELARED include prepubertal teratoma and spermatocytic tumor. Yolk sac prepubertal shows specific gains and loss and result from progression of teratoma
spermatocytic occurs due to gain in ch.9
List of tumor markers looking foreward to
OCT 4 ONLY MARKS FETAL GERM CELL
Plap – placental alkaline phosphatase
Podoplanin –membranous- negative for EC
Sall 4 – nuclear
CD30 is positive in embroyonal, gypican in yst, sox 2 in yst
Ema- metastatic high grade carcinoma
117 is non specific as at also stains immature Sertoli cells
INRATUBULAR- TUBELES ARE EXPANDED , obliteration of normal components , including Sertoli cells, tubules surrounded by lymphocytes
EMBRONAL CA- distortion og seminiferous tubules , enlarged beyond normal diameter, necrosis, clacification,
Gross – solid, homogenous, lobulated, cream/tan or pale yellow, bulge on c/s. Necrosis, hemorrhage +/-
MICRO --Monomorphic primitive germ cell and lymphocytes tumour cells - pale to clear cytoplasm, distinct cytoplasmic membranes, polygonal non overlapping nuclei, granular chromatin
One or more large , centrally located nucleoli.
Granulomatous reaction +/-
Morphologic variants: microcystic, cribiform, solid tubular, interstitial --- same prognosis
Syncytiotrophoblasts in 10-20% (OCT4 +) --- same prognosis
Atypia --- same prognosis
IHC algorithm for germ cell tumours
Oct4 ACTS AS GATEKEEPER
Nuclear – OCT3/4, SALL4, SOX17
Cytoplasmic membrane - KIT(CD117), PLAP, Podoplanin
HMW KERATIN IS POSITIVE IN NON-SEMOINOMA GERM CELL TUMOR
SOX 2 POSITIVE IN EMBROUONAL
-GROSS enlarged testis ,variegated appearance, solid, white to tan, hemorrhagic, necrotic and cystic
HISTO- large, pleomorphic vesicular nuclei, single or multiple macronucleoli, dense amphophilic cytoplasm, poorly defined cytoplasmic membranes, mitotic figures, apoptotic bodies. Nuclear crowding, pleomorphism
Cd30, oct ¾, sox 2 (NUCLEAR) help to distinguish from gct
REACTIVITY TO Cd30(membranos) disappears after chemo but oct3.4 persists
Gross-- solid to partially cystic, usually with a greyish-white to tan cut surface may have a myxoid quality. haemorrhage and necrosis +/-
a. gross
b. Schiller duval bodies- endodermal sinus pattern
c. Pleomorphism and hyaline globules in yolk sac tumor of testis.
Gross- haemorrhagic nodules containing foci
of solid, greyish-tan tumour.
Micro-biphasic appearance –mononucleated (cytotrophoblasts and intermediate trophoblasts) and multinucleated syncytiotrophoblasts - in a haemorrhagic background
Syntiotrophoblast reactive to hcg
Ae1/ae3 – cytoplasmic
Cam5.2 is low molecular weight keratin.. Used along with ae1/3 to screen carcinoma
Hcg- cytoplasmic ,
Inhibin- cytoplasmic, gata- nuclear,
- nodular and firm. The cut surfaces are heterogeneous with solid and cystic areas corresponding to the tissue types present histologically
A teratoma with somatic-type malignancy is a teratoma that develops a distinct secondary component that resembles a somatic·type malignant neoplasm, as seen in other organs and tissues (e.g. sarcomas and ca1cinomas).
sarcomas are most common; most common ca - adenoca
SARCOMAS ( RHABDOMYOSARCOMA) are must common
Closely associated with yst and embroyonal component
They lack cells with cytological atypia hich is seen germ cell associated teratoma
Most tumours are 0. 5-5 cm and well circumscribed.They have a homogeneous ,soft, yellow t o tan or brownish-green cut surface, but haemorrhage and necrosis are seen in about 25% of them . Lobulation with visible wh ite bands between lobules may be present
NESTS OF PALLISADING CELLS- CALL-EXNER LIKE ARRANGEMENT
SERTOLI CELLS
Sertoliform cells expresses sex cord stromal markers ---------------------------------------------------adenocarcinoma related markers