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At least 19 recordsLinked to original sources
PubMed1990

Clinical applications of the pathological properties of small cell carcinoma, large cell carcinoma, and adenoid cystic carcinoma of the lung.

Lung cancer has considerable treatment problems, with a poor 5-yr survival rate after surgery. Application of histopathological and immunohistopathological subtyping have proven to be powerful tools for the assessment of prognosis. Results in 33 patients with small cell carcinoma, 44 with large cell carcinoma, and five with adenoid cystic carcinoma of the lung are discussed. The 5-yr survival rates in patients with small cell carcinoma of the oat cell type and intermediate type were 24 and 44%, respectively. Argyrophilic granules and neuron-specific enolase, neuroendocrine markers, were detected more frequently in the oat cell type rather than in the intermediate type. In contrast, keratin, epithelial membrane antigen, and carcinoembryonic antigen, epithelial origin markers, were present more frequently in the intermediate type than in the oat cell type. The 5-yr survival rates with large cell carcinoma of the compact growth type and the loose structure type were 46 and 28%, respectively, based on evidence of morphologically intercellular cohesion. The epithelial origin markers were detectable and more frequent in the compact growth type than in the loose structure type. The growth patterns of adenoid cystic carcinoma are classified as tubular, cribriform, and solid. The solid pattern was the most aggressive with extensive perineural invasion. We propose that the pathological properties of lung cancer should be examined as a prognostic implication of subtyping.

Adult↗
PubMed2000

[Large cell carcinoma].

Large cell carcinoma is defined as an undifferentiated carcinoma without the characteristic features of squamous cell, small cell, or adeno-carcinomas. Diagnosis is largely based on exclusion of the other cell types of lung cancer by light microscopy. Large cell carcinoma grows rapidly and is usually quite large by the time it is diagnosed. Most of colony stimulating factor-producing lung cancers previously reported are large cell carcinomas. These colony stimulating factors are considered to contribute to the progressive nature of large cell carcinoma. The radiographic appearance of large cell carcinoma is often larger than 4 cm in diameter. The margins of the mass are poorly defined and lobulated while cavitation remains infrequent. Giant cell carcinoma, which is a variant of large cell carcinoma, is a particularly aggressive subtype with a poor prognosis. Metastases occur fairly late in the course of large cell carcinoma. The sites of metastases (brain, bone, adrenal glands, and liver) are similar to those involved with adenocarcinoma, although the gastrointestinal tract metastases are more commonly involved in large cell carcinoma.

Carcinoma, Large Cell↗
PubMed1989

Differential DNA sequence deletions from chromosomes 3, 11, 13, and 17 in squamous-cell carcinoma, large-cell carcinoma, and adenocarcinoma of the human lung.

Activation of protooncogenes and inactivation of putative tumor suppressor genes are genetic lesions considered to be important in lung carcinogenesis. Fifty-four cases of non-small-cell lung cancer (23 adenocarcinomas, 23 squamous-cell carcinomas, and 8 large-cell carcinomas) were examined for loss of DNA sequences at 13 polymorphic genetic loci. Loss of heterozygosity was seen more frequently in squamous-cell carcinoma than in adenocarcinoma. The loss of DNA sequences from the short arm of chromosome 17 (D17S1 locus) was detected in 8 of 9 heterozygous cases of squamous-cell carcinoma and in only 2 of 11 heterozygous cases of adenocarcinomas. Furthermore, in 7 of these 8 squamous-cell carcinomas, loss of heterozygosity from chromosome 17 was accompanied by loss of DNA sequences from chromosome 11. The spectrum of allelic sequences lost from chromosome 11 was, however, similar in every type of carcinoma studied, and the data show two regions commonly deleted from chromosome 11 (11pter-p15.5 and 11p13-q13) that may have a role in the pathogenesis of all these types of non-small-cell bronchogenic carcinoma. Loss of DNA sequences from chromosome 3 was seen in 16 of 31 cases where the constitutive DNA was heterozygous-i.e., informative. These data included only 6 of 16 cases where loss of heterozygosity involved a chromosomal locus previously shown to be lost consistently in small-cell lung cancer (DNF15S2). Loss of heterozygosity at the chromosome 13q locus, D13S3, was seen in 9 of 21 informative cases, and in 2 cases, both adenocarcinomas, duplication of the intact DNA sequences suggested the possibility that mitotic recombination had occurred. Frequent DNA sequence deletions, including those from chromosome 17, in squamous-cell carcinomas may reflect the extensive mutagenic and clastogenic effects of tobacco smoke that may lead to inactivation of putative tumor-suppressor genes.

Adenocarcinoma↗
PubMed1982

Vindesine in the treatment of squamous cell carcinoma, adenocarcinoma, and large cell carcinoma of the lung.

The antineoplastic activity of vindesine was evaluated in a phase II trial in patients with squamous cell carcinoma, adenocarcinoma, and large cell carcinoma of the lung. Sixty-three patients participated in the trial: 22 with squamous cell carcinoma, 25 with adenocarcinoma, and 16 with large cell carcinoma. Most of the patients had not received prior treatment; six had received single-agent chemotherapy. The dose of vindesine was 4 mg/m2 every 2 weeks, reduced or increased according to hematologic and neurologic side effects. Fifty-four patients were evaluable. Objective response was observed in two of 19 patients with squamous cell carcinoma (11%), in six of 22 patients with adenocarcinoma (27%), and in one of 13 patients with large cell carcinoma (8%). In patients with adenocarcinoma the median duration of response was 196 days (range, 71-450+). Twenty-five percent of the evaluable patients received greater than or equal to 100% of the scheduled dose. In 39% of the patients, dose reductions were necessary because of leukopenia, and in 63%, dose modifications were necessary because of neurotoxic effects. It is concluded that vindesine as a single-agent chemotherapy is active against adenocarcinoma of the lung. Activity in squamous cell carcinoma and large cell carcinoma appears to be less, but not totally absent.

Adenocarcinoma↗
PubMed2001

Clinical characterization of pulmonary large cell neuroendocrine carcinoma and large cell carcinoma with neuroendocrine morphology.

BACKGROUND: Large cell carcinoma has been classified as four potential types based on its neuroendocrine morphology and evidence of neuroendocrine differentiation discernible by immunohistochemistry or electron microscopy. However, the clinical relation among these four categories has not been clearly defined. In 1999, the World Health Organization (WHO) categorized large cell neuroendocrine carcinoma as a variant of large cell carcinoma. MATERIAL AND METHODS The authors analyzed 119 cases of large cell carcinoma from a total of 2070 primary lung carcinoma cases resected surgically between 1969-1999. Using light microscopy, electron microscopy, and immunohistochemical staining, the authors reclassified these cases into large cell neuroendocrine carcinoma (LCNEC), large cell carcinoma with neuroendocrine differentiation (LCCND), large cell carcinoma with neuroendocrine morphology (LCCNM), and classic large cell carcinoma (CLCC). RESULTS: In multivariate analyses, the authors found that large cell carcinoma with neuroendocrine features, which combined LCNEC, LCCND, and LCCNM, impacted both the overall survival and disease-free survival of patients. The clinical behavior of LCCNM was similar to that of LCNEC. CONCLUSIONS: Large cell carcinomas with neuroendocrine features appear to be more clinically aggressive than CLCCs. The authors' findings suggest that the histologic identification of neuroendocrine features in tumor tissue from patients diagnosed with large cell carcinoma of the lung may have clinical relevance.

Adult↗
PubMed2003

Large cell neuroendocrine carcinoma and large cell carcinomas with neuroendocrine morphology of the lung: prognosis after complete resection and systematic nodal dissection.

BACKGROUND: Large cell neuroendocrine carcinoma (LCNEC) and large cell carcinoma with neuroendocrine morphology of the lung are both currently classified as subtypes of large cell carcinomas according to the World Health Organization IASLC classification system for lung and pleural tumors. Prognosis is reported as similar to that of small cell carcinomas. There is no consensus on management of this subset and adjuvant chemotherapy is recommended by some for early stage LCNEC to impact long-term prognosis. We retrospectively reviewed a cohort of patients at our institution who had this type of tumor to determine factors that might influence survival. METHODS: Twenty-one cases of LCNEC and large cell carcinoma with neuroendocrine morphology were identified in the files of the Royal Brompton Hospital between 1986 and 1999. All patient data were reviewed, and complete follow-up was achieved with 20 of these patients. RESULTS: Of the 21 patients identified, 20 underwent resection with systematic nodal dissection in 18. There was no in-hospital mortality. Of those patients fully staged by systematic nodal dissection, 9 were stage I, 5 were stage II and 4 were stage III. Median follow-up was 25 months (range, 2 to 120 months). At the time of review, 11 patients were alive and free of disease. One patient was alive and free of disease when lost to follow-up. Nine patients had died, 7 related and 2 unrelated to disease. The 5-year actuarial survival for the entire group was 47%. The actuarial survival of accurately staged, stage I patients at 5 years was 88%. The actuarial survival of patients in stage II and III was 28% at 5 years. CONCLUSIONS: LCNEC and large cell carcinoma with neuroendocrine morphology are aggressive tumors, but patients with completely resected disease after systematic nodal dissection have a better prognosis than previously described. Patients with more advanced disease have a poor prognosis.

Aged↗
PubMed1994

A placebo-controlled randomized double-blind study of adjuvant intrapleural BCG in patients with resected T1N0, T1N1, or T2N0 squamous cell carcinoma, adenocarcinoma, or large cell carcinoma of the lung. LCSG Protocol 771.

This article reviews the design and findings of LCSG Protocol 771, a randomized double-blind comparison of postoperative adjuvant intrapleural bacillus Calmette-Guérin (BCG) against saline solution placebo control in 473 patients with resected T1N0, T1N1, or T2N0 non-small cell lung cancer. Patients were randomized from August 30, 1977, through October 20, 1980, and follow-up ended on January 1, 1990. There was no evidence of improved survival or time to recurrence among patients given BCG in contrast to earlier promising findings. A calculation suggests that false-positive results due to chance are not uncommon in small preliminary studies, indicating the need for larger confirmatory trials such as LCSG Protocol 771. Other contributions from this Protocol are also reviewed, including data on BCG toxicity, immunologic effects, patterns of recurrence, and identification of prognostic risk groups.

Adenocarcinoma↗
PubMed1989

Primary composite squamous cell carcinoma and large cell neuroendocrine carcinoma of the hypopharynx.

Neuroendocrine carcinomas are rare neoplasms of the larynx and hypopharynx. Tumours composed of both neuroendocrine and squamous cell elements are very rare. We report a case of a primary hypopharyngeal carcinoma composed of both squamous cell and large cell neuroendocrine carcinoma and discuss the treatment of this patient and management of neuroendocrine carcinomas of the larynx and hypopharynx.

Carcinoma↗
PubMed1990

[Immunohistochemical and immunoelectron microscopic observation of human lung carcinomas using biotinized peanut lectin (PNA)].

Ninety-three cases of various types of human primary lung carcinomas have been studied by immunohistochemical technique and 5 cases of human primary lung adenocarcinomas by immunoelectron microscopic method with biotinized peanut lectin (PNA). The results showed that PNA staining was weak positive or negative in the normal bronchial epithelial cells which are adjacent to the carcinoma studied but strong or moderate positive in the carcinoma proper (P less than 0.05). The total positive rate of the lung carcinoma in this series is 81%. About 85% of the positive adenocarcinoma the PNA receptors were distributed along the luminal border, which corresponded with the linear electron-dense deposits on the luminal surface of the adenocarcinoma cell's membrane by immunoelectron microscopy. Squamous cell carcinoma, large cell carcinoma and small cell carcinoma, large cell carcinoma and small cell carcinoma were dominant in PNA cytoplasmic positive, while clear cell carcinoma in whole cell membrane positive. Some of the squamous cell carcinoma, large and small cell carcinoma showed microlumen by PNA staining that could not be found easily by conventional HE staining. It is suggested that these carcinomas mentioned above were poorly-differentiated adenocarcinoma or other types of carcinomas combined with adenocarcinoma. The results also assumed that the increasing of PNA receptor may be proportional to the differentiation of lung carcinoma cell. Therefore PNA receptor may be considered as a marker of carcinoma cell differentiation. It could be helpful in early diagnosis of lung carcinoma and prediction of the prognosis.

Adenocarcinoma↗
PubMed2006

Surfactant protein A detection in large cell carcinoma of the lung.

Large cell carcinomas of the lung are undifferentiated malignant epithelial tumors that lack cytologic features of small cell carcinoma, glandular cell carcinoma, or squamous cell differentiation. Lung surfactant protein A (SP-A) is produced by alveolar type II cells and Clara cells. Most bronchioloalveolar carcinomas of the lung react positively for SP-A. Positive SP-A staining of large cell carcinoma of the lung could indicate that at least part of these tumors have the same cellular origin or differentiation as bronchioloalveolar carcinoma. The authors determined the SP-A staining of 63 large cell carcinomas of the lung by IHC. In 20 of the 63 (32%), the tumors stained positive for SP-A. This may imply that about one third of large cell carcinomas of the lung have a similar cellular origin or differentiation as bronchioloalveolar carcinoma. The significance of this finding for prognosis and new forms of treatment remains to be determined.

Carcinoma, Large Cell↗
PubMed1985

Large cell carcinoma of the lung.

The diagnosis of large cell carcinoma of the lung on the basis of hematoxylin and eosin (H & E) stains represents a heterogeneous group, both endodermally and non-endodermally derived, totalling about 16% of lung cancers. By the use of special stains, such as Kreyberg and Grimelius stains, this percentage can be sharply reduced, leaving a core group of about 10%, including giant cell and clear cell variants. This core group may show a variety of ultramicroscopic organelles that are insufficiently developed to alter the light microscopic characteristics on which the diagnosis depends. In a study of 1000 slides, large cell carcinoma constituted 6% of the squamous cell carcinoma slides and 21% of the adenocarcinoma slides, which was reduced to 3% by mucin stains. Giant cells predominated in 5% and clear cells in 10% of large cell carcinoma slides. Large cells also occurred in 12% of small cell carcinoma slides.

Adenocarcinoma↗
PubMed2006

Characteristics of loss of heterozygosity in large cell neuroendocrine carcinomas of the lung and small cell lung carcinomas.

Large cell neuroendocrine carcinoma (LCNEC) of the lung is a new entity. Besides morphological characteristics, its molecular biological features have been investigated by many researchers and compared to those of other neuroendocrine carcinomas, small cell lung carcinoma (SCLC) and carcinoid tumor (CT). However, there are few reports that show the significantly different genetic characteristics between them. The purpose of the present paper was to study the frequency of loss of heterozygosity (LOH) at chromosome 3p (3p14.2) in 38 neuroendocrine carcinomas of the lung (13 LCNEC, 11 SCLC and 14 CT) and 10 large cell carcinomas (LCC). The frequencies of LOH at 3p14.2 were 69.2% in LCNEC, 81.8% in SCLC, 50.0% in LCC and 7.14% in CT. Those at 22q13.3 were 30.8% in LCNEC, 72.7% in SCLC, 45.5% in LCC and 7.14% in CT. In particular, the frequency of SCLC with LOH at both 3p14.2 and 22q13.3 (63.6%) was significantly higher than that of LCNEC (15.4%). LCNEC and SCLC had different characteristics of LOH patterns at 3p14.2 and 22q13.3. The combined analysis of the LOH at 3p14.2 and 22q13.3 is thought to be useful for differential diagnosis between LCNEC and SCLC.

Biomarkers, Tumor↗
PubMed1982

Vindesine in the treatment of squamous cell carcinoma (WHO I), adenocarcinoma (WHO III), and large cell carcinoma (WHO IV) of the lung.

The antineoplastic activity of vindesine was evaluated in 57 patients with non-small-cell carcinoma of the lung, 53 patients were fully evaluable for response and toxicity. Twenty-seven patients had squamous cell carcinoma (WHO I), 14 had adenocarcinoma (WHO III), and 12 had large cell carcinoma (WHO IV). Forty percent of patients were previously treated. Vindesine was administered at a weekly i.v. dose of 3 mg/m2. Partial remissions were observed in 2 of 12 patients with large cell carcinoma and in 1 of 27 patients with squamous cell carcinoma. Among 14 patients with adenocarcinoma, 3 minor responses were observed. Drug-related toxic effects (mainly leukopenia with manageable and reversible neurotoxicity) required modification of dose in 41% of patients: this finding and previous treatment may have adversely affected the response rate. It is concluded that vindesine as a single agent has some activity in large cell carcinoma. Activity in the other histologic types was minimal but not totally absent and deserves further evaluation, possibly in non-pretreated patients.

Adenocarcinoma↗
PubMed2001

Adjuvant chemotherapy for large cell carcinoma with neuroendocrine features.

BACKGROUND: In 1999, the World Health Organization categorized large cell neuroendocrine carcinoma, large cell carcinoma with neuroendocrine differentiation, and large cell carcinoma with neuroendocrine morphology as a variant of large cell carcinoma. Patients with large cell carcinoma with neuroendocrine features have poor prognoses, comparable to those for small cell lung carcinoma. Small cell lung carcinoma is sensitive to chemotherapy; however, it is still unclear whether large cell carcinoma with neuroendocrine features is responsive to adjuvant chemotherapy. METHODS: The authors analyzed 73 patients with large cell carcinoma with neuroendocrine features who underwent resection of the tumor and studied the effect of adjuvant chemotherapy for large cell carcinoma with neuroendocrine features. RESULTS: In patients with Stage I disease, the overall survival for patients with adjuvant chemotherapy based on cisplatin, carboplatin, or cyclophosphamide, which were used as standard chemotherapy for small cell lung carcinoma, were significantly higher than the overall survival for patients without adjuvant chemotherapy. In patients with Stage II, III, and IV disease, there was no significant difference between patients with adjuvant chemotherapy and without adjuvant chemotherapy. CONCLUSIONS: Adjuvant chemotherapy based on cisplatin, carboplatin, or cyclophosphamide prolongs survival of patients with large cell carcinoma with neuroendocrine features in early stage.

Adult↗
PubMed2005

Pulmonary large cell carcinoma with rhabdoid phenotype.

Large cell carcinoma of the lung with a rhabdoid phenotype is very rare. We present a 55-year-old man with multiple nodules in his lung. He had an emergency operation because of abundant hemoptysis. The microscopic appearance was a large cell carcinoma with a pure rhabdoid phenotype. There were no foci of any other carcinomatous components. Tumor cells had abundant eosinophilic cytoplasmic globules and eccentric nuclei and did not adhere to each other. Histochemically, these cells were periodic acid-Schiff-negative. Immunohistochemically, vimentin and neuron-specific enolase were positive. Epithelial membrane antigen was focally and weakly positive, p53 was positive in 60% of tumoral cells, and Ki-67 (MIB-1 labeling index) was 50%. The patient died of disseminated disease 2 months after the operation.

Carcinoma, Large Cell↗
PubMed2006

[A clinical study of advanced large cell neuroendocrine carcinoma].

Large cell neuroendocrine carcinoma (LCNEC) is a newly recognized clinicopathologic entity. The clinical features of advanced LCNEC are still unclear, because most of the previous reports have described resected cases. The aim of this study was to clarify the clinical characteristics and response to chemotherapy in patients with advanced LCNEC. From June 2002 to July 2004, nine patients (seven men and two women, median age 61) with advanced LCNEC were admitted to our hospital. We reviewed the clinical manifestations, tumor markers, and treatment of these patients. Seven of nine patients (78%) were current or ex-smokers. As for tumor markers, the levels of progastrin-releasing peptide (proGRP) and neuron-specific enolase (NSE) were elevated in six patients (67%) and five patients (56%), respectively. The diagnosis of LCNEC was made based on the resected specimens in 8 patients including resection of brain metastasis in 1 and CT-guided needle biopsy in 1. One patient was stage IIIA, 1 was stage IIIB, 3 were stage IV, and 4 had postoperative recurrence. Treatment included chemotherapy alone in 7 patients, chemotherapy plus whole brain radiation in 1, and postoperative radiotherapy in 1. Of 7 patients treated by chemotherapy alone who had received carboplatin-based chemotherapy. 5 showed partial response, yielding response rate of 71.4%. The proGRP level was frequently elevated in patients with advanced LCNEC and the response rate of LCNEC to carboplatin-based chemotherapy was comparable to that of small cell lung cancer.

Adult↗
PubMed1997

Cigarette smoking and large cell carcinoma of the lung.

Large cell carcinoma is the fourth most common histological type of lung cancer in the United States. Cigarette smoking causes large cell lung cancer, but it is uncertain whether the effect varies with the amount and duration of smoking. This uncertainty stems from ambiguity in the histopathological classification of large cell cancer, especially before 1971, and the relatively infrequent occurrence of large cell cancer in epidemiological studies. The present case-control investigation demonstrates that the risk of large cell cancer increases with both the frequency and number of years of cigarette smoking. The odds ratio associated with smoking two or more packs/day was 37.0 (95% confidence interval, 16.4-83.2) in men and 72.9 (35.4-150.2) in women. It is concluded that cigarette smoking is the predominant cause of large cell lung cancer.

Adult↗