Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The increasing panel of systemic therapies enables the individual management of cancer patients, even in advanced stages. However, diagnostic tools indicating early the efficacy of therapy are still needed. In prospectively collected sera of 161 patients with recurrent non-small cell lung cancer (NSCLC) receiving second-line chemotherapy, the courses of nucleosomes, cytokeratin-19 fragments (CYFRA 21-1), carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), and progastrin-releasing peptide (ProGRP) were investigated and correlated with therapy response. At high specificity for detection of progressive disease, most sensitive biomarkers were identified and included in a combination model. High levels and insufficient decreases of nucleosomes and CYFRA 21-1 during the first cycle of therapy indicated poor outcome. Combination of nucleosome concentrations at day 8 and CYFRA 21-1 before start of the second cycle enabled the early detection of progressive disease with a sensitivity of 34.4% at 95% specificity (AUC 0.79) prior to imaging techniques. When cutoffs were fixed at the 90th percentile of responding patients, the combination model achieved sensitivities of 19% at 100% specificity and of 52% at 88% specificity. Thus, nucleosomes and CYFRA 21-1 showed to be valuable for the individual management of patients with recurrent NSCLC.
Lung Cancer 2009 Jan
PMID:Nucleosomes and CYFRA 21-1 indicate tumor response after one cycle of chemotherapy in recurrent non-small cell lung cancer. 1857 61

Bronchioloalveolar carcinoma (BAC) is a subset of lung adenocarcinoma that has a distinct clinical presentation, tumor biology, response to therapy, and prognosis compared with other subtypes of non-small-cell lung carcinoma. BAC disproportionately affects women, never-smokers, and is characterized by growth along alveolar septae without evidence of stromal, vascular, or pleural invasion. Microscopically, BACs have been divided into mucinous, nonmucinous, and mixed types. We describe a case of young female who received radiation therapy to the mediastinum and chemotherapy for Hodgkin lymphoma and now develops mucinous bronchioalveolar adenocarcinoma of the left lung which to the best of our knowledge has not been previously described after radiotherapy and chemotherapy for Hodgkin lymphoma. The tumor cells express Galectin-3, CD138, p16INK4a, thyroid transcription factor-1, cytokeratin 7, epithelial membrane antigen, carcinoembryonic antigen, E-cadherin, neuron-specific enolase, and S100 whereas no expression of cytokeratin 20, calretinin, and CDX2 is seen.
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PMID:Expression of Galectin-3, CD138, p16INK4a, and TTF-1 in mucinous bronchioloalveolar adenocarcinoma after Hodgkin lymphoma. 1899 17

The author reports a very rare case of cutaneous metastasis of sarcomatoid carcinoma of the lung. The skin metastasis was an initial presentation. A 67-year-old man consulted our hospital because of left chest skin mass. An excisional biopsy was performed, and it showed proliferation of malignant sarcomatoid spindle and polygonal cells in the deep dermis and subcutis remote from the epidermis and appendages. Immunohistochemically, the tumor cells were positive for pancytokeratins, cytokeratin (CK) 7, CK 18, vimentin, p53, Ki-67 (95%) and PDGFRA. They were negative for high molecular weight CK, CK 5/6, CK 14, CK 19, CK 20, epithelial membrane antigen, TTF-1, CEA, desmin, S100 protein, alpha-smooth muscle actin, p63, CD34, surfactant apoprotein A, chromogranin, synaptophysin, neuron-specific enolase, CD68, CD56, D2-40, calretinin and KIT. A pathological diagnosis of metastatic sarcomatoid carcinoma probably originating from the lung was made. Then, the patient was admitted to our hospital, and imaging modalities including computed tomography (CT) and magnetic resonance imaging (MRI) revealed a tumor in the left lung. No other tumors were detected in the imaging techniques. Lung biopsy was planned, but the patient suddenly died; the cause of death was unclear. Autopsy was not performed. The present report suggests that sarcomatoid carcinoma of the lung should be considered in cutaneous metastatic lesions.
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PMID:Sarcomatoid carcinoma of the lung presenting as a cutaneous metastasis. 1960 61

The author reports herein a case of occult very small lung carcinoma with a solitary brain metastasis that is clinically diagnosed as cavernous hemangioma, with an emphasis on pathologic findings. A 48-year-old Japanese man was admitted to our hospital complaining of mild paresis of left leg. Brain CT and MRI showed a solitary tumor (2 cm) with features of cavernous hemangioma in the right temporal lobe. Tumorectomy was performed, and it was pathologically undifferentiated carcinoma. An immunohistochemical analysis reveled that the carcinoma cells were positive for four types of pancytokeratin, cytokeratin (CK) 5/6, CK7, CK18, CK19, p63, and Ki-67 (78%). They were negative for high molecular weight CK, CK14, CK20, TTF-1, PE-10, melanosome, S100 protein, EMA, vimentin, CD34, myoglobin, CEA, p53, desmin, alpha-smooth muscle actin, chromogranin, synaptophysin, CD56, neuron-specific enolase, CD68, KIT, and PDGFRA. The positive CK7 and negative CK20 suggested lung origin, and cytokeratin profiles and positive CK5/6 and p63 suggested a squamous differentiation. The pathological diagnosis was undifferentiated carcinoma with squamous differentiation probably of lung origin. Later, systemic CT, MRI and PET were performed, and they detected a small lung tumor (8 mm) in the right apex. The lung biopsy revealed an undifferentiated carcinoma with focal squamous differentiation; the immunohistochemical findings were the same as those of the brain tumor. These findings suggest that occult very small lung carcinoma can metastasize to brain and such a metastasis may mimic cavernous hemangioma radiologically. Pathologic observations using many antibodies are very useful to determine the origin and histological type in solitary brain nodule.
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PMID:Occult very small lung carcinoma with a solitary brain metastasis that is clinically diagnosed as cavernous hemangioma: a case report. 1982 73

The author reports herein a case of small cell carcinoma of the brain without extracranial tumors by serial imaging modalities. A 75-year-old man presented with headache. Brain CT and MRI revealed a solitary cystic tumor (5 x 6 x 7 cm) in the left occipital lobe. Blood laboratory test revealed no significant findings. Preoperative diagnosis was a primary or metastatic brain tumor. Preoperative systemic examinations including CT, MRI and PET revealed no extracranial tumors. Tumorectomy was performed. Pathologically, the tumor was small cell carcinoma positive for four types of pancytokeratins, cytokeratin (CK) 7, CK 18, thyroid transcriptional factor-1 (TTF-1), CD56, chromogranin, synaptophysin, neuron-specific enolase, p53 protein, KIT, PDGFRA, and Ki-67 antigen (labeling = 100%). It was negative for high molecular weight CK, CK5/6, CK14, CK19, CK20, PE10, epithelial membrane antigen, vimentin, CEA, desmin, S100 protein, CA19-9, alpha-smooth muscle actin, CD34, p63, and CD68. The pathologic examination strongly suggested primary small cell lung carcinoma. However, repeated serial imaging modalities including systemic CT, MRI and PET revealed no extracranial tumors. The serial sputum cytology was always negative. The patient was treated with radiation and cisplatin-based chemotherapy, and no tumors were found seven months after the operation. The present case suggests that there are small cell carcinomas with a solitary brain metastasis without a radiologically detected primary site. In the present case, primary small cell brain carcinoma cannot be excluded completely, although such a case has not been reported in the literature.
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PMID:Small cell carcinoma of the brain without extracranial involvement by serial CT, MRI and PET. 2022 32

The purposes of this study were to assess the relationship of serum levels of pro-gastrin-releasing protein (ProGRP) and neuron-specific enolase (NSE) at relapse with survival after relapse and the response to salvage therapy and to assess whether serum levels of ProGRP and NSE at relapse are useful markers for detecting relapse earlier than are symptoms or radiographic findings in patients with small-cell lung cancer (SCLC). The subjects of this study were 103 patients with SCLC who had achieved a complete response (CR) or partial response (PR) to first-line chemotherapy. We retrospectively evaluated whether ProGRP or NSE increased earlier than symptoms or radiographic findings appeared, and the association between response to salvage therapy and levels of ProGRP or NSE at relapse. In addition, we evaluated the association between survival after relapse and clinical and demographic factors at relapse, including age, sex, response to first-line treatment, sensitivity to first-line treatment, stage, performance status (PS), and serum levels of ProGRP, NSE, and lactate dehydrogenase. At relapse, 69.3% of patients had elevated serum levels of ProGRP, 60.2% had elevated serum levels of NSE, and 81.3% had elevated serum levels of either ProGRP or NSE. However, almost all asymptomatic relapses were detected with radiographic studies. The rate of CR to salvage chemotherapy was significantly lower in patients with elevated levels of NSE (2.2%) than in patients without (26.7%; p=0.001). Univariate analysis showed that sensitivity to first-line treatment, serum levels of NSE, stage, and PS at relapse were prognostic factors for survival after relapse. Multivariate analysis showed that sensitivity to first-line treatment, serum levels of NSE, and PS at relapse were independent prognostic factors after relapse. In conclusion, serum levels of ProGRP and NSE at relapse are not useful markers for detecting relapse earlier than are symptoms or radiographic findings. On the other hand, the serum level of NSE at relapse is a useful predictive marker for CR to salvage chemotherapy and a useful prognostic factor after relapse in patients with SCLC who have achieved a CR or PR to first-line chemotherapy.
Lung Cancer 2011 Feb
PMID:Are levels of pro-gastrin-releasing peptide or neuron-specific enolase at relapse prognostic factors after relapse in patients with small-cell lung cancer? 2053 24

The propensity for tumor biomarkers to be detected in serum at an early disease stage has become an area of interest for clinicians. This study aimed to evaluate the efficiency of 7 tumor biomarkers, namely, carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), cytokeratin 19 (CYFRA-21-1), alpha-fetoprotein, carbohydrate antigen-125 (CA-125), carbohydrate antigen-19.9 (CA-19.9), and ferritin, independently or in combination for the diagnosis of lung cancer. Electrochemiluminescence immunization was used to determine biomarker levels expressed in 530 patients with pulmonary disease and 229 healthy subjects. The observed levels of CEA, NSE, CYFRA-21-1, CA-125, and CA-19.9 in patients with pathologically confirmed lung cancer were significantly higher than those in patients with benign pulmonary disease or control subjects. Adenocarcinoma, squamous cell carcinoma, and small cell carcinoma of the lung were associated with the highest observed levels of CA-125, CYFRA-21-1, and NSE, respectively. Combining biomarkers successfully led to the diagnosis of lung cancer. CEA + NSE + CA-125 showed the highest sensitivity for small cell carcinoma, at 83.33%, whereas CEA + NSE + CYFRA-21-1 + CA-125 showed 94.11% sensitivity for squamous cell carcinoma. The combination of 6 biomarkers, namely, CEA + NSE + CYFRA-21-1 + CA-125 + ferritin + CA-19.9, showed 80.49% sensitivity for adenocarcinoma. Combining biomarkers significantly aided in the diagnosis of lung cancer. However, this increased sensitivity on combination was accompanied by a decreased specificity for lung cancer subtypes. Combining biomarkers appropriately increases their sensitivity and helps with the diagnosis of lung cancer.
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PMID:Biomarkers in the lung cancer diagnosis: a clinical perspective. 2266 14

About 80 % of lung cancers are carcinomas that are classified histologically as non-small-cell lung carcinoma (NSCLC) and targeted chemotherapy of this cancer is currently based on sensitivity of the primary tumor to specific drugs. The purpose of this study was to compare the levels of four serum markers of cancer and the levels of six molecular markers which are possibly associated with drug selection in the primary tumors and metastatic lymph nodes of 39 consecutive NSCLC patients who were admitted to a single institution in China. Serum markers of cancer (neuron-specific enolase, carcinoembryonic antigen (CEA), cancer antigen 125, cytokeratin fragment 21-1) were measured by an automated electrochemiluminescence system and molecular markers (multidrug resistance protein 1, LDL receptor-related protein, ribonucleotide reductase M1, epidermal growth factor receptor, excision repair cross-complementing gene 1, and breast cancer 1) were measured by immunohistochemistry of the primary tumors and metastatic lymph nodes. The results indicate that the serum level of CEA was higher in NSCLC patients with adenocarcinoma relative to those with squamous cell carcinoma, but no significant differences in the other serum markers. Expression of excision repair cross-complementing gene 1 was significantly different in the primary tumors and metastatic sites of NSCLC patients with adenocarcinoma, but there were no other significant differences. This study provides an initial step toward the development of individualized chemotherapy of NSCLC based on measurement of molecular markers in the primary tumors and metastatic lymph nodes.
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PMID:Differential expression of ERCC-1 in the primary tumors and metastatic lymph nodes of patients with non-small cell lung cancer adenocarcinoma. 2289 Aug 30

The author herein reports a large cell neuroendocrine carcinoma (LCNEC) of the lung diagnosed in an axillary lymph node without clinical data, with an emphasis of KIT and PDGFRA. A 64-year-old woman presented with axillary and cervical lymph nodes swelling. An excisional biopsy of an axillary lymph node was performed under the clinical diagnosis of malignant lymphoma. The HE section showed a presence of large malignant cells arranged in a medullary pattern. The tumor cells had nucleoli. The HE diagnosis was large cell lymphoma or metastatic undifferentiated carcinoma, in particular large cell carcinoma of the lung. The tumor cells were positive for cytokeratins, p53 protein, thyroid transcriptional factor-1, neuron-specific enolase, synaptophysin, CD56, KIT, and PDGFRA. In contrast, they were negative for CD3, CD15, CD30, CD45, CD20, CD45RO, CEA, CA19-9, and chromogranin (Dako). Ki-67 labeling (Dako) was 100%. Therefore, a diagnosis of LCNEC of the lung was made. A molecular genetic analysis for KIT (exons 9, 11, 13, and 17) and PDGFRA (exons 12 and 18) identified no mutations. Later, a lung tumor and pleural effusion were detected, and the cytology of the effusion and sputum revealed carcinoma cells compatible with LCNEC. The patient was diagnosed as lung LCNEC, and treated by chemotherapy (cisplatin) and radiation (45 Gray). The present report is the first one with an examination of protein expression and gene mutations of KIT and PDGFRA in a metastatic focus of LCNEC of the lung.
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PMID:Pathologic diagnosis of large cell neuroendocrine carcinoma of the lung in an axillary lymph node: a case report with immunohistochemical and molecular genetic studies. 2369 39

Neuroendocrine (NE) phenotypes characterize a spectrum of lung tumors, including low-grade typical and intermediate-grade atypical carcinoid, high-grade large-cell NE carcinoma and small cell lung carcinoma. Currently, no effective treatments are available to cure NE lung tumors, demanding identification of biological features specific to these tumors. Here, we report that autophagy has an important role for NE lung tumor cell proliferation and survival. We found that the expression levels of the autophagy marker LC3 are relatively high in a panel of lung tumor cell lines expressing high levels of neuron-specific enolase (NSE), a key NE marker in lung tumors. In response to bafilomycin A1 and chloroquine, NE lung tumor cells exhibited cytotoxicity whereas non-NE lung tumor cells exhibited cytostasis, indicating a distinct role of autophagy for NE lung tumor cell survival. Intriguingly, in certain NE lung tumor cell lines, the levels of processed LC3 (LC3-II) were inversely correlated with AKT activity. When AKT activity was inhibited using AKTi or MK2206, the levels of LC3-II and SQSTM1/p62 were increased. In contrast, torin 1, rapamycin or mTOR knockdown increased p62 levels, suggesting that these two pathways have opposing effects on autophagy in certain NE lung tumors. Moreover, inhibition of one pathway resulted in reduced activity of the other, suggesting that these two pathways crosstalk in the tumors. These results suggest that NE lung tumor cells share a common feature of autophagy and are more sensitive to autophagy inhibition than non-NE lung tumor cells.
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PMID:Autophagy sensitivity of neuroendocrine lung tumor cells. 2412 19


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