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Pathologic Evaluation of Lung Cancer 65 Table 4–2. World Health Organization Classification of Nonepithelial Tumors of the Lung Soft Tissue Lymphoproliferative Miscellaneous Tumor-Like Tumors Diseases Tumors Lesions Localized fibrous tumor Epithelioid hemangioendothelioma Pleuropulmonary blastoma Chondroma Calcifying fibrous pseudotumor of the pleura Congenital peribronchialmyofibroblastic tumor Diffuse pulmonary lymphangiomatosis Desmoplastic round cell tumor Source: Travis et al, 1999. Lymphoid interstitial pneumonia (LIP) Nodular lymphoid hyperplasia Low-grade marginal zone B-cell lymphoma of the mucosaassociatedlymphoid tissue (MALT) Lymphomatoid granulomatosis Hamartoma Sclerosing hemangioma Clear cell tumor Germ cell tumors: teratoma, mature; teratoma, immature Thymoma Malignant melanoma Tumorlet Minute meningothelioid nodules Langerhans cell histiocytosis Inflammatory pseudotumor (inflammatory myofibroblastic tumor) Localized organizing pneumonia Amyloid tumor (nodular amyloid) Hyalinizing granulomaLymphangioleiomyomatosis Micronodular pneumocyte hyperplasia Endometriosis Bronchial inflammatory polyp ratio, abnormalities in nuclear contour and nuclear chromatin, increased numbers of nucleoli and mitoses, and loss of normal maturation with alteration of polarity. Squamous dysplasia is graded as mild, moderate, or severe depending on the thickness of the involved epithelium and the severity of the changes. Carcinoma in situ is full-thickness involvement of the squamous mucosa by neoplastic cells that show all the morphologic features of squamous cell carcinoma but are confined by the basement membrane. These cells have the potential to invade into the underlying stroma, at which point they would be classified as squamous cell carcinoma. Carcinoma in situ cells may extend into submucosal glands, but such extension is not considered invasion as long as the basement membrane is not breached.
66 P. Tamboli and J.Y. Ro Atypical Adenomatous Hyperplasia AAH is defined as a lesion measuring 5.0 mm or less that is composed of atypical epithelial cells lining the alveoli and respiratory bronchioles (Travis et al, 1999). The morphologic appearance of this lesion is similar to that of nonmucinous bronchioloalveolar adenocarcinoma (BAC). In AAH, the alveolar septae are thickened and lined by a monotonous layer of cuboidal or low columnar cells with scant cytoplasm, enlarged hyperchromatic nuclei, and inconspicuous nucleoli (Figure 4–3). When examined with an electron microscope, these cells show the features of either type II pneumocytes or Clara cells. AAH has been referred to in the past by various names, including atypical bronchioloalveolar cell hyperplasia, bronchioloalveolar adenoma, atypical alveolar hyperplasia, alveolar epithelial hyperplasia, and atypical alveolar cuboidal cell hyperplasia. AAH is thought to be the most likely precursor for pulmonary adenocarcinoma, especially nonmucinous BAC. There is no conclusive evidence of this association, but there is much circumstantial evidence, including the frequent association of AAH with adenocarcinoma, the presence of multifocal AAH in lungs removed for adenocarcinoma, and the observation of a morphologic transformation from AAH to adenocarcinoma (Kitamura et al, 1999). A study using analysis of the human androgen receptor gene has shown AAH to be a monoclonal proliferation (Niho et al, 1999). Additional corroborating evidence of the malignant potential of AAH and its similarity to adenocarcinoma includes reports indicating that AAH has the following features: p53 mutations (Kitamura et al, 1999), expression of carcinoembryonic antigen (Kitamura et al, 1999), expression of blood group antigens, increased proliferative activity as measured by Ki-67 antibody, higher mean nuclear area as measured by nuclear morphometry (Kitamura et al, 1999), loss of heterozygosity of loci on chromosomes 3p, 9p, and 17p, telomerase activity, and the presence of mutations of codon 12 of the K-ras gene. The lesions included in the differential diagnosis of AAH are reactive alveolar epithelial hyperplasia, nodular type II pneumocyte hyperplasia, bronchiolization of the alveolar septae, and small BAC. Of these, small BAC is the most important differential diagnostic consideration because in the 1997 TNM staging system for lung cancer, multiple tumor nodules within the same lobe are considered pT4 disease but the presence of a tumor nodule in a different lobe is classified as M1 disease (Sobin and Wittekind, 1997). Thus, in the case of a separate nodule in another lobe (i.e., not the lobe containing the main tumor), confusing AAH for a small BAC or vice versa could potentially affect management decisions for the patient. Morphologic features that favor BAC are loss of alveolar architecture with prominent papillary growth, marked cell
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Lung Cancer Frank V. Fossella, MD R
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Frank V. Fossella, MD Department of
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vi Foreword possible. Since the res
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x Contents Chapter 7 Surgical Treat
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xii Contributors Joe B. Putnam, Jr.
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2 J.B. Putnam, Jr., F.V. Fossella,
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Page 39 and 40: 26 F.V. Fossella common sites of lu
Page 41 and 42: 28 F.V. Fossella history and physic
Page 43 and 44: 30 F.V. Fossella Computed Tomograph
Page 45 and 46: 32 F.V. Fossella Pulmonary Function
Page 47 and 48: 34 F.V. Fossella The use of flexibl
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Page 71 and 72: 58 P. Tamboli and J.Y. Ro Chapter O
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Page 115 and 116: 102 W.R. Smythe nation for these su
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116 W.R. Smythe Henschke CI, McCaul
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7 SURGICAL TREATMENT OF LOCALLY ADV
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120 S.G. Swisher Treatment Options
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122 S.G. Swisher Initial Assessment
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124 S.G. Swisher Figure 7-1. Region
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126 S.G. Swisher Table 7-2. (contin
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128 S.G. Swisher upper paratracheal
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130 S.G. Swisher is performed only
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132 S.G. Swisher chance for long-te
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134 S.G. Swisher Pancoast tumors th
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136 S.G. Swisher A B Figure 7-2. Do
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138 S.G. Swisher a combination of t
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140 S.G. Swisher Dartevelle PG, Cha
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8 NONSURGICAL TREATMENT OF EARLY-ST
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144 R. Komaki morbid conditions pre
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146 R. Komaki and 26 patients had c
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148 R. Komaki Around 1998, by using
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150 R. Komaki Table 8-5. Survival a
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152 R. Komaki A total of 610 patien
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154 R. Komaki tially obstructed air
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156 R. Komaki report of Radiation T
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9 TREATMENT OF PATIENTS WITH ADVANC
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160 R. Zinner chemotherapy, in pati
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Table 9-1. Chemotherapy in Older Pa
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164 R. Zinner results of additional
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Table 9-3. Third-Generation-Agent M
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Table 9-4. Third-Generation Agents
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Table 9-5. Third-Generation Platinu
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Table 9-6. Comparisons between Diff
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174 R. Zinner may play an important
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Table 9-8. Third-Generation Cisplat
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178 R. Zinner wards higher survival
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180 R. Zinner KEY PRACTICE POINTS
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182 R. Zinner DeVore RF, Fehrenbach
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184 R. Zinner Perng RP, Chen YM, Mi
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10 TREATMENT OF LIMITED-STAGE SMALL
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188 R. Komaki Age is not a signific
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190 R. Komaki lished between 1979 a
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Table 10-1. Complete Response Rates
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194 R. Komaki twice daily to a tota
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196 R. Komaki Intergroup study 0096
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198 R. Komaki Figure 10-1. Survival
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200 R. Komaki cisplatin with concur
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202 R. Komaki KEY PRACTICE POINTS
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204 R. Komaki tients (Pts) with lim
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206 R. Komaki Wagner H, Kim K, John
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208 G.R. Blumenschein, Jr. recurs a
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210 G.R. Blumenschein, Jr. syndrome
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212 G.R. Blumenschein, Jr. toxicity
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214 G.R. Blumenschein, Jr. the year
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216 G.R. Blumenschein, Jr. is chara
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218 G.R. Blumenschein, Jr. new cyto
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12 PALLIATIVE CARE IN PATIENTS WITH
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222 J.B. Putnam, Jr. therapy. Patie
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224 J.B. Putnam, Jr. tion—includi
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226 J.B. Putnam, Jr. rates were 47%
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228 J.B. Putnam, Jr. Dyspnea The ma
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230 J.B. Putnam, Jr. Small-bore cat
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232 J.B. Putnam, Jr. A B Figure 12-
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234 J.B. Putnam, Jr. C D Figure 12-
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236 J.B. Putnam, Jr. B Figure 12-3.
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238 J.B. Putnam, Jr. KEY PRACTICE P
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240 J.B. Putnam, Jr. Rendina EA, De
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242 A.A. Vaporciyan, J.F. Kelly, an
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14 PREVENTION AND EARLY DETECTION O
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258 E.S. Kim and F.R. Khuri A secon
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260 E.S. Kim and F.R. Khuri Smoking
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262 E.S. Kim and F.R. Khuri Reversa
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264 E.S. Kim and F.R. Khuri yet to
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266 E.S. Kim and F.R. Khuri nation
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268 E.S. Kim and F.R. Khuri Methodo
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270 E.S. Kim and F.R. Khuri have be
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272 E.S. Kim and F.R. Khuri the tre
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274 E.S. Kim and F.R. Khuri changes
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276 E.S. Kim and F.R. Khuri KEY PRA
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278 E.S. Kim and F.R. Khuri Hong WK
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15 MOLECULAR EVENTS IN LUNG CANCER
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282 W.N. Hittelman, J.M. Kurie, and
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300 Index Anterior spinal column re
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302 Index Cardiac murmurs, 104 Card
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304 Index Diagnosis. See also under
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306 Index Growth. See Tumor growth
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308 Index Magnetic resonance (MR) i
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310 Index p16 gene, 285 p19 arf gen
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312 Index Pulmonary resection (cont
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314 Index Squamous metaplasia, 263-
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316 Index Vitamin A, 262 Vocal cord
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