Non Small Cell Lung Cancer Histopathology ד"ר יהודית זנדבנק
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1 Non Small Cell Lung Cancer Histopathology ד"ר יהודית זנדבנק
2 Lecture outlines WHO histological classification Macro/Micro assessment Early diagnosis Minimal pathology Main subtypes SCC, AdCa, LCLC Histology / Cytology IHC DD Molecular genetics Prognosis and histopathology Neuroendocrine tumor concept Targeted therapy
3 The most simple classification of lung cancer: Small cell lung cancer (SCLC) v` Non-small cell lung cancer (NSCLC)
4 WHO histological classification Squamous cell carcinoma - Papillary - Clear cell - Small cell - Basaloid
5 Adenocarcinoma - Mixed subtype - Acinar - Papillary - Bronchioloalveolar *Nonmucinous *Mucinous *Mixed
6 -Solid adenocarcinoma with mucin production *Fetal *Mucinous (colloid) *Mucinous cystadenocarcinoma *Signet ring cell adenocarcinoma *Clear cell adenocarcinoma
7 Large cell carcinoma -Large cell neuroendocrine carcinoma *Combined large cell neuroendocrine ca. -Basaloid carcinoma -Lymphoepithelioma-like carcinoma -Clear cell carcinoma -Large cell carcinoma with rhabdoid phenotype
8 Adenosquamous cell carcinoma Sarcomatoid carcinoma -Pleomorphic -Spindle cell -Giant cell -Carcinosarcoma -Pulmonary blastoma
9 Salivary gland tumours -Mucoepidermoid -Adenoid cystic -Epithelial myoepithelial
10 Why classify?
11 Classification Prognosis Treatment Pathogenesis/biology Epidemiology
12 Macroscopic and Microscopic assessment of NSCLC Tumor size Tumor necrosis Pleural involvement Resection margin evaluation Assessment of sampled lymph nodes Search for intrapulmonary metastases Histological heterogeneity Grading Vascular, lymphatic involvement
13 Early lesions, Pulmonary epithelium Bronchial (ciliated, mucous, neuroendocrine, reserve, metaplastic) Bronchioles/alveoli (Clara cells, types I and II alveolar lining cells)
14 Early lesion, Bronchial: Squamous metaplasia Dysplasia Carcinoma in situ Invasive malignancy
15 Normal bronchial mucosa
16 Bronchial mucosa basal cell hyperplasia
17 Normal bronchial mucosa Squamous metaplasia
18 Bronchial mucosa Squamous cell carcinoma in situ (severe dysplasia)
19 Early lesion, bronchioles/alveoli Atypical Adenomatous Hyperplasia Spread of neoplastic cells along alveolar walls (bronchioloalveolar carcinoma) True invasive adenocarcinoma THIS PATTERN IS BECOMING COMMONER
20 Atypical Adenomatous Hyperplasia (AAH)
21 Bronchiolalveolar carcinoma (BAC)
22 Minimal pathology Bronchoscopic biopsies Core needle biopsies
23 Minimal pathology (cont.) No tumor Minimal amount of tumor Morphology Immunohistochemistry Lung tumors - heterogeneous
24 Adeno Ca.?? SCC
25 >90% smokers Squamous cell carcinoma Central and peripheral in increase 44% in males 25% in females Macroscopy large, grey, firm, cavitary, post obstructive pneumonia Tumor spread - locally aggressive - less locoregional metastases - common locoregional recurrence
26 Squamous cell carcinoma Immunohistochemistry HMW/CK, CK5/6, CEA positive TTF1, CK7, LMW/CK rarely (+ve)
27 SCC Differential diagnosis Large cell carcinoma Solid adenocarcinoma (focal mucin content acceptable) Thymic carcinoma in case of massive mediastinal involvement SCC metastases Squamous metaplasia with atypia in reactive conditions, e.g.. DAD
28 SCC histological criteria for prognosis prediction Better prognosis than adenocarcinoma The more necrosis the worse the prognosis Well differentiated SCC more locoregional spread Poorly differentiated SCC early metastases to distant sites Alveolar filling of peripheral SCC more favorable prognosis
29 SCC molecular genetics EGFR gene mutations 84% K-RAS - rare Her2 rare p53 gene function disruption common Rb gene pathway disruption - common
30 Squamous Cell Carcinoma
31 Squamous cell carcinoma Histology / Cytology
32 Squamous Cell Lung Cancer:FNA
33 Adenocarcinoma (AdCa) Surpassed SCC as most common lung cancer. Most in smokers But in women non smokers Women 42% Men 28% ~20% present with distant metastases Local recurrence not as common as SCC
34 AdCa (cont.) Mixed subtypes 80% Mixed degree of differentiation Therefore ample sampling is necessary When only bronchioloalveolar carcinoma seen ample sampling to look for invasive component
35 AdCa - macroscopy Peripheral Central Diffuse pneumonia-like, BAC Diffuse bilateral disease simulating interstitial pneumonia, BAC Growth along pleurae, simulating mesothelioma In background of underlying fibrosis
36 AdCa - immunohistochemistry Pan CK LMW/CK CK7 EMA CEA TTF1 SPB1
37 AdCa differential diagnosis Atypical Alveolar Hyperplasia v` BAC (>5mm) Prominent bronchiolar metaplasia in fibrotic lesions, e.g. interstitial pneumonia Metastatic adenocarcinoma Mesothelioma, epithelial
38 AdCa - histogenesis Central - bronchial epithelium - bronchial glands Periphery - type II pneumocytes - clara cells
39 AdCa prognostic histological factors Poor differentiation- increased local recurrence - increased lymph node metastases Grading insignificant in peripheral T1 AdCas but High grade histology, vascular invasion, mf, few intra-tumoral lymphocytes, extensive necrosis are unfavorable prognosticators Unfavorable papillary and micropapillary patterns
40 AdCa molecular genetics EGFR gene mutations K-RAS - ~30% P53 P16ink4 K-RAS mutations contraindicate therapy with EGFR tyrosine kinase inhibitors
41 Adenocarcinoma
42 Adenocarcinoma
43 Adenocarcinoma: FNA
44 Adenocarcinoma: mucin stain
45 Adenocarcinoma with lepidic features Restricted to cases without pleural, vascular or stromal invasion ~20% 5 yr survival of localized, resected BAC is 100% Recent studies - AdCa with predominant BAC and small (<0.5cm) central scarring in tumor of </=3cm have a similar favorable prognosis (~30%) - AdCa <2cm with BAC, without central desmoplastic reaction, 100% survival at 10 yrs
46 Bronchioloalveolar carcinoma macroscopy
47 Mucinous carcinoma Non mucinous carcinoma
48 Mucinous Bronchioloalveolar carcinoma cytology/cell block CK20 TTF1 CK7 BAC cell block
49 Large cell lung cancer (LCLC) Most peripheral 9% Locoregional invasion common to pleura, chest wall Metastases Poorly differentiated neoplasms Originate from a common pluripotential progenitor cell
50 LCLC differential diagnosis Poorly differentiated SCC Poorly differentiated ADC/solid LCNEC No precursor lesions
51 Non-small Cell Lung Cancer:NOS
52 Large cell carcinoma
53 Non-small Cell Lung Cancer:NOS
54 The concept of Neuroendocrine tumors Carcinoid Atypical carcinoid (AC) Large cell neuroendocrine tumor (LCNEC) Small cell lung cancer (SCLC) -All in different categories in the WHO classification. -WHO nomenclature to be used.
55 Low grade neuroendocrine tumors Carcinoid v` Atypical carcinoid 2-10 mitotic figures/10 high power fields Necrosis small foci Cytologic atypia non significant Thus small biopsies may be non diagnostic between the two diagnoses. Both: 20-40% are not smoking related May occur in patients with MEN May be associated with NE cell hyperplasia +/- tumorlets
56 High grade neuroendocrine tumors LCNEC - >11mf/10hpf Most LCNEC and SCLC 70-80mf/10hpf Typical morphology for each tumor Histological heterogeneity, common Most are smoking related To be differentiated from NSCLC with NE differentiation
57
58 Treatment Selection in Advanced NSCLC The OLD Way Empiric Comparison of RR, PFS, and OS only in randomized, controlled trials Best numbers = Standard of care The NEW Way Rational Emphasis on targeted therapy Molecular targets Histology guides therapeutic options
59 Conclusions Targeted therapies have demonstrated a survival benefit in selected patients with NSCLC Treatment of NSCLC should be individualized Histology Molecular markers
60 Targeted Therapies Bevacizumab Panitumumab Cetuximab Erlotinib Sunitinib Sorafenib Sorafenib Temsirolimus Chemotherapy Inhibition of programmed cell death (apoptosis) Tumor cell proliferation Tumor cell invasion metastasis Development of tumor vasculature (angiogenesis)
61 KRAS and EGFR EGFR and KRAS mutations in NSCLC are mutually exclusive KRAS is downstream in the EGFR pathway KRAS mutations are seen in a subset of patients with NSCLC More common in smokers than non-smokers More common in adenocarcinomas NSCLC patients with KRAS mutations may be less likely to respond to EGFR-TKIs
62 EGFR Ligand Receptor antibodies Ligand-binding domain Tyrosine kinase inhibitors (ATP-binding cleft) PI3K K K Grb-2 SOS Ras Raf PTEN Akt MEK mtor Survival STAT 3/5 MAPK Proliferation Adapted from: Pao W and Miller VA. J Clin Oncol. 2005;23:
63 Markers of Interest for EGFR tyrosine kinase inhibitors: EGFR EGFR expression by IHC Least helpful EGFR gene copy number by FISH EGFR mutations Sensitizing: exons 19, 21, and others Predictive of resistance: exon 20, T790
64 Squamous Cell Carcinoma: EGFR Positive
65 EGFR gene copy number/ FISH assay
66 Molecular genetic abnormalities (potential therapeutic targets): SCLC NSCLC Oncogenes, Myc Myc, K-ras, Her2 Tumor suppressor genes p53, Rb, p3, p53,1q 3p, 9p, 11p, Rb,
67 Pathology/Early microscope Molecular biology
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