Uploadvirus (talk | contribs) |
Kwamikagami (talk | contribs) Undid revision 425091018 by Uploadvirus (talk) - we need intelligible English here. Rv. per MOS & agreement to use these names. |
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Lung cancers have been historically classified using two major paradigms. [[Histological]] classification systems group lung cancers according to the appearance of the cells and surrounding tissues when they are viewed under a microscope. [[Clinical]] classification systems divide lung cancers into groups based on medical criteria, particularly their response to different treatment regimens. |
Lung cancers have been historically classified using two major paradigms. [[Histological]] classification systems group lung cancers according to the appearance of the cells and surrounding tissues when they are viewed under a microscope. [[Clinical]] classification systems divide lung cancers into groups based on medical criteria, particularly their response to different treatment regimens. |
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Before the mid-1900's, lung cancer was considered to be a single disease entity, with all forms treated similarly. In the 1960's, [[small |
Before the mid-1900's, lung cancer was considered to be a single disease entity, with all forms treated similarly. In the 1960's, [[small-cell lung carcinoma]] (SCLC) was recognized as a unique form of lung cancer, based both on its appearance ([[histology]]) and its [[clinical]] properties, including much greater susceptibility to [[chemotherapy]] and [[radiation]], more rapid growth rate, and its propensity to metastasize widely early on in its course. Since then, most [[oncologists]] have based patient treatment decisions on a dichotomous division of lung cancers into SCLC and [[non-small-cell lung carcinoma]]s (NSCLC), with the former being treated primarily with chemoradiation, and the latter with surgery. |
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An explosion of new knowledge, accumulated mainly over the last 20 years, has proved that lung cancers should be considered an extremely [[heterogeneous]] family of [[neoplasms]]<ref name='RoggliVollmer'>Roggli VL, Vollmer RT, Greenberg SD, McGavran MH, Spjut HJ, Yesner R. Lung cancer heterogeneity: a blinded and randomized study of 100 consecutive cases. Hum Pathol 1985; 16: 569-79.</ref> with widely varying genetic, biological, and clinical characteristics, particularly their responsiveness to the large number of newer treatment protocols. Well over 50 different histological variants are now recognized under the 2004 revision of the [[World Health Organization]] ("WHO-2004") typing system, currently the most widely used lung cancer classification scheme.<ref name='who2004' /> Recent studies have shown beyond doubt that the old clinical classification paradigm of "SCLC vs. NSCLC" is now obsolete, and that correct "subclassification" of lung cancer cases is necessary to assure that lung cancer patients receive optimum management.<ref name='RossiMarchioni'>Rossi G, Marchioni A, Sartori1 G, Longo L, Piccinini S, Cavazza A. Histotype in non-small cell lung cancer therapy and staging: The emerging role of an old and underrated factor. Curr Resp Med Rev 2007; 3: 69-77.</ref><ref name='Vincent'>Vincent MD. Optimizing the management of advanced non-small-cell lung cancer: a personal view. Curr Oncol 2009; 16: 9-21.</ref> |
An explosion of new knowledge, accumulated mainly over the last 20 years, has proved that lung cancers should be considered an extremely [[heterogeneous]] family of [[neoplasms]]<ref name='RoggliVollmer'>Roggli VL, Vollmer RT, Greenberg SD, McGavran MH, Spjut HJ, Yesner R. Lung cancer heterogeneity: a blinded and randomized study of 100 consecutive cases. Hum Pathol 1985; 16: 569-79.</ref> with widely varying genetic, biological, and clinical characteristics, particularly their responsiveness to the large number of newer treatment protocols. Well over 50 different histological variants are now recognized under the 2004 revision of the [[World Health Organization]] ("WHO-2004") typing system, currently the most widely used lung cancer classification scheme.<ref name='who2004' /> Recent studies have shown beyond doubt that the old clinical classification paradigm of "SCLC vs. NSCLC" is now obsolete, and that correct "subclassification" of lung cancer cases is necessary to assure that lung cancer patients receive optimum management.<ref name='RossiMarchioni'>Rossi G, Marchioni A, Sartori1 G, Longo L, Piccinini S, Cavazza A. Histotype in non-small cell lung cancer therapy and staging: The emerging role of an old and underrated factor. Curr Resp Med Rev 2007; 3: 69-77.</ref><ref name='Vincent'>Vincent MD. Optimizing the management of advanced non-small-cell lung cancer: a personal view. Curr Oncol 2009; 16: 9-21.</ref> |
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Approximately 98% of lung cancers are [[carcinoma]], which are tumors composed of cells with [[epithelial]] characteristics.<ref name='TravisTravis'>Travis WD, Travis LB, DeVesa SS. Lung Cancer. Cancer 1995; 75: 191-202.</ref> LCLC's are one of 8 major groups of lung carcinomas recognized in WHO-2004:<ref name='who2004'>{{cite book |title=Pathology and Genetics of Tumours of the Lung, Pleura, Thymus and Heart |editor1-last=Travis |editor1-first=William D |editor2-last=Brambilla |editor2-first=Elisabeth |editor3-last=Muller-Hermelink |editor3-first=H Konrad |editor4-last=Harris |editor4-first=Curtis C |publisher=IARC Press |location=Lyon |year=2004 |series=World Health Organization Classification of Tumours |isbn=92 832 2418 3 |url=http://www.iarc.fr/en/publications/pdfs-online/pat-gen/bb10/bb10-cover.pdf |accessdate=27 March 2010}}</ref> |
Approximately 98% of lung cancers are [[carcinoma]], which are tumors composed of cells with [[epithelial]] characteristics.<ref name='TravisTravis'>Travis WD, Travis LB, DeVesa SS. Lung Cancer. Cancer 1995; 75: 191-202.</ref> LCLC's are one of 8 major groups of lung carcinomas recognized in WHO-2004:<ref name='who2004'>{{cite book |title=Pathology and Genetics of Tumours of the Lung, Pleura, Thymus and Heart |editor1-last=Travis |editor1-first=William D |editor2-last=Brambilla |editor2-first=Elisabeth |editor3-last=Muller-Hermelink |editor3-first=H Konrad |editor4-last=Harris |editor4-first=Curtis C |publisher=IARC Press |location=Lyon |year=2004 |series=World Health Organization Classification of Tumours |isbn=92 832 2418 3 |url=http://www.iarc.fr/en/publications/pdfs-online/pat-gen/bb10/bb10-cover.pdf |accessdate=27 March 2010}}</ref> |
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*Squamous |
*Squamous-cell carcinoma |
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*Small |
*Small-cell carcinoma |
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*Adenocarcinoma |
*Adenocarcinoma |
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*Large |
*Large-cell carcinoma |
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*Adenosquamous carcinoma |
*Adenosquamous carcinoma |
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*Sarcomatoid carcinoma |
*Sarcomatoid carcinoma |
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*Carcinoid tumor |
*Carcinoid tumor |
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*Salivary gland |
*Salivary gland-like carcinoma |
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==The Rhabdoid Phenotype== |
==The Rhabdoid Phenotype== |
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==Diagnosis== |
==Diagnosis== |
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While occasional scattered rhabdoid cell formation occurs with considerable frequency in lung carcinomas, this is not considered to be of clinical significance.<ref name="SainiKumar"/><ref name='ShimazakiAida'>Shimazaki H, Aida S, Sato M, Deguchi H, Ozeki Y, Tamai S. Lung carcinoma with rhabdoid cells: a clinicopathological study and survival analysis of 14 cases. ''Histopathology'' 2001;38:425-34.</ref> According to current classification criteria, a tumor can only be diagnosed as LCLC-RP when an undifferentiated [[large-cell lung carcinoma]] contains a rhabdoid |
While occasional scattered rhabdoid cell formation occurs with considerable frequency in lung carcinomas, this is not considered to be of clinical significance.<ref name="SainiKumar"/><ref name='ShimazakiAida'>Shimazaki H, Aida S, Sato M, Deguchi H, Ozeki Y, Tamai S. Lung carcinoma with rhabdoid cells: a clinicopathological study and survival analysis of 14 cases. ''Histopathology'' 2001;38:425-34.</ref> According to current classification criteria, a tumor can only be diagnosed as LCLC-RP when an undifferentiated [[large-cell lung carcinoma]] contains a rhabdoid-cell component that makes up at least 10% of the tumor mass.<ref name='CavazzaColby'>Cavazza A, Colby TV, Tsokos M, Rush W, Travis WD (1996). Lung tumors with a rhabdoid phenotype. Am J Clin Pathol 105:182-188.</ref> |
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Microscopic characteristics of rhabdoid cells include<ref name="who2004"/><ref name='SainiKumar'>Saini G, Kumar M, Julka PK, Puri T, Sharma M, Rath GK. Rhabdoid variant of lung cancer: clinicopathological details of a case and a review of literature. ''J Cancer Res Ther'' 2009;5:54-7.</ref><ref name='KanekoHonda'>Kaneko T, Honda T, Fukushima M, Haniuda M, Komatsu H, Kodama T. Large cell carcinoma of the lung with a rhabdoid phenotype. ''Pathol Int'' 2002;52:643-7.</ref>: |
Microscopic characteristics of rhabdoid cells include<ref name="who2004"/><ref name='SainiKumar'>Saini G, Kumar M, Julka PK, Puri T, Sharma M, Rath GK. Rhabdoid variant of lung cancer: clinicopathological details of a case and a review of literature. ''J Cancer Res Ther'' 2009;5:54-7.</ref><ref name='KanekoHonda'>Kaneko T, Honda T, Fukushima M, Haniuda M, Komatsu H, Kodama T. Large cell carcinoma of the lung with a rhabdoid phenotype. ''Pathol Int'' 2002;52:643-7.</ref>: |
Revision as of 00:33, 21 April 2011
Large-cell lung carcinoma with rhabdoid phenotype | |
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Specialty | Oncology ![]() |
Large-cell lung carcinoma with rhabdoid phenotype (LCLC-RP) is a rare histological variant of large-cell lung carcinoma (LCLC), wherein at least 10% of the malignant cells making up the tumor contain distinctive eosinophilic whorled perinuclear inclusions composed of aggregates of intermediate filaments,[1][2] giving the cells a microscopic resemblance to rhabdomyosarcoma, an unrelated malignant tumor of skeletal muscle.[3]
Classification
Lung cancers have been historically classified using two major paradigms. Histological classification systems group lung cancers according to the appearance of the cells and surrounding tissues when they are viewed under a microscope. Clinical classification systems divide lung cancers into groups based on medical criteria, particularly their response to different treatment regimens.
Before the mid-1900's, lung cancer was considered to be a single disease entity, with all forms treated similarly. In the 1960's, small-cell lung carcinoma (SCLC) was recognized as a unique form of lung cancer, based both on its appearance (histology) and its clinical properties, including much greater susceptibility to chemotherapy and radiation, more rapid growth rate, and its propensity to metastasize widely early on in its course. Since then, most oncologists have based patient treatment decisions on a dichotomous division of lung cancers into SCLC and non-small-cell lung carcinomas (NSCLC), with the former being treated primarily with chemoradiation, and the latter with surgery.
An explosion of new knowledge, accumulated mainly over the last 20 years, has proved that lung cancers should be considered an extremely heterogeneous family of neoplasms[4] with widely varying genetic, biological, and clinical characteristics, particularly their responsiveness to the large number of newer treatment protocols. Well over 50 different histological variants are now recognized under the 2004 revision of the World Health Organization ("WHO-2004") typing system, currently the most widely used lung cancer classification scheme.[2] Recent studies have shown beyond doubt that the old clinical classification paradigm of "SCLC vs. NSCLC" is now obsolete, and that correct "subclassification" of lung cancer cases is necessary to assure that lung cancer patients receive optimum management.[5][6]
Approximately 98% of lung cancers are carcinoma, which are tumors composed of cells with epithelial characteristics.[7] LCLC's are one of 8 major groups of lung carcinomas recognized in WHO-2004:[2]
- Squamous-cell carcinoma
- Small-cell carcinoma
- Adenocarcinoma
- Large-cell carcinoma
- Adenosquamous carcinoma
- Sarcomatoid carcinoma
- Carcinoid tumor
- Salivary gland-like carcinoma
The Rhabdoid Phenotype
Colby and colleagues were the first to report a primary lung cancer with a rhabdoid phenotype in a paper published in 1995.[8] LCLC-RP were first recognized as a distinct entity under the 3rd WHO classification system, published in 1999.[9]
Diagnosis
While occasional scattered rhabdoid cell formation occurs with considerable frequency in lung carcinomas, this is not considered to be of clinical significance.[10][11] According to current classification criteria, a tumor can only be diagnosed as LCLC-RP when an undifferentiated large-cell lung carcinoma contains a rhabdoid-cell component that makes up at least 10% of the tumor mass.[12]
Microscopic characteristics of rhabdoid cells include[2][10][13]:
- Oval to polygonal cell shape
- Eosinophilic, hyaline-like perinuclear agglomerations of intermediate filaments
- Compressed, eccentric nuclei
- Prominent central macronucleoli (one or two)
- Abundant eosinophilic cytoplasm
- Reticular chromatin pattern
The differential diagnosis of LCLC-RP includes secondary metastatic lesions, melignant melanoma of the lung with rhabdoid phenotype, mucinous adenocarcinomas (particularly those featuring signet-ring cells), rhabdomyosarcoma, epitheloid angiosarcoma, mesothelioma, and plasmacytoma.[10][11][13][14] On radiological imaging, most cases of LCLC-RP are single "coin lesions" or discrete masses, but cases presenting as multiple nodules throughout the lung have also been noted.[15] LCLC-RP may also be a tumor variant that is particularly susceptible to massive central necrosis and cavitation, with rhabdoid cells flourishing and progressing only in a "rim" remaining at the edge of the necrotic tumor mass.[16]
Results of immunohistochemistry staining in rhabdoid lung cancers tends to reflect the multiphasic nature of these tumors. Typically, markers expressed in LCLC-RP include those seen in "generic" NSCLC's, such as epithelial membrane antigen (EMA, 61%) and various cytokeratins (CK's, 80%), and markers associates with the underlying "parent" pulmonary carcinoma. Expression of immunomarkers in the rhabdoid cells, however, have often been noted to be weaker and more diffuse than those in the more differentiated tumor cells.[10][13] They also more frequently express "non-carcinomatous" markers typically associated with "dedifferentiated" neoplasms. Interestingly, expression of thyroid transcription factor-1 (TTF-1), a commonly used marker for primary lung cancers, appears to be less frequent in rhabdoid carcinomas than in most other histotypes of pulmonary cancers.[17]
Vimentin, an intermediate filament protein usually found in sarcoma, is ubiquitously (nearly 100%) expressed diffusely throughout the cytoplasm of the rhabdoid cells, and is often intermingled with CK's in their whorled inclusions. Neuroendocrine-related markers (i.e. neuron-specific enolase (NSE), neural cell adhesion molecule (NCAM), chromogranin A (CgA), and synaptophysin, are also quite frequently expressed in a significant proportion of rhabdoid cells.[10][11][13]
Histogenesis and Genetics
The histogenesis of most lung cancers is not well understood. Carcinomas of the lung are thought to arise from the uncontrolled growth of mutated, transformed multipotent "cancer stem cells" with epithelial characteristics. When viewed under a light microscope, the transformed cancer cells in LCLC are undifferentiated, lacking the specific cytological and tissue architectural characteristics of other types, subtypes, and variants of lung cancer.[2] Election microscopic studies, however, have shown that many LCLC do have ultrastructural characteristics of other tumor types (i.e. adenocarcinoma, squamous cell carcinoma).[18], and that rhabdoid carcinomas often show similar features.[19]
Some evidence suggests that cells with the rhabdoid phenotype result from further mutations occurring in some cells of the "parent" tumor, which leads to "emergence" of distinct cells with the rhabdoid phenotype within the parent neoplasm, often in the peripheral part of the tumor.[14][16][19] Missense mutations occurring in the cytokeratin 8 gene (RTK 8)[20] at specific codons affects the way the protein products of this gene assume their normal shape and undergo assembly into filamentous structures within the cytoplasm. These defective "protofilament" products apparently accumulate to form the distinctive whorled paranuclear inclusions of the rhabdoid cell.[21] It seems likely that mutations (and possibly post-tranlational modifications) affecting cytokeratins 8 and 18, and possibly vimentin, protofilaments are intimately involved in the genesis of the characteristic inclusions, and therefore, the rhabdoid phenotype. The particulars of this process are poorly understood, but depend in part on the origin of the tumor[22] and stochastic genomic phenomena.[23][24]
Rhabdoid cells often express protein products suggestive of aggressive, dedifferentiated cells, including neuroendocrine tumor-related products[11] and granulocyte-macrophage colony stimulating factor (GM-CSF).[19][25] Vimentin, which is an intermediate filament protein usually associated with non-carcinomatous tumors (i.e. sarcoma), is ubiquitous in rhabdoid cells.[26]. Co-expression of cytokeratins and vimentin are associated with cells undergoing epithelial-mesenchymal transition (EMT).[27][28]
While undifferentiated large-cell lung carcinoma is the most common parent lung tumor from which a rhabdoid phenotype evolves,[10] malignant cells with a rhabdoid phenotype are known to occur in many different histological variants of lung cancer, including adenocarcinoma[17], sarcomatoid carcinoma,[13][17], squamous cell carcinoma,[29], combined large-cell neuroencrine carcinoma,[29] and mucinous bronchioloalveolar carcinoma [30] and combined small-cell lung carcinoma.[29]
Treatment
Because LCLC-RP is so rare, no clinical trials have ever been conducted that specifically address treatment of this lung cancer variant. Because LCLC-RP is considered a form of non-small-cell lung carcinoma (NSCLC), most physicians adhere to published NSCLC treatment guidelines in rhabdoid carcinoma cases. When possible, radical surgical resection is the primary treatment of choice in NSCLC's, with or without adjuvant, neoadjuvant, or palliative chemotherapy and/or radiotherapy, depending on the disease stage and performance status of the individual patient.[31]
In numerous clinical trials of (generic) NSCLC, several different platinum-based chemotherapy regimens have been shown to be more-or-less equally effective.[31] LCLC's, as a subtype of NSCLC, have traditionally been included in many of these clinical trials, and have been treated like other NSCLC's. More recent trials, however, have shown that some newer agents may have particular effectiveness in prolonging survival of LCLC patients.[5][6] Pemetrexed, in particular, has shown significant reduction in the hazard ratio for death when used in patients with LCLC.[32] Taxane-based (paclitaxel, docetaxel) chemotherapy was shown to induce a complete and sustained response in a liver metastasis in a case of LCC-RP. A later-appearing metastasis within mediastinal lymph nodes in the same case also showed a durable response to a taxane alone.[10]
There have also been reports of rhabdoid carcinomas expressing vascular endothelial growth factor (VEGF),[16] suggesting that targeted molecular therapy with VEGF blocking monoclonal antibodies such as bevacizumab may be active in these variants.[33][34][35] However, evidence suggests that caution must be used when treating a cavitated rhabdoid tumor, one that contains significant components of squamous cell differentiation, or large tumors with containing major blood vessels, due to the potential high risk of life-threatening pulmonary hemorrhage.[33]
A recent study reported a case wherein 2 courses of adjuvant therapy with cisplatin and paclitaxel, followed by oral gefitinib, were used after complete resection. The patient had had no recurrence 34 months later.[25]
Prognosis
LCLC-RP are considered to be especially aggressive tumors with a dismal prognosis.[5][17][24] Many published cases have shown short survival times after diagnosis.[11][36] Some studies suggest that, as the proportion of rhabdoid cells in the tumor increases, the prognosis tends to worsen,[11] although this is most pronounced when the proportion of rhabdoid cells exceeds 5%.[11] With regard to "parent" neoplasms other than LCLC, adenocarcinomas with rhabdoid features have been reported to have worse prognoses than adenocarcinomas without rhabdoid features,[37] although an "adenocarcinoma with rhabdoid phenotype" tumor variant has not been specifically recognized as a distinct entity under the WHO-2004 classification system.[2]
Interestingly, there are case reports of rhabdoid carcinomas recurring after unusually long periods, which is unusual for a fast growing, aggressive tumor type. One report described a very early stage patient whose tumor recurred 6 years after initial treatment.[16] Although rapidly progressive, fulminant courses seem to be the rule in this entity, long term survival has also been noted, even post-metastectomy in late stage, distant metastatic disease.[13]
Epidemiology
Although reliable and comprehensive incidence statistics are nonexistent, LCLC-RP is known to be a rare tumor, with only a few hundred cases reported in the scientific literature to date.[10][18] LCLC's make up about 10% of all lung cancers in most series,[2][7][38][39] equating to approximately 22,000 cases per year in the U.S.[40] Of these, it is estimated that approximately 1% eventually develop the rhabdoid phenotype during tumor evolution.[18] In one large series of 902 surgically resected lung cancers, only 3 cases (0.3%) were diagnosed as LCLC-RP. In another highly selected series of large-cell lung carcinoma cases, 4 of 45 tumors (9%) were diagnosed as the rhabdoid phenotype using the 10% criterion, while another 10 (22%) had at least some rhabdoid cell formation.[11] It appears, therefore, that LCLC-RP probably comprises between 0.1% and 1.0% of all lung malignancies.
LCLC with rhabdoid phenotype appears to be highly related to tobacco smoking, and to be more common in males than in females.[17]
References
- ^ Rubenchik I, Dardick I, Auger M. Cytopathology and ultrastructure of primary rhabdoid tumor of lung. Ultrastruct Pathol 1996;20:355-60.
- ^ a b c d e f g Travis WD, Brambilla E, Muller-Hermelink HK, Harris CC (Eds.): World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of the Lung, Pleura, Thymus and Heart. IARC Press: Lyon 2004. Cite error: The named reference "who2004" was defined multiple times with different content (see the help page).
- ^ Beckwith JB, Palmer NF. Histopathology and prognosis of Wilms tumors: Results from the First National Wilms' Tumor Study. Cancer 1978;41:1937-48.
- ^ Roggli VL, Vollmer RT, Greenberg SD, McGavran MH, Spjut HJ, Yesner R. Lung cancer heterogeneity: a blinded and randomized study of 100 consecutive cases. Hum Pathol 1985; 16: 569-79.
- ^ a b c Rossi G, Marchioni A, Sartori1 G, Longo L, Piccinini S, Cavazza A. Histotype in non-small cell lung cancer therapy and staging: The emerging role of an old and underrated factor. Curr Resp Med Rev 2007; 3: 69-77.
- ^ a b Vincent MD. Optimizing the management of advanced non-small-cell lung cancer: a personal view. Curr Oncol 2009; 16: 9-21. Cite error: The named reference "Vincent" was defined multiple times with different content (see the help page).
- ^ a b Travis WD, Travis LB, DeVesa SS. Lung Cancer. Cancer 1995; 75: 191-202. Cite error: The named reference "TravisTravis" was defined multiple times with different content (see the help page).
- ^ Colby TV, Koss MN, Travis WD. Carcinoid and other neuroendocrine tumors. In: Travis WD, editor. Tumors of Lower Respiratory Tract. Washington DC: Armed Forces Institute of Pathology; 1995. p. 311.
- ^ Brambilla E, Travis WD, Colby TV, Corrin B, Shimosato Y. The new World Health Organization classification of lung tumours. Eur Respir J 2001;18:1059-68
- ^ a b c d e f g h Saini G, Kumar M, Julka PK, Puri T, Sharma M, Rath GK. Rhabdoid variant of lung cancer: clinicopathological details of a case and a review of literature. J Cancer Res Ther 2009;5:54-7.
- ^ a b c d e f g h Shimazaki H, Aida S, Sato M, Deguchi H, Ozeki Y, Tamai S. Lung carcinoma with rhabdoid cells: a clinicopathological study and survival analysis of 14 cases. Histopathology 2001;38:425-34. Cite error: The named reference "ShimazakiAida" was defined multiple times with different content (see the help page).
- ^ Cavazza A, Colby TV, Tsokos M, Rush W, Travis WD (1996). Lung tumors with a rhabdoid phenotype. Am J Clin Pathol 105:182-188.
- ^ a b c d e f Kaneko T, Honda T, Fukushima M, Haniuda M, Komatsu H, Kodama T. Large cell carcinoma of the lung with a rhabdoid phenotype. Pathol Int 2002;52:643-7.
- ^ a b Attems JH, Lintner F. Pseudomesotheliomatous adenocarcinoma of the lung with rhabdoid features. Pathol Res Pract 2001;197(12):841-6.
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- ^ Vogel AM, Gown AM, Caughlan GJ, Haas JE, Beckwith JB. Rhabdoid tumors of the kidney contain mesenchymal specific and epithelial specific intermediate filament proteins. Lab Invest 1984; 50: 232–238.
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- ^ Zinner RG, Novello S, Peng G, Herbst R, Obasaju C, Scagliotti G. Comparison of patient outcomes according to histology among pemetrexed-treated patients with stage IIIB/IV non-small-cell lung cancer in two phase II trials. Clin Lung Cancer 2010;11:126-31.
- ^ a b Johnson DH, Fehrenbacher L, Novotny WF, Herbst RS, Nemunaitis JJ, Jablons DM, et al. Randomized phase II trial comparing bevacizumab plus carboplatin and paclitaxel with carboplatin and paclitaxel alone in previously untreated locally advanced or metastatic non-small-cell lung cancer. J Clin Oncol 2004;22:2184–91.
- ^ Sandler A, Gray R, Perry MC, Brahmer J, Schiller JH, Dowlati A, et al. Paclitaxel-carboplatin alone or with bevacizumab for non-small-cell lung cancer. N Engl J Med 2006;355:2542–50.
- ^ Reck M, von Pawel J, Zatloukal P, Ramlau R, Gorbounova V, Hirsh V, et al. Phase III trial of cisplatin plus gemcitabine with either placebo or bevacizumab as first-line therapy for nonsquamous non-small-cell lung cancer: AVAil. J Clin Oncol 2009;27:1227–34.
- ^ Chetty R, Bhana B, Batitang S, Govender D. Lung carcinomas composed of rhabdoid cells. Eur J Surg Oncol 1997;23:432-4.
- ^ Sheikh SS, Al-Khatti AA, Amr SS. Metachronus malignant rhabdoid tumor of the ileum and adenocarcinoma of lung: a unique case report. Ann Diagn Pathol 2008;12:57-61.
- ^ Iyoda A, Hiroshima K, Toyozaki T, Haga Y, Fujisawa T, Ohwada H. Clinical characterization of pulmonary large cell neuroendocrine carcinoma and large cell carcinoma with neuroendocrine morphology. Cancer 2001;91:1992-2000.
- ^ Takei H, Asamura H, Maeshima A, Suzuki K, Kondo H, Niki T, Yamada T, Tsuchiya R, Matsuno Y (2002). Large cell neuroendocrine carcinoma of the lung: a clinicopathologic study of eighty-seven cases. J Thorac Cardiovasc Surg 2002;124:285-92.
- ^ American Cancer Society. Cancer Facts & Figures 2009. Atlanta: American Cancer Society; 2009.