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7 Cards in this Set

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Precursor lesions of lung tumors
• Usually associated with bronchial lesions; often present in uninvolved bronchus near carcinoma
• No distinct criteria for dysplasia versus CIS
• Gross: either unremarkable or papillary, granular with loss of folds
• Micro: focal to full thickness replacement of epithelium by squamous cells with increased nuclear to cytoplasmic ratio, nuclear pleomorphism, mitotic activity but intact basement membrane; no invasive growth although may extend into ducts of submucosal glands

Bronchioalveolar atypical adenomatous hyperplasia
• Diagnostic variability exists
• Aka adenoma, well differentiated bronchioalveolar carcinoma of Clara cell or type II pneumocyte type
• Associated with coexisting bronchioloalveolar carcinoma and papillary adenocarcinoma
• If malignant appearing but noninvasive, call “bronchioloalveolar carcinoma of nonmucinous type”
• Micro: alveolar lining cells replaced by cuboidal cells with uniform, mildly to highly atypical nuclei, scanty cytoplasm, minimal mitotic figures
Lung adenocarcinoma vs mesothelioma: IHC
• (+) for calretinin, WT1, CK5/6
• (-) for BerEP4, B72.3, LeuM1, CEA
• (+) for BerEP4, B72.3, CEA, LeuM1, TTF
• (-) for calretinin, CK 5/6, WT1.

EM: long, slender microvilli in mesothelioma; short in adenocarcinoma
Smoking related cancers
Carcinomas of

• Lung
• Lip
• Tongue
• Pharynx
• Larynx
• Esophagus
• Bladder
• pancreas
• kidney
• Floor of mouth
Lung: carcinomas, in general
• 95% of lung tumors are bronchogenic carcinoma
• In US, lung cancer is #1 cause of cancer death; causes 30% of cancer deaths in men
• Peak ages 50-69 years

Risk factors:
• Cigarette smoking:
• Causes most cases of lung cancer (RR smokers: non is 10-20:1; risk related pack years)
• 10% of smokers have atypia or hyperplasia of bronchial epithelium
• Carcinogens in tobacco smoke are benzo [a] pyrene (an initiator) and phenol derivatives (promoters)
• Usually associated with squamous cell and small cell carcinoma, less likely with adenocarcinoma
Other causes:
• Radiation exposure,
• Uranium
• Asbestos
• exposure to nickel, chromate, coal, mustard gas, arsenic, beryllium, iron, vinyl chloride, radon radiation, gold miners
Symptoms: cough, weight loss, chest pain, shortness of breath, increased sputum production
Systemic symptoms:
• Lambert-Eaton myasthenic syndrome (muscle weakness due to antibodies to neuronal calcium channel), sensory peripheral neuropathy, acanthosis nigricans, leukemoid reaction, hypertrophic pulmonary osteoarthropathy (clubbing), superior vena cava syndrome (compression/invasion of SVC causes venous congestion, circulatory compromise, dusky head, arm edema), pain in distribution of ulnar nerve and Horner’s syndrome (enophthalmos, ptosis, miosis, anhidrosis) due to apical lung tumors called Pancoast tumors
• broad classification is non-small cell carcinoma (80%) versus small cell carcinoma (20%)
• Many have mixed histologic subtypes
Spread: along bronchus distally and proximally, into lung parenchyma to mediastinum or pleura, causing pleural seeding, pleural effusion, involvement of diaphragm and chest wall
Metastases: 50% have nodal involvement at resection (usually hilar, mediastinal and supraclavicular); also metastases to adrenals (50%), liver (30%), brain, bone; also opposite lung, pericardium, kidneys
Treatment: complete excision for non-small cell lung carcinoma; radiation therapy (usually non-curative), chemotherapy (rarely curative, even for small cell carcinoma)
Survival: overall 5 year survival is 10-15%; only 30% have limited disease at diagnosis
For stage I non-small cell carcinoma, 5 year survival is 60%, poor prognostic factors are p53+, HER2+, angiolymphatic invasion or tumor size > 3 cm
Poor prognostic factors (clinical): high TNM stage, weight loss >10% of body weight, age < 40 years or women (usually are high stage), small cell or giant cell subtypes, angiolymphatic invasion, pleural effusion, lack of lymphoplasmacytic reaction
Favorable subtypes: non-mucinous bronchioloalveolar, well differentiated squamous cell
Gross: arise near hilus; hemorrhage, necrosis, cavities are common; 2-5% are multiple; peripheral tumors are usually adenocarcinomas
Micro (see also specific subtypes): begins with atypia, then warty excrescence, then fungates into lumen, penetrates wall of bronchus growing along broad front to produce a cauliflower like intraparenchymal mass; 80% have vascular invasion
Molecular: dominant oncogenes are K-ras (adenocarcinomas), c-myc (small cell carcinomas), p53, Rb, 3p suppressor gene; non-small cell carcinogenesis may be related to loss of Cables protein expression at 18q11-12
Metastasis to lung
• Lung is a common site
• Usually multiple, bilateral, sharply outlined, rapidly growing, more pleomorphic and necrotic than lung primaries, negative for TTF1
• Often multiple discrete nodules in periphery of lung; also lymphangitis carcinomatosa (peribronchial and perivascular patterns via lymphatics); rarely intralymphatic microscopic foci that may cause pulmonary hypertension
• Treatment: excision of isolated nodules
• Nodular metastases: breast, GI tract, kidney, sarcoma, melanoma
• Lymphangitis carcinomatosis: stomach, breast, choriocarcinoma, pancreas, prostate; case report with hepatocellular carcinoma
• Central cavitation: squamous cell carcinoma of upper aerodigestive tract, colonic adenocarcinoma, leiomyosarcoma
• Intrabronchial masses: breast, kidney, colon
• Tumor emboli: breast, stomach, liver, choriocarcinoma
• Lepidic pattern: colon, pancreas
Lymphomatoid granulomatosis
• Maybe angioimmunoproliferative lesion?
• Lymphoproliferative disorder that is malignant or likely prem-alignant, resembles PTLDs.
• Middle aged men and women with well defined, bilateral rounded mass densities on chest Xray
• Associated with transplant-related immunosuppression, Sjogren’s syndrome, HIV
• 80% of cases have extrapulmonary involvement (skin, CNS, kidneys, liver, spleen, adrenal glands, heart, GI tract)
• Rarely, there is only extrapulmonary involvement
• Usually no hilar or mediastinal lymph node involvement
• May be an EBV related, B cell proliferation; T cells present are usually reactive
• May have reversal of T helper / suppressor ratio
• Large number of atypical lymphoid cells is a poor prognostic factor
• Median survival 14 months; death due to sepsis, destruction of lung tissue; similar infiltrates found in other organs
Treatment: chemotherapy
Micro: nodular inflammatory infiltrate of large atypical lymphoid cells (prominent nuclei, mitotic activity), plasma cells, immunoblasts, involving walls of pulmonary vessels (angioinvasive, angiocentric, angiodestructive); no multinucleated giant cells
Positive stains: EBV (50-70%)
Lung: Small cell carcinoma
Small cell carcinoma
AKA undifferentiated carcinoma, oat cell carcinoma
10-20% all of lung carcinoma,
Usually men, median age 60 years, 99% occur in smokers, very aggressive with early mediastinal lymph node involvement
Apparently derived from primitive cells of basal bronchial epithelium with partial differentiation towards neuroendocrine cells
Associated with paraneoplastic syndromes due to production of ADH (hyponatremia), ACTH (Cushing’s syndrome), parathyroid hormone (hyperparathyroidism), calcitonin (hypocalcemia), gonadotropins (gynecomastia), serotonin (carcinoid syndrome), encephalomyelitis, sensory neuropathy, Lambert-Eaton syndrome
Diagnosis is based on H & E staining, not the presence of neuroendocrine markers
5 year survival (n=55): stage I - 33%, II - 44%, IIIA - 22%, IIIB - 0%, IV - 12%
Biopsies often crushed; cytology may be helpful
Flow cytometry: CD56+ (neural cell adhesion molecule), CD45-, which differentiates from lymphoma.
Treatment: chemotherapy, radiation; cure rates of 15-25% for limited disease; most live 1 year; preoperative chemotherapy and surgery if T1-2, N0-1, M0
Poor prognostic factors: elevated serum LDH, alkaline phosphatase, albumin, hemoglobin, white blood count
Gross: usually central/hilar; white-tan, soft, friable, extensive necrosis; peripheral nodules have fairly well-defined border and fleshy cut surface
Micro: sheets, ribbons, clusters, rosettes or peripheral pallisading of small to medium sized (2-4x neutrophils) round/oval cells with minimal cytoplasm, salt and pepper chromatin without prominent clumps, hyperchromatic, indistinct nucleoli, nuclear molding, smudging, frequent mitotic figures; Azzopardi phenomena (basophilic nuclear chromatin spreading to wall of blood vessels), indistinct cell borders; stroma is scanty, vascular, delicate; no glands, replacement of epithelium is less common than subepithelial growth; necrosis and apoptotic debris are common
More cytoplasm is present in cells in metastases or resections than in small biopsies
May have larger cells with similar morphology, small mixtures of squamous cell carcinoma or adenocarcinoma; rarely scattered giant cells, prominent nucleoli

Positive stains: pan-keratin (100%, dot like pattern), CK-BB (91%), TTF1 (89%), histamine decarboxylase (78%, Mod Path 2003;16:72), neuron specific enolase (77%), CD117 (75%, 50% after chemotherapy), chromogranin (58%, may be weak), synaptophysin (57%), calretinin (49%), thrombomodulin (27%), keratin5 (27%), CD56/Leu7 (variable), gastrin releasing peptide, N-CAM, bcl-2 (variable)
Negative stains: CD3, CD20, CD45, CD99/MIC2, pancreatic polypeptide, vimentin, mesothelin, p63
EM: occasional round, membrane bound, dense core neurosecretory granules, 100-200 nm in diameter; may have bundles of tonofibrils; may form glandular spaces
DD: atypical carcinoid tumor (less nuclear atypia, <20 mitotic figures per 10 HPF, no extensive necrosis, more intense neuroendocrine staining)