This document discusses the classification and histological subtypes of lung tumors according to the WHO. It covers precursor lesions like atypical adenomatous hyperplasia and adenocarcinoma in situ. Invasive adenocarcinoma subtypes include lepidic, acinar, papillary, micropapillary and solid. Molecular markers are discussed for adenocarcinoma. Minimally invasive adenocarcinoma is defined as invasive foci ≤0.5cm. Invasive mucinous adenocarcinoma contains large glands filled with mucin. The histological subtypes of lung cancers are small cell lung cancer, non-small cell lung cancer including squamous cell carcinoma, adenocarc
This document discusses three types of atypical lymphocytes:
1) Type I plasmacytoid cells which are differentiated but functionally incompetent B cells.
2) Type II mononuclear cells seen in infectious mononucleosis with irregular borders and pale cytoplasm.
3) Type III transformed or blastoid lymphocytes seen in leukemia with vacuolated cytoplasm and finely reticular chromatin.
Atypical lymphocytes are seen in the blood of dengue patients and are thought to be activated B cells producing antibodies against the dengue virus. An increased atypical lymphocyte count correlates with elevated IgG levels and can help differentiate dengue from other viral infections.
Salivary glands produce saliva and are composed of major and minor glands. The major glands are the parotid, submandibular, and sublingual glands. Salivary gland cytology can detect both benign and malignant lesions. Common benign findings include pleomorphic adenoma, Warthin's tumor, and basal cell adenoma cells. Malignant lesions include adenoid cystic carcinoma, mucoepidermoid carcinoma, and adenocarcinoma. Fine needle aspiration cytology allows diagnosis of salivary gland lesions with high sensitivity and specificity to guide treatment.
This document discusses lung tumors, specifically focusing on lung cancer. It covers the main types of lung cancer including small cell carcinoma, non-small cell carcinoma (squamous cell carcinoma, adenocarcinoma, large cell carcinoma), and carcinoid tumors. For each type, it discusses risk factors, histology, gross appearance, microscopic patterns, etiology, and clinical features. Common sites of metastasis are also listed. The document provides an overview of lung cancer pathology and clinical manifestations.
Squash cytology of cns paediatric tumoursSumanth Deva
This document provides an overview of squash cytology techniques for diagnosing pediatric central nervous system tumors, describing the smear patterns and key cytological features of common tumor types like medulloblastoma, atypical teratoid/rhabdoid tumors, choroid plexus papilloma, and choroid plexus carcinoma. Squash cytology allows rapid examination of biopsy samples during neurosurgery to aid diagnosis and surgical decision making.
Bronchial cytology and fine needle aspiration are important techniques for diagnosing lung lesions. Bronchial cytology examines the central airways using bronchoscopy while fine needle aspiration can sample peripheral lung lesions. Normal respiratory cells include ciliated bronchial cells and alveolar macrophages. Benign lesions may show goblet cell or basal cell hyperplasia. Non-neoplastic lung diseases like sarcoidosis and pulmonary alveolar proteinosis can also be diagnosed through their characteristic cytology findings. Cytology is useful for identifying infection causes as well as diagnosing and classifying lung tumors.
Cytologic assessment of bronchopulmonary lesionsAseem Jain
This document provides an overview of cytologic assessment of bronchopulmonary lesions. It discusses the normal histology of the respiratory system and various cytologic sampling techniques used to evaluate the lungs, such as sputum samples, bronchial brushings, washings and lavage. The cytology of normal respiratory cells and endogenous material is described. A variety of benign pulmonary conditions and infectious processes are outlined. Specific lung diseases like tuberculosis, sarcoidosis and nocardiosis are discussed through their characteristic cytologic findings.
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 discusses three types of atypical lymphocytes:
1) Type I plasmacytoid cells which are differentiated but functionally incompetent B cells.
2) Type II mononuclear cells seen in infectious mononucleosis with irregular borders and pale cytoplasm.
3) Type III transformed or blastoid lymphocytes seen in leukemia with vacuolated cytoplasm and finely reticular chromatin.
Atypical lymphocytes are seen in the blood of dengue patients and are thought to be activated B cells producing antibodies against the dengue virus. An increased atypical lymphocyte count correlates with elevated IgG levels and can help differentiate dengue from other viral infections.
Salivary glands produce saliva and are composed of major and minor glands. The major glands are the parotid, submandibular, and sublingual glands. Salivary gland cytology can detect both benign and malignant lesions. Common benign findings include pleomorphic adenoma, Warthin's tumor, and basal cell adenoma cells. Malignant lesions include adenoid cystic carcinoma, mucoepidermoid carcinoma, and adenocarcinoma. Fine needle aspiration cytology allows diagnosis of salivary gland lesions with high sensitivity and specificity to guide treatment.
This document discusses lung tumors, specifically focusing on lung cancer. It covers the main types of lung cancer including small cell carcinoma, non-small cell carcinoma (squamous cell carcinoma, adenocarcinoma, large cell carcinoma), and carcinoid tumors. For each type, it discusses risk factors, histology, gross appearance, microscopic patterns, etiology, and clinical features. Common sites of metastasis are also listed. The document provides an overview of lung cancer pathology and clinical manifestations.
Squash cytology of cns paediatric tumoursSumanth Deva
This document provides an overview of squash cytology techniques for diagnosing pediatric central nervous system tumors, describing the smear patterns and key cytological features of common tumor types like medulloblastoma, atypical teratoid/rhabdoid tumors, choroid plexus papilloma, and choroid plexus carcinoma. Squash cytology allows rapid examination of biopsy samples during neurosurgery to aid diagnosis and surgical decision making.
Bronchial cytology and fine needle aspiration are important techniques for diagnosing lung lesions. Bronchial cytology examines the central airways using bronchoscopy while fine needle aspiration can sample peripheral lung lesions. Normal respiratory cells include ciliated bronchial cells and alveolar macrophages. Benign lesions may show goblet cell or basal cell hyperplasia. Non-neoplastic lung diseases like sarcoidosis and pulmonary alveolar proteinosis can also be diagnosed through their characteristic cytology findings. Cytology is useful for identifying infection causes as well as diagnosing and classifying lung tumors.
Cytologic assessment of bronchopulmonary lesionsAseem Jain
This document provides an overview of cytologic assessment of bronchopulmonary lesions. It discusses the normal histology of the respiratory system and various cytologic sampling techniques used to evaluate the lungs, such as sputum samples, bronchial brushings, washings and lavage. The cytology of normal respiratory cells and endogenous material is described. A variety of benign pulmonary conditions and infectious processes are outlined. Specific lung diseases like tuberculosis, sarcoidosis and nocardiosis are discussed through their characteristic cytologic findings.
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 presentation i have made to understand the approach to a kidney biopsy in depth. kidney biopsy is not done in all centers and that's why its difficult to understand it. i have put some cases also to understand it better.
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.
This document summarizes key information about renal biopsies and nephrectomies:
1) Renal biopsies are typically performed under ultrasound guidance by a nephrologist and radiologist to evaluate renal function abnormalities. Adequate biopsy specimens contain at least 10 glomeruli and two arteries. Tissue is processed for light microscopy, immunofluorescence, and electron microscopy.
2) Nephrectomies are performed for renal tumors, nonfunctioning transplants, or native kidneys. Radical nephrectomies remove the entire kidney and surrounding tissues while partial nephrectomies resect tumors. Specimens are examined grossly and microscopically, with sections
This document discusses different types of intestinal polyps. It begins by defining a polyp as an abnormal growth projecting from a mucous membrane. The main types discussed are epithelial polyps, which include adenomas, serrated lesions like hyperplastic polyps and sessile serrated adenomas/polyps, and hamartomas. Adenomas are further classified based on histology and risk of malignancy. Serrated lesions have distinct histologic features and molecular profiles. Certain polyp types are associated with hereditary cancer syndromes like familial adenomatous polyposis. Accurate classification and reporting of polyps helps determine cancer risk and appropriate surveillance for patients.
Immunofluorescence is a technique that allows visualization of specific proteins or antigens in tissue sections. It involves binding antibodies conjugated to fluorescent dyes. There are two main types - direct immunofluorescence detects in vivo antibodies bound to tissue, while indirect detects circulating antibodies in patient serum. Immunofluorescence microscopy uses filters and dichroic mirrors to generate fluorescent images. It has various applications in histopathology for diseases like renal biopsy, skin biopsy, and more. Specific patterns of immunofluorescence staining can help diagnose glomerular diseases like post-infectious glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy.
This document discusses the histology and classification of non-neoplastic lymphadenopathy. It begins by describing the histology of lymph nodes, including the capsule, cortex, paracortex, and medulla. Guidelines for examining lymph nodes through grossing, fixation, sectioning and staining are provided. Non-neoplastic lymphadenopathy is classified into lymphadenitides caused by various infectious agents like viruses, bacteria, mycobacteria, fungi and protozoa, and lymphadenopathies associated with clinical syndromes. Specific conditions are then discussed in detail, including their etiology, clinical features, histopathology, special staining, and differential diagnosis.
This document discusses various histopathological patterns seen under the microscope. It defines terms like trabecular, syncytial, alveolar, herringbone, stromiform, fascicular, glandular, cribriform, tubular, papillary, micropapillary, Indian file, hobnail, and follicular patterns. It also explains structures like rossettes, microcysts, and different types of rossettes seen in various tumors. Examples of tumors showing each pattern are provided. The document aims to help differentiate between the most common histopathological patterns.
The document discusses various pathologies of the prostate, including:
- Benign prostatic hyperplasia (BPH), which is a noncancerous enlargement of the prostate due to aging. Histologic features include glandular and stromal hyperplasia.
- Prostatic intraepithelial neoplasia (PIN), which is considered a precursor lesion to prostate cancer. It is graded as low or high grade.
- Prostate adenocarcinoma, which microscopically appears as small, simple glandular structures. The Gleason grading system is used to characterize prostate cancers.
- Other rare pathologies that can involve the prostate such as lymphoma, small cell carcinoma,
Skin cancer is the most common cancer worldwide. The three main types are basal cell carcinoma, squamous cell carcinoma, and melanoma. Risk factors include fair skin, sun exposure, and family history. Symptoms include new skin growths or changes to existing moles. Diagnosis involves inspection and biopsy of suspicious lesions. Treatment options depend on cancer type and stage but commonly include surgery, chemotherapy, and radiation therapy to remove or destroy cancer cells.
This is a presentation on the topic of cytology of the breast, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Tumor diagnosis involves several methods including clinical examination, imaging tests, biochemical assays, and morphologic and molecular techniques. Histological examination of tissue samples through methods like biopsy and cytology is the gold standard for cancer diagnosis and involves analyzing cell and tissue morphology under a microscope with techniques like immunohistochemistry and flow cytometry. Molecular diagnostic tests also allow detection of genetic markers associated with specific cancer types.
The document discusses several pediatric neoplasms that appear as small round blue cell tumors due to their primitive histological features. These include neuroblastoma, Wilms tumor, rhabdomyosarcoma, Ewing's sarcoma, medulloblastoma, retinoblastoma, and lymphoma. For each tumor, the document outlines characteristics such as common age of diagnosis, clinical features, histopathological appearance under the microscope, immunohistochemistry profiles, genetics where relevant, and important prognostic factors. Differential diagnosis of these small round blue cell tumors in children is provided for accurate diagnosis and treatment.
1) The document discusses Acute Myeloid Leukemia (AML), including its classification, epidemiology, etiology, clinical presentation, laboratory findings, and specific subtypes defined by genetic abnormalities such as AML with t(8;21), inv(16), and t(15;17).
2) It describes the key features of different AML subtypes including their morphology, immunophenotype, genetics, and prognosis. Specific attention is given to abnormal cells, staining patterns, and genetic translocations that characterize each subtype.
3) The FAB and WHO classification systems are introduced and compared, noting the WHO system incorporates immunophenotyping, cytogenetics, and molecular characteristics
Paraneoplastic syndromes are conditions that develop in patients with advanced cancer due to the local or distant spread of the tumor or hormones secreted by the tumor. They can be the earliest sign of an occult tumor, cause significant health problems, and mimic metastatic disease. Common paraneoplastic syndromes include endocrinopathies like Cushing syndrome, nerve and muscle disorders like myasthenia gravis, and dermatologic conditions like acanthosis nigricans. The underlying mechanisms involve tumor secretions, immunological responses, or coagulation abnormalities.
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
This document discusses testicular seminoma, a type of germ cell tumor that originates in the testis. It describes the signs and symptoms, gross pathology, histopathology, immunohistochemistry, differential diagnosis, staging, and treatment protocol for testicular seminoma. Microscopically, seminoma appears as sheets of pale tumor cells separated by fibrovascular septae with lymphocytic infiltration and a characteristic "tigroid" background. Immunohistochemistry stains such as OCT3/4, CD117, and D2-40 are useful for diagnosis. Staging involves determining if the cancer has spread from the testis and treatment typically involves surgery followed by radiation or chemotherapy.
Broncho-Alveolar Lavage Fluid Analysis provides information on the status of the respiratory tract beyond what can be seen bronchoscopically. It involves instilling saline into segments of the lung and analyzing the cell types in the returned fluid. A satisfactory sample contains at least 2x10^6 cells including over 10 macrophages per field. Differential cell counts can indicate conditions like pneumonia, cancer, sarcoidosis, and alveolar hemorrhage. Special stains can identify pathogens, lipids, proteins, and minerals for diagnostic purposes. Complications are generally minor but loss of lung function is a risk in severely compromised patients.
This document discusses neoplasia and the clinical and laboratory diagnosis of cancer. It covers topics such as the local and hormonal effects of tumors, cancer cachexia, paraneoplastic syndromes, grading and staging of tumors, histologic and cytologic diagnostic methods, immunohistochemistry, molecular diagnostics, circulating tumor cells, tumor markers, and the potential for molecular profiling of tumors to improve cancer diagnostics.
Histopathological subtypes and molecular alterations in pulmonary adenocarcinomaMeghana P
This document discusses the histopathological subtypes and molecular alterations in pulmonary adenocarcinoma. It describes the various histologic subtypes including lepidic, acinar, papillary, micropapillary, solid, colloidal, fetal, and enteric adenocarcinoma. Preinvasive lesions like atypical adenomatous hyperplasia and adenocarcinoma in situ are also discussed. Common molecular alterations in each subtype including mutations in EGFR, KRAS, P53, HER2, and BRAF are described. Gene rearrangements involving ALK, ROS1, RET, and NRG1 are also summarized. Different subtypes are associated with smoking status, gender, and
Non–small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers. Histologically, NSCLC is divided into adenocarcinoma, squamous cell carcinoma (SCC) (see the image below), and large cell carcinoma. Small cell lung cancer (SCLC), previously known as oat cell carcinoma, is considered distinct from other lung cancers, which are called non–small cell lung cancers (NSCLCs) because of their clinical and biologic characteristics.
This presentation i have made to understand the approach to a kidney biopsy in depth. kidney biopsy is not done in all centers and that's why its difficult to understand it. i have put some cases also to understand it better.
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.
This document summarizes key information about renal biopsies and nephrectomies:
1) Renal biopsies are typically performed under ultrasound guidance by a nephrologist and radiologist to evaluate renal function abnormalities. Adequate biopsy specimens contain at least 10 glomeruli and two arteries. Tissue is processed for light microscopy, immunofluorescence, and electron microscopy.
2) Nephrectomies are performed for renal tumors, nonfunctioning transplants, or native kidneys. Radical nephrectomies remove the entire kidney and surrounding tissues while partial nephrectomies resect tumors. Specimens are examined grossly and microscopically, with sections
This document discusses different types of intestinal polyps. It begins by defining a polyp as an abnormal growth projecting from a mucous membrane. The main types discussed are epithelial polyps, which include adenomas, serrated lesions like hyperplastic polyps and sessile serrated adenomas/polyps, and hamartomas. Adenomas are further classified based on histology and risk of malignancy. Serrated lesions have distinct histologic features and molecular profiles. Certain polyp types are associated with hereditary cancer syndromes like familial adenomatous polyposis. Accurate classification and reporting of polyps helps determine cancer risk and appropriate surveillance for patients.
Immunofluorescence is a technique that allows visualization of specific proteins or antigens in tissue sections. It involves binding antibodies conjugated to fluorescent dyes. There are two main types - direct immunofluorescence detects in vivo antibodies bound to tissue, while indirect detects circulating antibodies in patient serum. Immunofluorescence microscopy uses filters and dichroic mirrors to generate fluorescent images. It has various applications in histopathology for diseases like renal biopsy, skin biopsy, and more. Specific patterns of immunofluorescence staining can help diagnose glomerular diseases like post-infectious glomerulonephritis, membranoproliferative glomerulonephritis, and IgA nephropathy.
This document discusses the histology and classification of non-neoplastic lymphadenopathy. It begins by describing the histology of lymph nodes, including the capsule, cortex, paracortex, and medulla. Guidelines for examining lymph nodes through grossing, fixation, sectioning and staining are provided. Non-neoplastic lymphadenopathy is classified into lymphadenitides caused by various infectious agents like viruses, bacteria, mycobacteria, fungi and protozoa, and lymphadenopathies associated with clinical syndromes. Specific conditions are then discussed in detail, including their etiology, clinical features, histopathology, special staining, and differential diagnosis.
This document discusses various histopathological patterns seen under the microscope. It defines terms like trabecular, syncytial, alveolar, herringbone, stromiform, fascicular, glandular, cribriform, tubular, papillary, micropapillary, Indian file, hobnail, and follicular patterns. It also explains structures like rossettes, microcysts, and different types of rossettes seen in various tumors. Examples of tumors showing each pattern are provided. The document aims to help differentiate between the most common histopathological patterns.
The document discusses various pathologies of the prostate, including:
- Benign prostatic hyperplasia (BPH), which is a noncancerous enlargement of the prostate due to aging. Histologic features include glandular and stromal hyperplasia.
- Prostatic intraepithelial neoplasia (PIN), which is considered a precursor lesion to prostate cancer. It is graded as low or high grade.
- Prostate adenocarcinoma, which microscopically appears as small, simple glandular structures. The Gleason grading system is used to characterize prostate cancers.
- Other rare pathologies that can involve the prostate such as lymphoma, small cell carcinoma,
Skin cancer is the most common cancer worldwide. The three main types are basal cell carcinoma, squamous cell carcinoma, and melanoma. Risk factors include fair skin, sun exposure, and family history. Symptoms include new skin growths or changes to existing moles. Diagnosis involves inspection and biopsy of suspicious lesions. Treatment options depend on cancer type and stage but commonly include surgery, chemotherapy, and radiation therapy to remove or destroy cancer cells.
This is a presentation on the topic of cytology of the breast, prepared by Dr Ashish Jawarkar, he is MD in pathology and a teacher at Parul institute of Medical sciences and research Vadodara.
Tumor diagnosis involves several methods including clinical examination, imaging tests, biochemical assays, and morphologic and molecular techniques. Histological examination of tissue samples through methods like biopsy and cytology is the gold standard for cancer diagnosis and involves analyzing cell and tissue morphology under a microscope with techniques like immunohistochemistry and flow cytometry. Molecular diagnostic tests also allow detection of genetic markers associated with specific cancer types.
The document discusses several pediatric neoplasms that appear as small round blue cell tumors due to their primitive histological features. These include neuroblastoma, Wilms tumor, rhabdomyosarcoma, Ewing's sarcoma, medulloblastoma, retinoblastoma, and lymphoma. For each tumor, the document outlines characteristics such as common age of diagnosis, clinical features, histopathological appearance under the microscope, immunohistochemistry profiles, genetics where relevant, and important prognostic factors. Differential diagnosis of these small round blue cell tumors in children is provided for accurate diagnosis and treatment.
1) The document discusses Acute Myeloid Leukemia (AML), including its classification, epidemiology, etiology, clinical presentation, laboratory findings, and specific subtypes defined by genetic abnormalities such as AML with t(8;21), inv(16), and t(15;17).
2) It describes the key features of different AML subtypes including their morphology, immunophenotype, genetics, and prognosis. Specific attention is given to abnormal cells, staining patterns, and genetic translocations that characterize each subtype.
3) The FAB and WHO classification systems are introduced and compared, noting the WHO system incorporates immunophenotyping, cytogenetics, and molecular characteristics
Paraneoplastic syndromes are conditions that develop in patients with advanced cancer due to the local or distant spread of the tumor or hormones secreted by the tumor. They can be the earliest sign of an occult tumor, cause significant health problems, and mimic metastatic disease. Common paraneoplastic syndromes include endocrinopathies like Cushing syndrome, nerve and muscle disorders like myasthenia gravis, and dermatologic conditions like acanthosis nigricans. The underlying mechanisms involve tumor secretions, immunological responses, or coagulation abnormalities.
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
This document discusses testicular seminoma, a type of germ cell tumor that originates in the testis. It describes the signs and symptoms, gross pathology, histopathology, immunohistochemistry, differential diagnosis, staging, and treatment protocol for testicular seminoma. Microscopically, seminoma appears as sheets of pale tumor cells separated by fibrovascular septae with lymphocytic infiltration and a characteristic "tigroid" background. Immunohistochemistry stains such as OCT3/4, CD117, and D2-40 are useful for diagnosis. Staging involves determining if the cancer has spread from the testis and treatment typically involves surgery followed by radiation or chemotherapy.
Broncho-Alveolar Lavage Fluid Analysis provides information on the status of the respiratory tract beyond what can be seen bronchoscopically. It involves instilling saline into segments of the lung and analyzing the cell types in the returned fluid. A satisfactory sample contains at least 2x10^6 cells including over 10 macrophages per field. Differential cell counts can indicate conditions like pneumonia, cancer, sarcoidosis, and alveolar hemorrhage. Special stains can identify pathogens, lipids, proteins, and minerals for diagnostic purposes. Complications are generally minor but loss of lung function is a risk in severely compromised patients.
This document discusses neoplasia and the clinical and laboratory diagnosis of cancer. It covers topics such as the local and hormonal effects of tumors, cancer cachexia, paraneoplastic syndromes, grading and staging of tumors, histologic and cytologic diagnostic methods, immunohistochemistry, molecular diagnostics, circulating tumor cells, tumor markers, and the potential for molecular profiling of tumors to improve cancer diagnostics.
Histopathological subtypes and molecular alterations in pulmonary adenocarcinomaMeghana P
This document discusses the histopathological subtypes and molecular alterations in pulmonary adenocarcinoma. It describes the various histologic subtypes including lepidic, acinar, papillary, micropapillary, solid, colloidal, fetal, and enteric adenocarcinoma. Preinvasive lesions like atypical adenomatous hyperplasia and adenocarcinoma in situ are also discussed. Common molecular alterations in each subtype including mutations in EGFR, KRAS, P53, HER2, and BRAF are described. Gene rearrangements involving ALK, ROS1, RET, and NRG1 are also summarized. Different subtypes are associated with smoking status, gender, and
Non–small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers. Histologically, NSCLC is divided into adenocarcinoma, squamous cell carcinoma (SCC) (see the image below), and large cell carcinoma. Small cell lung cancer (SCLC), previously known as oat cell carcinoma, is considered distinct from other lung cancers, which are called non–small cell lung cancers (NSCLCs) because of their clinical and biologic characteristics.
The document discusses pathology of oral cancer, including histological features and classifications. It notes that over 90% of oral cancers are squamous cell carcinoma, which can be well, moderately, or poorly differentiated. Other variants include verrucous, basaloid, and sarcomatoid squamous cell carcinoma. Prognostic factors discussed include tumor size and extent, lymph node involvement, histologic grade, and the presence of perineural or vascular invasion. Accurate classification of histologic type and grade is important for determining prognosis and treatment for oral cancers.
This document discusses salivary gland tumors. It begins with definitions of tumors and classifications of salivary glands and salivary gland tumors. It then covers the incidence, clinical features, histopathological features, and treatment plans for various benign and malignant salivary gland tumors. The document emphasizes that surgical resection is usually the primary treatment for salivary gland tumors, with adjuvant radiotherapy sometimes used as well.
This document discusses various tumors of the salivary glands. It begins by describing the major salivary glands and then covers topics such as pleomorphic adenoma, carcinoma ex pleomorphic adenoma, Warthin's tumor, mucoepidermoid carcinoma, adenoid cystic carcinoma, acinic cell carcinoma, non-Hodgkin's lymphoma, and squamous cell carcinoma. Key points are that pleomorphic adenoma is the most common tumor of the major salivary glands, adenoid cystic carcinoma is most common in the minor salivary glands, and mucoepidermoid carcinoma is the most common malignant tumor overall.
This document provides information on tumors of the salivary glands. It discusses the anatomy and histology of salivary glands, classification of salivary gland tumors, and specifics on certain tumor types including pleomorphic adenoma and Warthin's tumor. Pleomorphic adenoma is the most common benign salivary gland tumor, characterized by epithelial and mesenchymal differentiation. Warthin's tumor commonly occurs bilaterally in the parotid glands of older smoking males. The document covers epidemiology, etiology, histogenesis, clinical features, investigation, pathology and treatment of various salivary gland tumors.
There are five main histological types of bronchogenic carcinoma: squamous cell carcinoma, adenocarcinoma, bronchioalveolar carcinoma, small cell carcinoma, and large cell carcinoma. Squamous cell carcinoma typically presents as a central hilar tumor with necrosis and keratinization. Adenocarcinoma usually presents as a peripheral nodule and shows gland formation and mucin production. Bronchioalveolar carcinoma has a lepidic growth pattern along alveoli. Small cell carcinoma appears as a central hilar nodule with sheets of small blue cells. Large cell carcinoma forms a peripheral lobulated mass with large, anaplastic cells showing no clear cell type.
Salivary gland tumors can be benign or malignant. Benign tumors are more common and include pleomorphic adenomas, Warthin's tumors, and oncocytomas. These typically present as slow-growing masses in the parotid or submandibular glands. Malignant tumors are less common but can be diagnosed based on symptoms like rapid growth, pain, nerve palsies, or lymph node involvement. The most common sites for minor salivary gland tumors are the hard palate and other areas of the oral cavity. A thorough examination is needed to determine if a salivary gland tumor is benign or malignant.
This document discusses urinary bladder tumors. It begins by covering the anatomy and histology of the bladder. It then describes the WHO classification of bladder tumors, which includes urothelial, squamous, glandular, urachal, mullerian, and mesenchymal tumors, among others. Non-invasive urothelial lesions like carcinoma in situ, papillomas, and non-invasive papillary carcinomas are summarized. Invasive urothelial carcinoma is also covered, noting the range of architectural patterns and cell types seen microscopically. Variants with divergent differentiation like squamous or glandular are also common. The document provides an overview of bladder tumor pathology.
Recent advances in lung tumors and tumor like lesionsEkta Jajodia
This document summarizes recent advances in lung tumors and tumor-like lesions. It discusses the WHO classification of common lung cancers including squamous cell carcinoma, small cell carcinoma, adenocarcinoma, and carcinoid tumors. It also reviews tumor-like lung lesions and the IASLC/ATS/ERS classification of lung adenocarcinoma. Molecular subtypes of lung cancer characterized by mutations in genes such as EGFR, KRAS, ALK are described. Guidelines for molecular testing to select patients for targeted therapy are provided.
1) Salivary gland tumors are mostly benign (80%), with the majority originating in the parotid glands.
2) Pleomorphic adenoma is the most common benign tumor, representing 80% of parotid gland tumors.
3) Mucoepidermoid carcinoma is the most common malignant salivary gland tumor in both adults and children, typically presenting as a slow-growing mass in the parotid gland or palate.
Most solitary pulmonary nodules are found to be granulomas, lung cancers, or hamartomas. Benign nodules can be diagnosed if they are less than 3 cm and have certain calcification patterns like central, laminated, or popcorn patterns. Probability of malignancy is high with positive FDG PET scans and low with negative scans. For indeterminate nodules, follow-up CT scans are recommended. Nodules under 10 mm with low likelihood of cancer can be observed, while intermediate or high likelihood nodules should be biopsied or resected.
Neoplastic polyps can be benign or malignant. Adenomas are benign epithelial tumors that have the potential to become cancerous over time. There are several types of adenomas classified by their histological features, including tubular, villous, and tubulovillous. Large or villous adenomas have a higher risk of already containing cancer. Removal of adenomas is important as nearly all colon cancers develop from these polyps. Risk factors for the adenoma containing high-grade dysplasia or cancer include large size over 1 cm, villous histology, presence of high-grade dysplasia, and having multiple polyps.
The document provides information on the classification of salivary gland tumors. It begins with an introduction and then discusses the etiology, histogenesis, theories of histogenesis, morphogenesis, genetics, WHO classification from 1972-2017, general features of benign and malignant tumors, problems in clinical diagnosis, investigations including imaging techniques and histopathological investigation. It also provides examples of common tumors like pleomorphic adenoma and adenoid cystic carcinoma. Finally, it briefly outlines the TNM staging system for salivary gland tumors.
An adenoma is a benign tumor of glandular epithelium where cells are arranged in a recognizable glandular structure. Adenomas may cause excess secretion from affected glands. The major difference between adenomas and malignant tumors is that adenomas do not metastasize or spread. Sometimes adenomas develop into adenocarcinomas. Symptoms of adenomas vary and include lumps, excess secretion, or no symptoms. Adenomas can be diagnosed via colonoscopy or imaging and appear as sessile, flat, or pedunculated polyps.
Atypical pulmonary metastasis: the radiologic findingsThorsang Chayovan
Pulmonary metastasis is common, with the lungs acting as a filter for cancer cells from the lymphatic system. While multiple, round nodules in random distribution are typical, atypical presentations can include poorly-defined lesions, cavitation, calcification, hemorrhage, pneumothorax, airspace opacities, tumor emboli, endobronchial growths, solitary masses, or vessels within tumors. Certain primary cancers like sarcomas are also linked to specific radiologic appearances of pulmonary metastases. Awareness of atypical presentations helps avoid misdiagnosis versus primary lung disease.
Salivary gland tumours are a relatively rare and morphologically diverse group of lesions. So here are slides containing information about salivary gland tumours with images.
lymphnodes having metastatis from primary tumors. incidence of metastasis from various tumors to lymph nodes. how to differentiate metastatic lymph node from primary lymph node tumor(lymphoma) overview of TNM staging with example.
This document summarizes details of a laryngectomy specimen from a 52-year-old male patient with carcinoma of the larynx. On gross examination, the specimen showed a moderately differentiated squamous cell carcinoma involving the supraglottis, glottis, both vocal cords and subglottis. The carcinoma infiltrated the underlying outer cortex of the thyroid cartilage and adjacent minor salivary gland tissue. The document also provides background information on laryngeal carcinoma, including risk factors, common sites of involvement, histological subtypes, and staging guidelines.
1) Salivary gland tumors are diverse in histopathology and include both benign and malignant neoplasms. The parotid gland is the most common site.
2) Pleomorphic adenoma is the most common benign parotid tumor, comprising 80% of cases. Surgical excision is the primary treatment but recurrence is common after enucleation without a margin.
3) Mucoepidermoid carcinoma is the most common malignant salivary gland tumor. Treatment involves surgical resection with or without adjuvant radiation or chemotherapy depending on grade and stage. Prognosis depends on these factors with 5-year survival rates ranging from 90% for low grade to 40% for high grade disease.
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
it describes the bony anatomy including the femoral head , acetabulum, labrum . also discusses the capsule , ligaments . muscle that act on the hip joint and the range of motion are outlined. factors affecting hip joint stability and weight transmission through the joint are summarized.
Assessment and Planning in Educational technology.pptxKavitha Krishnan
In an education system, it is understood that assessment is only for the students, but on the other hand, the Assessment of teachers is also an important aspect of the education system that ensures teachers are providing high-quality instruction to students. The assessment process can be used to provide feedback and support for professional development, to inform decisions about teacher retention or promotion, or to evaluate teacher effectiveness for accountability purposes.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
Macroeconomics- Movie Location
This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
6. •New entities or terminology:
- Thoracic SMARCA4-deficient undifferentiated tumor
- Bronchiolar adenoma/ciliated muconodular papillary tumor
- Lymphoepithelioma-like carcinoma → Lymphoepithelial
carcinoma
- Enteric adenocarcinoma → Enteric-type adenocarcinoma
CHANGES IN WHO 2021 CLASSIFICATION OF LUNG
TUMOURS
7. HISTOLOGICAL SUBTYPE OF LUNG
CARCINOMAS
•Small cell lung cancer (SCLC)
•Non-small cell lung cancer (NSCLC)
– Squamous cell cancer
– Adenocarcinoma
– Large cell carcinoma
– Other subtypes
9. ADENOCARCINOMA : Molecular /
cytogenetics :
EGFR mutation
KRAS mutation
ALK rearrangement
TP53 point mutation
ROS1 gene fusions
BRAF mutation, V600E most common
NTRK mutation
PDL1mutation
STK11 mutation
KEAP 1 mutation
HER2 amplification
MET amplification
SMARCA4 loss of function
10. ADENOCARCINOMA : Molecular / cytogenetics
Genetic abnormalities seen in epidermal growth factor receptor (EGFR) and
downstream mitogen-activated protein kinases (MAPK) and phosphatidylinositol 3-
kinases (PI3K) signaling pathways.
ALK gene translocation with EML4 at 2p chromosome is also seen.
ALK translocated pulmonary adenocarcinoma shows solid growth pattern, often with
signet ring cell morphology.
Occur in young age ,non smokers and lacks mutation of EGFR,KRAS,TP53.
11. ATYPICAL ADENOMATOUS
HYPERPLASIA(AAH)
• This is defined as a small ,localised
proliferation of atypical pneumocytes
usually ≤ 5 mm lining the alveoli forming
small peripheral nodule .
• It is recognised as precursor lesion to invasive
adenocarcinoma.
12. ATYPICAL ADENOMATOUS
HYPERPLASIA(AAH)
•Atypical pneumocytes showing mild to
moderate atypia with enlarged cell and
increased N:C ratio; hyperchromatic nuclei.
• Atypical cells form a discontinuous
monolayer of cells c/a (skip lesion)
lining the alveoli.
• Mitotic activity is typically minimal
• There is minimal/no septal widening
and absence of septal inflammation
or fibrosis.
• Positive for TTF1
13. ADENOCARCINOMA IN
SITU(AIS)
•Defined as a localised (≤3cm) neoplastic
lesion growing along existing alveolar walls
in a lepidic growth pattern.
•Atypical cells form a continuous monolayer
of cells along alveoli ,no stromal invasion; no
necrosis
• shows mild to moderate cytologic atypia,
hyperchromasia, small nucleoli, increased
N:C ratio, hob nailing may be present.
Mucinous type adenocarcinoma in situ are
extremely rare
D/D-Minimally invasive adenocarcinoma-
invasive foci present
14. D/D OF ATYPICAL ADENOMATOUS
HYPERPLASIA (AAH)
•ADENOCARCINOMA IN SITU - is >0.5cm ( unlike AAH <0.5 cm) in size lesion, shows
cellular crowding and more abrupt transition to adjacent normal alveolar lining than AAH
and Columnar cells form a continuous monolayer along the alveoli.
•REACTIVE PNEUMOCYTE HYPERPLASIA- shows parenchymal inflammation and
fibrosis and the atypical pneumocytes tend to be more diffuse and do not form well
defined nodular areas. (unlike AAH.)
15. Minimally Invasive
Adenocarcinoma
• MIA is adenocarcinoma with lepidic growth pattern
predominantly with foci of invasion measuring
≤0.5 cm in greatest dimension and invasive
component should be non lipidic , as it can be
Acinar, papillary, micropapillary, solid , colloid,
fetal or mucinous.
• Acinar Pattern is the commonest invasive pattern
seen here.
• Image shows small invasive component consisting
of well differentiated glands (acinar pattern)seen
infiltrating through desmoplastic stroma.
16. The Entire Tumor Must Be Sampled for Diagnosis of AIS orMIA
Minimally invasive adenocarcinoma should be excluded if the tumor
Invades lymphatics, blood vessels, or pleura or
contains tumor necrosis
shows tumour spread through air spaces.
If multiple microinvasive areas are found in 1 tumor, the size of the
largest invasive area should be measured in its greatest dimension
and it should be 5 mm or less in size.
•Invasive adenocarcinoma, lepidic predominant pattern:
• Invasive foci must be 0.5 cm or more in size
•Adenocarcinoma in situ / Atypical adenomatous
hyperplasia
• No invasive component
Differential diagnosis of MIA
17. INVASIVEADENOCARCINOMA
• It is m/c lung cancer in nonsmokers and females , usually peripheral in location .
• Invasion should be present in at least 1 focus, measuring more than 5 mm in greatest
dimension .
(1) Histologic pattern of invasion should be other than lepidic pattern (ie,
acinar,papillary, micropapillary, and/or solid, colloid, fetal, enteric type).
(2) Document percentage (>5%) of each type present( lepidic to papillary to
acinar, micropapillary) as they are usually composed of complex heterogenous
mixture of patterns.
18. INVASIVE
ADENOCARCINOMA
shows peripherally located poorly circumscribed
mass containing a large area of central scarring.
•Greyish yellow on cut .
• There is a strong tendency for
multicentric, multilobar, and bilateral
lung involvement, which may reflect
aerogenous spread.
19. Lepidic Invasive
Adenocarcinoma
• Defined as non mucinous
adenocarcinoma that has lepidic
growth as its predominant
component means tumor cells
grow along the alveolar walls
• Tumor with lepidic predominant
pattern usually have good
prognosis.
20. Acinar Predominant
Adenocarcinoma
• Shows round / oval closely
packed glands with visible
lumen seen invading in to
desmoplastic stroma .
• Individual cells are round to
oval shows high N:C ratio,
pleomophism, hyperchromatic
nuclei, prominent nucleoli with
moderate amount of cytoplasm
and peripheral nuclear
polarization and apical
cytoplasm can be seen.
• Desmoplastic stroma is usually
present.
21. PapillaryAdenocarcinoma
• Presence of papillary structures with
true fibrovascular cores replacing the
alveolar lining or present within the
alveolar spaces
• The fibrovascular cores are lined by
cuboidal to columnar neoplastic cells
22. MicropapillaryAdenocarcinoma
Characterized by tumor cells growing in
small papillary tufts that lack fibrovascular
cores, these may be detached and/ or
connected to alveolar walls.
• The tumor cells are usually small
and cuboidal with mild to
moderate nuclear atypia.
• Small glandular structures may ‘‘float’’
within alveolar spaces .Vascular and
stromal invasion is frequent.
• Associated with poor prognosis.
23. SolidAdenocarcinoma
• Shows polygonal shaped tumor cells
arranged in sheets that lack recognizable
patterns of adenocarcinoma
• If the tumor is 100% solid, intracellular mucin
should be present in 5 or more tumor cells in
each of 2 hpf, confirmed with histochemical
stains for mucin
• Solid adenocarcinoma must be distinguished
from squamous cell carcinomas and large cell
carcinomas, both of which may show rare
cells with intracellular mucin
• Associated with poor prognosis.
24.
25.
26.
27. Invasive mucinous
adenocarcinoma
• Large glands filled with mucin are characteristic of the
mucinous adenocarcinoma
• Comprising of columnar epithelium and shows
intracytoplasmic mucin ,minimal cytological atypia.
• These tumors may show the same heterogeneous
mixture of lepidic, acinar, papillary, micropapillary, and
solid growth as in non mucinous tumors
• If there is at least 10% of each component, it
should be classified as ‘‘mixed invasive
mucinous and non mucinous adenocarcinoma
28. Colloid
Adenocarcinoma
• This is characterised by extracellular mucin
lakes that can expand and destroy existing
alveolar spaces.
• Contains malignant mucinous epithelium
which is of tall columnar type , growing along
the alveolar septa in a lepidic pattern,is often
difficult to visualise. Tumor cell clusters are
seen floating in pools of mucin.
29. Enteric Type
adenocarcinoma
• Is an extremely rare tumor that has a
striking resemblance to colorectal
adenocarcinomas.
• It is composed of moderate to well-
differentiated glands, often with cribriform
pattern, lined by eosinophilic tall columnar
cells with nuclear pseudostratification, dirty
necrosis and nuclear debris.
• Presence of other subtypes of primary lung
adenocarcinomas & CK7 negativity
facilitates distinction from metastatic
colorectal adenocarcinoma , frequently
express some or all markers of enteric
differentiation such as CDX2, MUC2 and
CK20, in addition to the pulmonary markers.
30. Fetal adenocarcinoma
• This is characterised by Irregular tubular
structures lined by columnar epithelial
cells with clear cytoplasm and oval
nuclei, optically clear nuclei rich in
biotin.
• Resembles fetal lung in pseudoglandular
stage
• Morular metaplasia, as in endometrioid
adenocarcinoma, can also be seen
• AFP+ ,PAX 8 – differentiate it from
endometrioid carcinoma.
32. D/D OF ADENOCARCINOMA
•Squamous cell lung carcinoma
• Is positive for p40 or p63; negative for TTF1
• shows large, more eosinophilic cells with intracellular bridges and contains keratin
•Small cell lung carcinoma
• Is positive for neuroendocrine markers, shows Small round blue cells, usually in sheets .
•High grade neuroendocrine tumor
• Increased mitotic activity (> 10/high power field), necrosis
• Positive for neuroendocrine markers and nuclear chromatin is clumped / salt and pepper
appearance
•Metastatic adenocarcinoma
• Negative for TTF1 (unless thyroid),Positive for markers from primary site(CDX2+ metastatic
colorectal adenoca, ER+ breast ca, GATA3+ urothelial ca)
•Metastatic papillary thyroid carcinoma
• psammoma bodies, nuclear features of PTC (orphan Annie)
• PAX8 and thyroglobulin positive
33. SQUAMOUS CELL CARCINOMA
•They have a strong association with cigarette smoking.
•SCC usually presents as a central tumour close to the hilum.
• They tend to produce symptoms earlier than adenocarcinoma and commonly show direct
spread into adjacent structures, in particular hilar lymph nodes. However, they are late to
metastasize compared with adenocarcinoma .
• can occur as endobronchial growth - associated with bronchial obstruction and post
obstructive pneumonia.
37. Basaloid variant : SCC
The tumor cells have a basophilic appearance and
are arranged in lobules with peripheral
palisading.
It is high-grade poorly-differentiated
variant that lacks obvious squamous
morphology ( like keratinization, keratin pearls,
intercellular bridges) but expresses squamous cell
markers (p40, p63) by immunohistochemistry.
Tumors with obvious squamous differentiation but a
majority basaloid component (>50%) are also
classified as Basaloid variant of SCC.
38. Basaloid variant : SCC
Basaloid squamous cell carcinoma
composed of inter anastamosing
cords of basaloid cells having central
areas of typical squamous cell
carcinoma.
Compressed lung parenchyma can be
seen at the top of the image.
It is characterized by a very
aggressive clinical course.
39. LYMPHOEPITHELIAL
CARCINOMA
•Lymphoepithelial carcinoma shows
syncytial growth pattern
•Large polygonal cells , round to oval
vesicular nuclei with multiple prominent
nucleoli and variably abundant
eosinophilic cytoplasm along with
lymphoid infiltrate and variable mitosis
•Squamous markers: CK5/6, p40, p63 +
•EBER1 +: desirable diagnostic criteria
40. IHC: Squamous cell carcinoma
•SCC strongly positive for p40, p63 and high molecular weight cytokeratin– CK 5/6
,Thrombomodulin .
•Always negative for TTF-1 and Napsin-A, Vimentin .
41. Differential Diagnosis of squamous cell
carcinoma
Metastatic squamous cell carcinoma( positive for markers
of origin.)
42. LARGE CELL CARCINOMA
LCCs are undifferentiated malignant epitheial carcinomas lacking cytologic features
of small-cell carcinoma and glandular or squamous differentiation.
They represent approximately 10% of Non Small Cell Lung Ca and have a strong
association with cigarette Smoking.
They commonly present as large peripheral tumours that shows a
fleshy, necrotic cut surface without cavitation.
This is a diagnosis of exclusion that can only be accurately made on a surgical
specimen rather than biopsy due to the heterogeneity of lung carcinomas“
43. LARGE CELL CARCINOMA : MOLECULAR ALTERATIONS
KRAS mutation
NRAS mutation
MET amplification
STK11mutation
PIK3CA Amplification & mutation
44. Large cell
carcinoma
Tumor cells are large,pleomorphic,
with abundant cytoplasm &
prominent nucleoli.
Atypical mitotic figures are usually
present.
46. D/D OF LARGE CELL CARCINOMA
• Large cell Neuroendocrine carcinoma – synaptophysin, chromogranin, NSE +
• Solid variant of adenocarcinoma –TTF1, NAPSIN +
• Basaloid squamous cell carcinoma – P40 +
• Metastatic carcinoma – positive markers for site of origin.
47. SARCOMATOID CARCINOMA
• Sarcomatoid carcinomas are a group of poorly differentiated non-small cell
carcinomas
• Strongly associated with tobacco smoking ,Classified into
Pleomorphic carcinoma
variants- Spindle cell carcinoma
Giant cell carcinoma
Carcinosarcoma
Pulmonary blastoma
48. • usually aggressive, poorly differentiated malignant
epithelial neoplasm composed of cells with significant
cytologic atypia and nuclear pleomorphism
•Contains at least 10% spindle cells and / or giant cells
Pleomorphic carcinoma
•Giant cells usually bizarre with multilobulated nuclei,
abundant eosinophilic cytoplasm accompanied by heavy
neutrophilic infiltrate
•Stroma is often myxoid, with collagen fibers, numerous
mitotic figures
•Massive necrosis common, Vascular invasion is
common, characterized by the presence of pleomorphic,
undifferentiated cells and numerous giant cells.
49. Subtype of Sarcomatoid carcinoma
Majority of cases are diagnosed in adults over the age
of 65 years
Carcinoma composed exclusively
of spindle-shaped tumor cells
Tumor cells often obliterate vessels
Spindle cell carcinoma
These tumors consist of spindle-shaped tumor cells
haphazardly arranged in irregular fascicles and
whorls.
50. Pulmonary giant cell
carcinoma
Consists of discohesive, pleomorphic,
mononucleated or multinucleated giant cells
,frequently intermingled with a rich
inflammatory infiltrate predominantly
composed of neutrophils. Prominent
Mitosis also seen
51. Pulmonary blastoma
• Usually seen in adults ,peripherally located, large
mass, characterised by well differentiated glands
resembling fetal lung lined by pseudostratified
columnar cells with subnuclear and supranuclear
glycogen vacuoles
• Cellular stoma composed of undifferentiated small
blastematous spindle cells with variable cellular atypia,
possible heterologous differentiation (skeletal muscle,
cartilage and bone)
Morules which are clusters of cells with
abundant acidophilic cytoplasm & ground
glass nuclei due to accumulation of biotin
are common
Positive stains
PAS (glycogen in epithelial cells)
Molecular Genetics
CTNNB1mutation,aggressive tumor with poor prog.
52. D/D OF Pulmonary blastoma
• Fetal type adenocarcinoma- no blastematous stroma
•Pleuropulmonary blastoma –occur in age <4 years, no epithelial component,DICER1 mutation
•Synovial sarcoma –TTF1- ,TFEL1 +
•Carcinosarcoma – absence of morules , CTNNB1 mutation -
53. More common in male with
smoking history & older age
Sites - Large airway and
peripheral lung
Biphasic tumor composed of a
mixture of well differentiated adenocarcinoma
and heterologous sarcomatoid differentiation
Rare tumor with poor prognosis
Osteosarcoma, chondrosarcoma, and
rhabdomyosarcoma are the
most common components, sometimes intermingled in the
same tumor.
Carcinosarcoma
54. ADENOSQUAMOUS
CARCINOMA
•Defined as carcinoma showing both squamous and
glandular differentiation, with each component
comprising at least 10%.
•Associated with cigarette smoking.
• They often present as a peripheral mass and can
show central scar formation .
•On immunohistochemistry, the adenocarcinoma
component should express TTF-1 and CK7, while the
squamous component is usually stained by p63 and
CK5/6.
55. OTHER EPITHELIAL TUMOURS
• Thoracic SMARCA4-Deficient ( WHO update)
Undifferentiated Tumor
• NUT carcinoma
56. Thoracic SMARCA4-Deficient
Undifferentiated Tumor
• occur in middle age, male & in smokers
•It is rapidly progressive tumor
• Present as large mass in mediastinum or pulmonary
hilum or pleura with or w/o chest wall involvement
•Often present with metastases.
57. SMARCA4-UT
•Poorly differentiated tumor usually with
rhabdoid morphology.
•Diffuse sheets of variably cohesive, large
,round to epithelioid cells,with large
eccentric nuclei with vesicular
chromatin & prominent nucleoli and
large paranuclear intracytoplasmic
inclusions & abundant eosinophilic
cytoplasm .
•Focal myxoid or desmoplastic stroma
can be seen
•Epithelial architecture(glands) should be
absent.
58. SMARCA4-UT
Loss of BRG1 (& BRM) expression .
Preserved INI-1 expression.
Commonly positive for SOX2, CD34 and/or SALL4.
• Negative or focal positivity for- Keratin (focal), claudin 4 (rare), TTF-1 (rare),
synaptophysin.
SMARCA4 (BRG1) - is a member of BAF chromatin- remodelling complex
Regulates transcription , promotes cell differentiation.
Biallelic inactivation of SMARCA4 gene.
TP53 mutation can also be seen .
60. NUT carcinoma
NUT carcinoma is an aggressive malignancy characterized by NUT gene
rearrangements
Somatic NUT reciprocal translocation leading to expression of an oncogenic NUT fusion
gene
Positive stains
NUT speckled nuclear positivity.
Keratins, particularly high molecular weight +
p63 and p40 ,MYC ,p16 +
Negative stains
CD99, synaptophysin, FLI1, EGFR, HER2, focal TTF1
61. NUT carcinoma
•Diffuse architecture with occasional spacing
and dyscohesion of tumor cells is present
• Cells are primitive looking, monotonous,
medium sized cells with frequent
cytoplasmic clearing ,prominent nucleoli.
•Scattered foci of abrupt keratinization can be
seen
•Background can shows necrosis with
prominent neutrophils.
62. D/D OF NUT carcinoma
•Focally keratinizing or basaloid squamous cell carcinoma :
NUT immunohistochemistry is important in differentiating these tumors
•Thymic carcinoma :
Thymic carcinomas usually express all of CD5, GLUT1 and CD117
•Small cell carcinoma:
Occasional positivity for synaptophysin and nuclear molding in NUT carcinoma is a diagnostic
pitfall
NUT immunohistochemistry can help differentiate
•Ewing sarcoma:
Occasional positivity for CD99 in NUT carcinoma is a pitfall
Ewing sarcomas express NKX2.2 by immunohistochemistry and harbor EWSR1 gene
rearrangement
63. Bronchial Adenoma / Ciliated
Muconodular Papillary Tumor
•Benign tumor
•Peripheral, peribronchiolar in location , not
associated with proximal bronchi
• affects middle age to elderly, no sex
predilection
•Tumor diameter is usually <2.5 cm
64. BA / CMPT
• shows papillary or glandular architecture
•Luminal epithelial cells may contain mucous
and or ciliated cells or cuboidal cells
•Shows continuous basal cell layer
surrounding luminal cells.→ p40 and TTF-1
positive.
•No nuclear atypia; rare mitoses
•Potential molecular alterations are: BRAF,
EGFR, KRAS, HRAS, ALK, AKT1
65.
66. BA/CMPT
Differential Diagnosis
•Adenocarcinoma (including AIS) – lacks continuous basal cell layer.
•Papilloma -central, endobronchial( unlike BA/CMPT which shows
parenchymal involvement)
•Peribronchiolar metaplasia
Lack of expression of BRAF, ALK
Often multicentric, no discrete nodule formation ( in contrast to
BA/CMPT.)
Occur in background of Interstitial lung ds or small airways disease.
67. Neuroendocrine Neoplasms
• Precursor lesion of neuroendocrine tumors
Diffuse idiopathic neuroendocrinal cell hyperplasia
• Neuroendocrine carcinomas
Small cell carcinoma
Large cell neuroendocrine carcinoma
• Neuroendocrine tumours
Carcinoid tumor , NOS
TYPICAL
ATYPICAL
68.
69. Small Cell Carcinoma
• Arises from neuroendocrine cells.
• Centrally located masses , extension to lung
parenchyma can be seen.
• Tan-white ,soft, friable mass, extensively necrotic.
• Involvement of hilar & mediastinal nodes
70. MUTATIONS: SMALL CELL CARCINOMA
Tp53 mutation
Ch.3p deletion
Loss of function mutation of RB gene
L-MYC amplification
Telomerase activation
Small cell carcinomas have highest mutational burden.
71. Paraneoplastic syndromes
Due to abnormal production of:
– increased ACTH secretion (Cushing's syndrome)
– increased ADH (SIADH - hyponatremia)
– Superior venacava syndrome.( obstruction of svc -facial &limb edema)
– Encephalomyelitis
– Lambert-Eaton syndrome (ab against voltage gated calcium channels,ms
weakness)
– Carcinoid sx (due to serotonin &bradykinin-flushing,wheezing, diarrhoea)
– Subacute sensory neuropathy
Small cell carcinoma is very aggressive tumor with early distant
metastasis
72. Shows sheets and clusters of small round
,hyperchromatic cells with dispersed finely
granular( salt & pepper) chromatin,
inconspicuous nucleoli and scant cytoplasm
and forming rossette
Small cell carcinoma
• shows nuclear moulding, high mitotic rate.
• Stroma: thin, delicate, scant, fibrovascular.
• Necrosis and apoptosis of individual cells
common
73. Crushed elongated deformed small blue cells
along with chromatin diffusion c/a “Crush
artifact” or “chromatin smearing or
streaming” is commonly seen
Azzopardi phenomena:
Basophilic nuclear DNA from necrotic tumor cells
gets deposited in the walls of vessels
small cell carcinoma
75. Differential diagnosis of small cell carcinoma
• Carcinoid tumors –ki67(MIB-1) Negative ( positive only < 10% cases).
• Large cell Neuroendocrine carcinoma - prominent nucleoli, abundant cytoplasm,
large nucleus.
• Lymphoma –Low molecular weight keratin negative.
• Basaloid variant of squamous cell carcinoma - HMW keratin + (Ck5/6,p63,p40 ),
TTF1 & Neuroendocrine markers negative.
• Poorly differentiated lung adenocarcinoma – CK 7++ (Strong),Neuroendocrine
markers -
76. Large cell neuroendocrine carcinoma
• Neuroendocrine architecture may include organoid, nesting,
palisading, trabecular, solid patterns and rosette-like
structures
• Large cells (~3x size of small cell carcinoma) with abundant
cytoplasm, nuclear pleomorphism, salt pepper
chromatin,prominant nucleoli.
• >10 mitoses / 2 mm2, extensive necrosis
• Chromogranin, synaptophysin, CD56, CD117 Cam5.2,
TTF1 + , High Ki67 index- helpful to differentiate from
carcinoid tumors, especially in small biopsies
77. Diffuse idiopathic neuroendocrinal cell
hyperplasia
•It is considered a preinvasive lesion that may progress into tumorlets or carcinoid
tumors (usually typical carcinoid).
•Histologic features comprise a diffuse intramucosal proliferation of pulmonary
neuroendocrine cells in monolayers or small groups that can penetrate through the
bronchial basement membrane to form tumorlets.
•Must be differentiated from secondary DIPNECH, which is a localized neuroendocrine
proliferation secondary to another chronic lung disease.
78. Diffuse idiopathic
neuroendocrinal cell hyperplasia
It is proliferation of neuroendocrine cells arise from
terminal bronchioles.
Cells are round, oval or spindle shaped, have a
moderate amount of eosinophilic cytoplasm and
have round to oval nuclei with a salt and pepper
chromatin.
Cells do not cross the mucosal basal lamina.
79. CARCINOID TUMORLET
• Tumorlet presenting as a small poorly defined
nodule of neuroendocrine cells that cross
beyond mucosal basal lamina
• They are benign,poorly defined nodules with
infiltrative margins in a fibrotic stroma, usually
found in relation to an airway.
• Tumor size < 5 mm with minimal mitosis &
absence of necrosis.
80. Differential diagnosis of carcinoid tumorlet
Typical carcinoid:
Tumor size 5 mm or more with < 2 mitoses/2 mm² and absence of necrosis
Atypical carcinoid:
Tumor size 5 mm or more with > 2 mitoses/2 mm² or presence of necrosis
81. • Typical Carcinoid tumor have central & peripheral
variants, mostly asymptomatic.
• Central carcinoids- present with recurrent
pneumonias or hemoptysis.
• association with (MEN)1 syndrome in 5%
• Grossly, carcinoids are usually >5mm or more in
size , well-circumscribed, round to oval mass
filling up the bronchial lumen. Appear as yellow
or fleshy, polypoid masses.
• tumor can infiltrate between cartilaginous
rings to extensively involve the bronchial
submucosa.
Carcinoid tumor
82. • Tumor cells are arranged in nested
pattern ,composed of intermediate
sized uniform polygonal cells,having
central nuclei, inconspicuous nucleoli,
moderate amount of granular
cytoplasm.
• characteristic of neuroendocrine tumor is
chromatin that is finely dispersed granular
or classically described as “salt and
pepper” chromatin.
• Ocassionally nuclear pleomorphism and
hyperchromasia can be seen but without or
<2 mitosis per 2 mm2 and lacks
necrosis.
Typical Carcinoid tumor
83. •Different patterns of Typical carcinoid
A. organoid nesting arrangement
B. Prominent spindle cell pattern
C. Trabecular pattern
D. Oncocytic features with abundant eosinophillic cytoplasm
84. Atypical carcinoid
• Histologic patterns similar to typical carcinoids: organoid,
trabecular, papillary.
• Tumor cells shows ,greater pleomorphism than typical
carcinoid , nuclei with salt and pepper chromatin and
inconspicuous nucleoli, along with moderate to abundant
eosinophilic cytoplasm. Spindle cells and clear cell
features can be seen
• Stroma is fine and highly vascularized; hyalinization,
cartilage or bone formation are possible
• shows 2 - 10 mitoses per 2 mm² or presence of
necrosis
Mitotic rate should be counted in the area with the highest
proliferation rate .
91. BENIGN PEComa /
SUGAR TUMOR
Also called as- Clear cell tumor
Benign peripheral lung mass derived from
perivascular epithelioid cells, occurs in
adults >40 years of age.
Gross- Small sharply outlined
glistening ,red- tan mass
c/s -shows foci of necrosis
92. SUGAR TUMOR
Microscopy :
Clear to eosinophilic, finely granular
cytoplasm containing abundant PAS+
glycogen.
Small, uniform, round nuclei with small
nucleoli, prominent sclerotic
vasculature.
There is absence of cellular atypia,
necrosis, and mitotic activity.
“Spider cells” with nuclear condensation
of eosinophilic cytoplasm with extensions
to the cell membrane.
96. Lymphangiomyomatosis (LAM) is a low-grade
destructive tumor that diffusely
involves lungs in women of reproductive age.
About 15% of patients with LAM have tuberous
sclerosis.
Cytological features are same as other pecomatous
tumours. The tumor cells may invade lymphatics and
blood vessel walls causing secondary hemorrhage and
destruction of the septal wall.
This results in formation of cystically-dilated airspaces
Lymphangioliomyomatosis
97. LAM shows proliferation of plump spindle-shaped
cells arranged in short fascicles around arterioles,
venules, and lymphatics which cause thickening of
alveolar septa.
Lymphangioleiomyomatosis
98. • Mutations in tuberous sclerosis genes
TSC1 and TSC2
• TFE3 (transcription factor 3 ) rearrangement –
associated PEComa shows aggressive
behaviour and poor prognosis
IHC : PEComatous Tumor
102. PROGNOSIS
Histologic type
Tumor size and location
Involvement of pleura
Surgical margins
Status and location of lymph nodes by station
Tumor grade
Lymphovascular invasion
Identification of gene mutations in lung cancer
Spread Through Airspace (STAS)
103. Spread Through Airspace (STAS)
• It is defined as tumor cells within airspaces beyond the edge of main tumor
•Present in 15-56% of NSCLC
• composed of 3 morphological Patterns: Micropapillary structures, Solid tumor
cell nests , Discohesive single tumor cells
•Spread through air spaces is more commonly associated with
adenocarcinomas
•SQCC, neuroendocrine neoplasms (all subtypes), pleomorphic carcinoma
can also show stas but less commonly
•Not included in total % of pattern or tumor size for staging because its just a
pattern of tumor spread.
104. Spread Through Airspace (STAS)
The extent of STAS was graded according to the distance from the edge of tumor with
a two-tiered system.
When all tumor clusters were present within 2500 μm (equivalent to one field of ×10
objective lens) from the edge of the tumor, STAS was graded as I, while it was graded
as II when any of tumor clusters were seen equal or greater than 2500 μm away from
the edge of tumor .
To differentiating STAS from artifacts. Artifacts were defined as; (1) tumor cell clusters
with jagged edges owing to tumor fragmentation or knife cuts during specimen
processing; (2) linear strips of cells that were lifted off the alveolar walls; (3) rare
isolated tumor clusters found at a distance rather than spreading in a continuous
manner.
105. Spread Through Airspace (STAS)
•Reduced recurrence free and overall survival in any
stage lung adenoCa
•Associated with aggressive pathologic features, KRAS
mutations
•Limited resection shows –
possibly higher risk for recurrence than lobectomy