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1. Cooks T, Arazi L, Schmidt M, Marshak G, Kelson I, Keisari Y: Growth retardation and destruction of experimental squamous cell carcinoma by interstitial radioactive wires releasing diffusing alpha-emitting atoms. Int J Cancer; 2008 Apr 1;122(7):1657-64
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  • [Title] Growth retardation and destruction of experimental squamous cell carcinoma by interstitial radioactive wires releasing diffusing alpha-emitting atoms.
  • In the present study, we examined the antitumoral effects caused by the release of alpha emitting radioisotopes into solid squamous cell carcinoma (SCC) tumors.
  • Using a novel method termed DART (Diffusing Alpha-emitters Radiation Therapy), we assessed the efficacy of short-lived daughters of (224)Ra releasing alpha particles, dispersing in the malignant tissue, to cause tumor growth retardation and destruction.
  • It was carried out using specially designed wires loaded with (224)Ra activities in the range of 7-42 kBq in a set of experiments performed on BALB/c and nude mice bearing metastatic SCC tumors derived from either mouse SQ2 or human CAL27 cell lines.
  • The insertion of a DART wire to the center of 6-7 mm primary tumors, retarded tumor growth, reduced lung metastatic load, prolonged life expectancy and in some cases caused tumor eradication.
  • Histological assessments revealed the tissue damage pattern, and indicated a role for the tumor vasculature in the dispersion of the atoms and the propagation of the damage.
  • Our findings indicate that Diffusing Alpha-emitting Radiation Therapy is effective in a model system using SCC primary tumors.
  • The in situ destruction of primary solid tumors by DART is evidently a necessary step toward curing cancer and might be augmented by chemotherapy and other modalities such as immunotherapy or antigrowth factors agents.
  • [MeSH-major] Alpha Particles / therapeutic use. Brachytherapy / methods. Carcinoma, Squamous Cell / radiotherapy. Neoplasms, Experimental / radiotherapy. Radioisotopes / therapeutic use
  • [MeSH-minor] Animals. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Polonium / therapeutic use. Radium / therapeutic use. Radon / therapeutic use. Treatment Outcome

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18059026.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radioisotopes; DQY03U61EJ / Polonium; Q74S4N8N1G / Radon; W90AYD6R3Q / Radium
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2. St John MA, Dohadwala M, Luo J, Wang G, Lee G, Shih H, Heinrich E, Krysan K, Walser T, Hazra S, Zhu L, Lai C, Abemayor E, Fishbein M, Elashoff DA, Sharma S, Dubinett SM: Proinflammatory mediators upregulate snail in head and neck squamous cell carcinoma. Clin Cancer Res; 2009 Oct 1;15(19):6018-27
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  • [Title] Proinflammatory mediators upregulate snail in head and neck squamous cell carcinoma.
  • PURPOSE: Inflammatory cytokines have been implicated in the progression of head and neck squamous cell carcinoma (HNSCC).
  • EXPERIMENTAL DESIGN: We evaluated the effect of IL-1beta on the molecular events of EMT in surgical specimens and HNSCC cell lines.
  • An inverse relationship between COX-2 and E-cadherin was shown in situ by double immunohistochemical staining of human HNSCC tissue sections.
  • Treatment of HNSCC cells with IL-1beta caused the downregulation of E-cadherin expression and upregulation of COX-2 expression.
  • IL-1beta-treated HNSCC cell lines showed a significant decrease in E-cadherin mRNA and an increase in the mRNA expression of the transcriptional repressor Snail.
  • This newly defined pathway for transcriptional regulation of E-cadherin in HNSCC has important implications for targeted chemoprevention and therapy.

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  • (PMID = 19789323.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA111851-04; United States / NCI NIH HHS / CA / R01 CA111851; United States / NCI NIH HHS / CA / R01 CA111851-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cadherins; 0 / Inflammation Mediators; 0 / Interleukin-1beta; 0 / Transcription Factors; 0 / snail family transcription factors
  • [Other-IDs] NLM/ NIHMS141348; NLM/ PMC2782528
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3. Weiss J, Sos ML, Seidel D, Peifer M, Zander T, Heuckmann JM, Ullrich RT, Menon R, Maier S, Soltermann A, Moch H, Wagener P, Fischer F, Heynck S, Koker M, Schöttle J, Leenders F, Gabler F, Dabow I, Querings S, Heukamp LC, Balke-Want H, Ansén S, Rauh D, Baessmann I, Altmüller J, Wainer Z, Conron M, Wright G, Russell P, Solomon B, Brambilla E, Brambilla C, Lorimier P, Sollberg S, Brustugun OT, Engel-Riedel W, Ludwig C, Petersen I, Sänger J, Clement J, Groen H, Timens W, Sietsma H, Thunnissen E, Smit E, Heideman D, Cappuzzo F, Ligorio C, Damiani S, Hallek M, Beroukhim R, Pao W, Klebl B, Baumann M, Buettner R, Ernestus K, Stoelben E, Wolf J, Nürnberg P, Perner S, Thomas RK: Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer. Sci Transl Med; 2010 Dec 15;2(62):62ra93
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  • [Title] Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer.
  • Lung cancer remains one of the leading causes of cancer-related death in developed countries.
  • Although lung adenocarcinomas with EGFR mutations or EML4-ALK fusions respond to treatment by epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) inhibition, respectively, squamous cell lung cancer currently lacks therapeutically exploitable genetic alterations.
  • We conducted a systematic search in a set of 232 lung cancer specimens for genetic alterations that were therapeutically amenable and then performed high-resolution gene copy number analyses.
  • We identified frequent and focal fibroblast growth factor receptor 1 (FGFR1) amplification in squamous cell lung cancer (n = 155), but not in other lung cancer subtypes, and, by fluorescence in situ hybridization, confirmed the presence of FGFR1 amplifications in an independent cohort of squamous cell lung cancer samples (22% of cases).
  • Using cell-based screening with the FGFR inhibitor PD173074 in a large (n = 83) panel of lung cancer cell lines, we demonstrated that this compound inhibited growth and induced apoptosis specifically in those lung cancer cells carrying amplified FGFR1.
  • We validated the FGFR1 dependence of FGFR1-amplified cell lines by FGFR1 knockdown and by ectopic expression of an FGFR1-resistant allele (FGFR1(V561M)), which rescued FGFR1-amplified cells from PD173074-mediated cytotoxicity.
  • Finally, we showed that inhibition of FGFR1 with a small molecule led to significant tumor shrinkage in vivo.
  • Thus, focal FGFR1 amplification is common in squamous cell lung cancer and associated with tumor growth and survival, suggesting that FGFR inhibitors may be a viable therapeutic option in this cohort of patients.
  • [MeSH-major] Lung Neoplasms / genetics. Lung Neoplasms / metabolism. Receptor, Fibroblast Growth Factor, Type 1 / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Animals. Apoptosis / genetics. Apoptosis / physiology. Blotting, Western. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / metabolism. Cell Line. Enzyme Inhibitors / therapeutic use. Gene Expression Regulation, Neoplastic / genetics. Humans. Male. Mice. Mice, Nude. Pyrimidines / therapeutic use. RNA Interference. Xenograft Model Antitumor Assays

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  • (PMID = 21160078.001).
  • [ISSN] 1946-6242
  • [Journal-full-title] Science translational medicine
  • [ISO-abbreviation] Sci Transl Med
  • [Language] eng
  • [Databank-accession-numbers] GEO/ GSE25016
  • [Grant] United States / NCI NIH HHS / CA / K08 CA097980; United States / NCI NIH HHS / CA / P01 CA129243; United States / NCI NIH HHS / CA / R01 CA121210
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / PD 173074; 0 / Pyrimidines; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 1; Adenocarcinoma of lung
  • [Other-IDs] NLM/ NIHMS569992; NLM/ PMC3990281
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4. Seward SM, Richardson DL, Leon ME, Zhao W, Cohn DE, Hitchcock CL: Metastatic squamous cell carcinoma of the vulva to the lung confirmed with allelotyping. Int J Gynecol Pathol; 2009 Sep;28(5):497-501
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  • [Title] Metastatic squamous cell carcinoma of the vulva to the lung confirmed with allelotyping.
  • A squamous-cell carcinoma (SCC) of the lung can be indistinguishable from metastatic SCC of gynecologic origin using common histopathologic techniques; however, establishing tumor origin can be clinically relevant.
  • A patient with a Bartholin gland SCC was found to also have a pulmonary SCC, concerning for metastasis versus synchronous pulmonary primary.
  • The patient received palliative chemotherapy instead of curative treatment.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / secondary. Lung Neoplasms / genetics. Lung Neoplasms / secondary. Vulvar Neoplasms / genetics. Vulvar Neoplasms / pathology
  • [MeSH-minor] Aged. Alleles. Bartholin's Glands / pathology. Biomarkers, Tumor / genetics. Female. Humans. In Situ Hybridization. Loss of Heterozygosity. Microdissection. Palliative Care. Papillomavirus Infections / complications. Sarcoidosis / complications

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  • (PMID = 19696623.001).
  • [ISSN] 1538-7151
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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5. Ugocsai K, Mándoky L, Tiszlavicz L, Molnár J: Investigation of HER2 overexpression in non-small cell lung cancer. Anticancer Res; 2005 Jul-Aug;25(4):3061-6
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  • [Title] Investigation of HER2 overexpression in non-small cell lung cancer.
  • Lung cancer is the leading cause of mortality worldwide.
  • Intrinsic or acquired drug resistance pose major challenges to the success of chemotherapy.
  • It has a possible role in tumor cell proliferation, tumor invasion, tumor metastasis and drug resistance.
  • We retrospectively investigated 88 samples of non-small cell lung cancer (NSCLC) and assessed the correlation between HER2 expression and tumor histology.
  • The expression of HER2 protein was analyzed by immunohistochemical staining (IHC) and HER2 DNA amplification was detected by using fluorescence in situ hybridization (FISH).
  • All of the HER2-overexpressing tumors histologically proved to be squamous cell carcinoma (SCC).
  • The HER2 expression in NSCLC was relatively low in the selected Hungarian population; consequently, there is no indication for introduction of trastuzumab for the treatment of lung cancer.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Receptor, ErbB-2 / biosynthesis
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies


6. Shabnam MS, Srinivasan R, Wali A, Majumdar S, Joshi K, Behera D: Expression of p53 protein and the apoptotic regulatory molecules Bcl-2, Bcl-XL, and Bax in locally advanced squamous cell carcinoma of the lung. Lung Cancer; 2004 Aug;45(2):181-8
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  • [Title] Expression of p53 protein and the apoptotic regulatory molecules Bcl-2, Bcl-XL, and Bax in locally advanced squamous cell carcinoma of the lung.
  • This pathway may be dysregulated leading to an altered ratio of pro- and anti-apoptotic molecules, hence rendering cells resistant to chemotherapy.
  • The objective of this study was to understand the role of Bcl-2 family members in mediation of apoptosis in squamous cell carcinoma of the lung.
  • RESULTS: Bronchoscopically obtained lung biopsies from 30 cases of histologically proven squamous cell carcinoma of the lung in stage III were assessed for the expression of Bcl-2, Bcl-XL, and Bax at the mRNA and protein levels by semi-quantitative reverse transcription (RT-PCR) and immunohistochemistry.
  • The AI ranged from <0.1 to 6.0% with a median of 1.3%.
  • CONCLUSION: The results of this study indicate that in locally advanced squamous cell carcinoma of the lung, Bax protein is up regulated and determines the level of apoptosis.
  • [MeSH-major] Apoptosis / physiology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Adult. Aged. Base Sequence. Biomarkers, Tumor / analysis. Biopsy, Needle. Bronchoscopy. Cohort Studies. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. India. Male. Middle Aged. Molecular Sequence Data. Neoplasm Staging. Probability. Prognosis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Risk Assessment. Sensitivity and Specificity. Statistics, Nonparametric. Survival Analysis. bcl-2-Associated X Protein

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  • (PMID = 15246189.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / BAX protein, human; 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein
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7. Zheng Z, Li X, Schell MJ, Chen T, Boulware D, Robinson L, Sommers E, Bepler G: Thymidylate synthase in situ protein expression and survival in stage I nonsmall-cell lung cancer. Cancer; 2008 Jun 15;112(12):2765-73
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  • [Title] Thymidylate synthase in situ protein expression and survival in stage I nonsmall-cell lung cancer.
  • TS messenger RNA and protein levels are predictive of response to 5-fluorouracil-containing therapy for patients with colorectal cancer and gastric cancer.
  • High levels of expression of 2 other genes important in DNA synthesis and repair, RRM1 and ERCC1, are prognostic of survival in early stage nonsmall-cell lung cancer (NSCLC) patients.
  • We hypothesized that intratumoral TS expression would be prognostic of outcome in stage I NSCLC.
  • METHODS: Cytoplasmic tumoral TS was determined by automated in situ protein quantification (AQUA) in 160 patients with completely resected NSCLC that had not received chemotherapy or radiation.
  • It was also determined by real-time quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) in 85 similar patients.
  • In a multivariate analysis adjusting for tumor stage, TS remained significantly prognostic of survival (P=.0013, adjusted P=.032).
  • CONCLUSIONS: In situ cytoplasmic TS protein expression in tumors of patients with resected stage I NSCLC is a clinically important determinant of survival.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Thymidylate Synthase / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Biomarkers, Tumor / analysis. Carcinoma, Large Cell / metabolism. DNA-Binding Proteins / metabolism. Endonucleases / metabolism. Female. Humans. Male. Neoplasms, Squamous Cell / metabolism. Prognosis. RNA, Messenger / metabolism. Smoking. Survival Analysis. Tumor Suppressor Proteins / metabolism

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  • [Copyright] Copyright (c) 2008 American Cancer Society.
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  • (PMID = 18442042.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102726; United States / NCI NIH HHS / CA / R01 CA102726
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / RRM1 protein, human; 0 / Tumor Suppressor Proteins; EC 2.1.1.45 / Thymidylate Synthase; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases
  • [Other-IDs] NLM/ NIHMS530227; NLM/ PMC3857609
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8. Junker K, Müller KM, Bosse U, Klinke F, Heinecke A, Thomas M: [Apoptosis and tumor regression in locally advanced non-small cell lung cancer with neoadjuvant therapy]. Pathologe; 2003 May;24(3):214-9
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  • [Title] [Apoptosis and tumor regression in locally advanced non-small cell lung cancer with neoadjuvant therapy].
  • Dysregulation of apoptosis is closely associated with malignant cell transformation.
  • On the other hand, apoptosis is induced by chemotherapy or irradiation.
  • Therefore, in 54 patients with locally advanced non-small cell lung cancer (NSCLC, 36 squamous cell carcinomas, 18 adenocarcinomas, stage IIIA/IIIB), apoptotic indices were comparatively analysed before onset and after termination of neoadjuvant therapy.
  • The results were compared with the response to neoadjuvant therapy (extent of therapy-induced tumour regression) as well as the survival times.
  • Neither before therapy nor after surgery did the apoptotic indices show a significant predictive value concerning different overall survival times.
  • These results suggest that neoadjuvant therapy does not modify the extent of apoptosis in lung cancer in the long term.
  • Only a few weeks after the completion of the neoadjuvant chemoradiotherapy this contributes to a net proliferation of the residual tumour tissue which is largely equivalent to that of the untreated tumour.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Adult. Aged. Apoptosis / drug effects. Female. Humans. In Situ Nick-End Labeling. Male. Middle Aged. Neoadjuvant Therapy. Neoplasm Staging

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  • (PMID = 12739056.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] Comparative Study; English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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9. Barroso A, Nogueira R, Lencastre H, Seada J, Parente B: Primary lymphoepithelioma-like carcinoma of the lung. Lung Cancer; 2000 Apr;28(1):69-74
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  • [Title] Primary lymphoepithelioma-like carcinoma of the lung.
  • Lymphoepithelioma is an undifferentiated carcinoma with prominent lymphoid stroma in the nasopharynx.
  • Primary LELC of the lung is very rare, and scant information is available in the scientific literature.
  • This paper details the case of a 25-year-old Caucasian male patient with the diagnosis (determined by thoracotomy) of primary LELC of the lung.
  • Immunohistochemical analysis was negative for Epstein-Barr virus, as was the in situ hybridization of the tumor cells.
  • Because the tumor (T4N2M0) could not be resected, the patient was treated with chemotherapy, carboplatin/5-fluorouracil, completing two cycles.
  • The patient's condition worsened when he developed contralateral pneumonia, which was then followed by pericardial effusion.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Diagnosis, Differential. Fatal Outcome. Fluorouracil / administration & dosage. Humans. Male. Tomography, X-Ray Computed

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  • (PMID = 10704712.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] IRELAND
  • [Chemical-registry-number] BG3F62OND5 / Carboplatin; U3P01618RT / Fluorouracil
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10. Rogers SJ, Box C, Chambers P, Barbachano Y, Nutting CM, Rhŷs-Evans P, Workman P, Harrington KJ, Eccles SA: Determinants of response to epidermal growth factor receptor tyrosine kinase inhibition in squamous cell carcinoma of the head and neck. J Pathol; 2009 May;218(1):122-30
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  • [Title] Determinants of response to epidermal growth factor receptor tyrosine kinase inhibition in squamous cell carcinoma of the head and neck.
  • Dramatic responses to epidermal growth factor receptor (EGFR) tyrosine kinase (TK) inhibitors may be seen in non-small cell lung cancers (NSCLCs) with a sensitizing mutation of the EGFR TK domain.
  • It is not known how to predict response in patients with squamous cell carcinoma of the head and neck (SCCHN), where EGFR TK mutations are less frequent and where response rates in unselected patients are disappointing.
  • We have characterized the intrinsic sensitivity of a panel of 18 SCCHN cell lines to gefitinib, an EGFR TK inhibitor, and have investigated correlations between putative markers of response and intrinsic sensitivity.
  • Induction of G1 arrest was only seen in cell lines with GI(50) < 1 microM.
  • While EGFR tyrosine kinase mutations were not detected, EGFR gene amplification was confirmed by fluorescence in situ hybridization in the most sensitive cell line.
  • E-cadherin expression was detected in cell lines with a range of sensitivities, whereas amphiregulin was secreted predominantly by sensitive cell lines.
  • Breast receptor kinase (BRK) was more highly expressed in the sensitive cell lines, but siRNA knockdown of neither BRK nor MET affected sensitivity.
  • Our data suggest that overexpression of EGFR and multiple related cell surface receptors may be associated with sensitivity to gefitinib and that differences between our data and the literature highlight that biomarkers of response are tumour type- and cell line-dependent.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Head and Neck Neoplasms / drug therapy. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Biomarkers, Tumor / analysis. Blotting, Western. Cell Line, Tumor. Drug Resistance, Neoplasm. Drug Screening Assays, Antitumor. Flow Cytometry / methods. Gene Expression. Genes, erbB-2. Humans. In Situ Hybridization, Fluorescence. Linear Models. Polymorphism, Genetic. Proto-Oncogene Proteins c-met / metabolism


11. Antoine M: [Contribution of immunohistochemistry to the management of lung cancer: from morphology to diagnosis and treatment]. Rev Pneumol Clin; 2007 Jun;63(3):183-92
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  • [Title] [Contribution of immunohistochemistry to the management of lung cancer: from morphology to diagnosis and treatment].
  • [Transliterated title] Qu'apporte l'immunohistochimie à la prise en charge du cancer bronchique? De la morphologie au diagnostic et au traitement.
  • We detail here the contribution of IHC to the classification of lung cancer: small-cell lung cancer and other neuroendocrine tumors, basaloid carcinoma, large-cell carcinoma.
  • The distinction is less clear for large-cell carcinoma or squamous-cell carcinoma, or for tumors with a pleural or mediastinal presentation.
  • By demonstrating the presence of carcinomatous cells within the neighboring structures (pleura) or lymph nodes, IHC contributes to lung cancer staging, particularly when there are few of these elements morphologically difficult to distinguish.
  • Finally, IHC contributes to prognosis (proliferation markers, differentiation markers) or prediction of therapeutic response (chemotherapy or targeted therapies).
  • IHC studies may also be requested in a forensic setting, for example to demonstrate that the lung cancer observed in a patient exposed to asbestosis is primary.
  • Other morphological techniques such as hybridization in situ or molecular biology techniques will further complete the histological diagnosis in the future.
  • [MeSH-major] Immunohistochemistry. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Carcinoma, Large Cell / pathology. Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / pathology. Carcinoma, Transitional Cell / pathology. Chorionic Gonadotropin, beta Subunit, Human / analysis. Forecasting. Humans. Lymph Nodes / pathology. Lymphoma / pathology. Mediastinal Neoplasms / pathology. Melanoma / pathology. Neoplasm Staging. Neuroendocrine Tumors / pathology. Pleural Neoplasms / pathology. Prognosis. Sarcoma / pathology. alpha-Fetoproteins / analysis

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  • (PMID = 17675942.001).
  • [ISSN] 0761-8417
  • [Journal-full-title] Revue de pneumologie clinique
  • [ISO-abbreviation] Rev Pneumol Clin
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / alpha-Fetoproteins
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12. Hirsch FR, Scagliotti GV, Langer CJ, Varella-Garcia M, Franklin WA: Epidermal growth factor family of receptors in preneoplasia and lung cancer: perspectives for targeted therapies. Lung Cancer; 2003 Aug;41 Suppl 1:S29-42
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  • [Title] Epidermal growth factor family of receptors in preneoplasia and lung cancer: perspectives for targeted therapies.
  • The Erb-B family of receptors plays an important role in lung carcinogenesis and tumor development, and EGFR and HER2 are highly expressed in bronchial preneoplasia.
  • In invasive tumors, EGFR are expressed in 50-90%, and mostly in squamous cell carcinomas, but also in adenocarcinomas and large cell carcinomas, while HER2 is less frequently expressed (20-30%) and mostly expressed in adenocarcinomas.
  • Bronchioloalveolar cell carcinomas may present a distinct EGFR profile compared to the other NSCLCs and evidence and consequences are discussed.
  • However, for EGFR and HER2 there is a positive correlation between gene copy numbers and level of protein expression demonstrated by fluorescence in situ hybridization analysis and immunochemistry.
  • The treatment status and therapeutic limitation with trastuzumab (Herceptin) in lung cancer compared to breast cancer is discussed.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / physiopathology. Gene Expression Regulation, Neoplastic. Lung Neoplasms / drug therapy. Lung Neoplasms / physiopathology. Precancerous Conditions / physiopathology. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, ErbB-2 / biosynthesis
  • [MeSH-minor] Gene Amplification. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence


13. Castro Kreder N, Van Bree C, Franken NA, Haveman J: Colour junctions as predictors of radiosensitivity: X-irradiation combined with gemcitabine in a lung carcinoma cell line. J Cancer Res Clin Oncol; 2003 Oct;129(10):597-603

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  • [Title] Colour junctions as predictors of radiosensitivity: X-irradiation combined with gemcitabine in a lung carcinoma cell line.
  • PURPOSE: To determine whether measurement of colour junctions by fluorescent in situ hybridisation (FISH) can predict radiosensitisation of gemcitabine (2'-2'-difluorodeoxycytidine).
  • METHODS: Human lung carcinoma cells (SW-1573) were irradiated with X-rays with or without incubation of 10 n M gemcitabine for 24 h.
  • Cell survival was determined with clonogenic assay.
  • RESULTS: A clear radiosensitisation by gemcitabine was observed on cell survival.
  • A significant decrease in the number of colour junctions was observed after gemcitabine treatment compared with radiation treatment alone.
  • The correlation between colour junction induction and cell survival was high for both with and without gemcitabine, but the gemcitabine-sensitised curve did not coincide with the non-sensitised curve.
  • [MeSH-minor] Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / radiotherapy. Cell Line, Tumor / drug effects. Cell Line, Tumor / radiation effects. Cell Survival / drug effects. Cell Survival / genetics. Cell Survival / radiation effects. Chromosome Aberrations / drug effects. Chromosome Aberrations / radiation effects. Combined Modality Therapy. Dose-Response Relationship, Radiation. Flow Cytometry. Humans. In Situ Hybridization, Fluorescence. Lung Neoplasms / drug therapy. Lung Neoplasms / radiotherapy. Radiation Dosage. Radiation Tolerance / drug effects

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  • (PMID = 14513371.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Radiation-Sensitizing Agents; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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14. Miyazu Y, Miyazawa T, Kurimoto N, Iwamoto Y, Kanoh K, Kohno N: Endobronchial ultrasonography in the assessment of centrally located early-stage lung cancer before photodynamic therapy. Am J Respir Crit Care Med; 2002 Mar 15;165(6):832-7
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  • [Title] Endobronchial ultrasonography in the assessment of centrally located early-stage lung cancer before photodynamic therapy.
  • To evaluate the utility of endobronchial ultrasonography (EBUS) in selecting appropriate candidates with centrally located early-stage lung cancer for photodynamic therapy (PDT) with curative intent, we performed EBUS before PDT in 18 biopsy-proven squamous cell carcinomas (including three carcinoma in situ) that had been considered to be appropriate candidates for PDT by conventional bronchoscopy and high-resolution computed tomography (HR-CT).
  • Long-term complete remission has been achieved in these patients with a median follow-up term after PDT of 32 months.
  • The remaining nine lesions were diagnosed as extracartilaginous by EBUS and were considered candidates for other therapies such as surgical resection, chemotherapy, and radiotherapy, although two were invisible by HR-CT, three were superficial, and five were < or = 1 cm in diameter on observation by bronchoscopy.
  • We conclude that EBUS is a useful technique that might be considered in addition to conventional bronchoscopy and HR-CT to improve the efficacy of PDT in patients with centrally located early-stage lung cancer.
  • [MeSH-major] Carcinoma, Squamous Cell / therapy. Carcinoma, Squamous Cell / ultrasonography. Endosonography. Lung Neoplasms / therapy. Lung Neoplasms / ultrasonography. Patient Selection. Photochemotherapy
  • [MeSH-minor] Aged. Carcinoma in Situ / pathology. Carcinoma in Situ / therapy. Carcinoma in Situ / ultrasonography. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Prospective Studies

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  • (PMID = 11897652.001).
  • [ISSN] 1073-449X
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Kumaki F, Kawai T, Hiroi S, Shinomiya N, Ozeki Y, Ferrans VJ, Torikata C: Telomerase activity and expression of human telomerase RNA component and human telomerase reverse transcriptase in lung carcinomas. Hum Pathol; 2001 Feb;32(2):188-95
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  • [Title] Telomerase activity and expression of human telomerase RNA component and human telomerase reverse transcriptase in lung carcinomas.
  • The aim of this study was to evaluate the usefulness of determination of telomerase activity and expression of human telomerase RNA component (hTERC) and human telomerase reverse transcriptase (hTERT) for the diagnosis of lung carcinomas.
  • The tissues studied consisted of 115 carcinomas and adjacent nonneoplastic lung, which were removed surgically without previous chemotherapy or radiotherapy.
  • Localization of expression was examined by using in situ hybridization and immunohistochemistry.
  • The correlation between telomerase activity in lung carcinoma and clinicopathologic features, including prognosis, was investigated.
  • Telomerase activity in lung carcinomas was detected in 107 of 115 (93%) lung carcinomas, but not in any adjacent noncancerous tissues, and was significantly higher in small cell carcinoma than in any other histologic type.
  • This activity also was significantly higher in poorly differentiated than in well-differentiated squamous cell carcinomas and adenocarcinomas.
  • Messenger RNAs for hTERC and hTERT were mainly detected in the cytoplasm of cancer cells by in situ hybridization, and TERT protein was localized in the nuclei of these cells by immunohistochemical staining.
  • Determinations of telomerase activity by in situ hybridization, immunohistochemistry, and TRAP assay are useful for evaluating the diagnosis and prognosis of lung carcinomas.
  • [MeSH-major] Adenocarcinoma / enzymology. Lung Neoplasms / enzymology. RNA. RNA, Messenger / metabolism. Telomerase / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Base Sequence. DNA-Binding Proteins. Female. Humans. Immunohistochemistry. In Situ Hybridization. Lymph Nodes / pathology. Lymphatic Metastasis / genetics. Lymphatic Metastasis / pathology. Male. Middle Aged. Molecular Sequence Data. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate

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  • (PMID = 11230706.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / telomerase RNA; 63231-63-0 / RNA; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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16. Schneider CP, Heigener D, Schott-von-Römer K, Gütz S, Laack E, Digel W, Guschall WR, Franke A, Bodenstein H, Schmidtgen C, Reck M: Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study. J Thorac Oncol; 2008 Dec;3(12):1446-53
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  • [Title] Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study.
  • INTRODUCTION: Relationships between clinical outcomes and epidermal growth factor receptor (EGFR)-related tumor markers were investigated in patients with advanced non-small cell lung cancer.
  • METHODS: Patients with stage IIIB/IV non-small cell lung cancer (0-2 prior regimens) received erlotinib (150 mg PO per day).
  • Response and survival were evaluated, and tumor samples were assessed by immunohistochemistry (EGFR, phosphorylated mitogen-activated protein kinase, and phosphorylated AKT protein expression), fluorescence in situ hybridization (FISH; EGFR gene copy number), and DNA sequencing (EGFR, KRAS gene mutations).
  • Two of 4 patients with EGFR mutations had tumor responses, versus 2/68 with wild-type EGFR (p = 0.014).
  • None of 17 patients with a KRAS mutation had a tumor response, but the impact of KRAS mutation status on survival outcomes was of borderline statistical significance.
  • CONCLUSIONS: The presence of EGFR mutations and EGFR FISH-positive tumors may predispose patients to achieving better outcomes on erlotinib, but may have a beneficial impact on prognosis (irrespective of treatment).
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Protein Kinase Inhibitors / therapeutic use. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adult. Aged. Aged, 80 and over. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / metabolism. Disease-Free Survival. Erlotinib Hydrochloride. Female. Gene Dosage. Germany. Humans. Immunoenzyme Techniques. In Situ Hybridization, Fluorescence. Male. Middle Aged. Mitogen-Activated Protein Kinases / metabolism. Mutation / genetics. Phosphorylation. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt / metabolism. Survival Rate. Treatment Outcome. ras Proteins / genetics. ras Proteins / metabolism

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  • (PMID = 19057271.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.6.5.2 / ras Proteins
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17. Kurdow R, Boehle AS, Haye S, Boenicke L, Schniewind B, Dohrmann P, Kalthoff H: Ganciclovir prodrug therapy is effective in a murine xenotransplant model of human lung cancer. Ann Thorac Surg; 2002 Mar;73(3):905-10
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  • [Title] Ganciclovir prodrug therapy is effective in a murine xenotransplant model of human lung cancer.
  • BACKGROUND: Therapy failures have been reported for retroviral gene transfer of herpes simplex virus thymidine kinase (HSV-TK) gene followed by systemic ganciclovir application in human lung cancer.
  • Use of the HSV-TK mutant TK30 in combination with a VSV-G pseudotyped retroviral vector was found to enhance the efficacy of prodrug therapy.
  • The present study evaluated this therapeutic strategy in human non-small cell lung cancer cell lines in a preclinical murine xenotransplant model.
  • METHODS: Intrathoracally induced by HSV-TK30 transduced non-small cell lung cancer cell lines Colo 699 (adenocarcinoma) and KNS 62 (squamous cell carcinoma) were monitored for local tumor growth, survival, and metastases.
  • RESULTS: Survival was significantly prolonged, and tumor growth and pleural metastases were reduced in HSV-TK30-positive tumors of both cell lines.
  • A significant therapeutic effect in bystander experiments was observed in squamous cell carcinoma.
  • CONCLUSIONS: Delivery of HSV-TK30 in a VSV-G pseudotyped retroviral vector and subsequent ganciclovir application provided therapeutic efficacy.
  • Despite of low transduction rates achievable in gene transfer in situ, prodrug therapy appears to be feasible in tumor cells with efficient bystander effects.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antiviral Agents / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Ganciclovir / therapeutic use. Genetic Vectors. Lung Neoplasms / drug therapy. Prodrugs. Thymidine Kinase / genetics

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  • [CommentIn] Ann Thorac Surg. 2002 Mar;73(3):704-6 [11899169.001]
  • (PMID = 11899199.001).
  • [ISSN] 0003-4975
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Connexin 43; 0 / Prodrugs; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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18. Keith RL: Chemoprevention of lung cancer. Proc Am Thorac Soc; 2009 Apr 15;6(2):187-93
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  • [Title] Chemoprevention of lung cancer.
  • Lung cancer is the leading cause of cancer death in the United States, and the majority of diagnoses are made in former smokers.
  • While avoidance of tobacco abuse and smoking cessation clearly will have the greatest impact on lung cancer development, effective chemoprevention could prove to be more effective than treatment of established disease.
  • Chemoprevention is the use of dietary or pharmaceutical agents to reverse or inhibit the carcinogenic process and has been successfully applied to common malignancies other than lung.
  • Despite previous studies in lung cancer chemoprevention failing to identify effective agents, our ability to determine higher risk populations and the understanding of lung tumor and pre-malignant biology continues to advance.
  • The World Health Organization/International Association for the Study of Lung Cancer classification for lung cancer now recognizes distinct histologic lesions that can be reproducibly graded as precursors of non-small cell lung cancer.
  • For example, carcinogenesis in the bronchial epithelium starts with normal epithelium and progresses through hyperplasia, metaplasia, dysplasia, and carcinoma in situ to invasive squamous cell cancer.
  • At this time, chemopreventive agents can only be recommended as part of well-designed clinical trials, and multiple trials are currently in progress and additional trials are in the planning stages.
  • This review will discuss the principles of chemoprevention, summarize the completed trials, and discuss ongoing and potential future trials with a focus on targeted pathways.
  • [MeSH-major] Chemoprevention / methods. Lung Neoplasms / prevention & control. Precancerous Conditions / drug therapy

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  • (PMID = 19349487.001).
  • [ISSN] 1546-3222
  • [Journal-full-title] Proceedings of the American Thoracic Society
  • [ISO-abbreviation] Proc Am Thorac Soc
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
  • [Number-of-references] 86
  • [Other-IDs] NLM/ PMC2674227
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19. Laurenzi L, Natoli S, Pelagalli L, Marcelli ME, Abbattista D, Carpanese L, Arcuri E: Long-term central venous catheterization via persistent left superior vena cava: a case report. Support Care Cancer; 2003 Mar;11(3):190-2

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  • [Title] Long-term central venous catheterization via persistent left superior vena cava: a case report.
  • We report a case of a cancer patient who displayed a persistent left superior vena cava (PLSVC) after implantation of a central venous catheter (Port-a-Cath), as revealed by angiography.
  • This anomaly is rather rare (0.3% of healthy individuals), and the few studies on the long-term maintenance of an implant in situ are not very informative.
  • Nevertheless, based on the acceptable venous caliber and the patient's serious clinical situation, we decided to leave the catheter in place and perform infusional chemotherapy and supportive therapy with careful and continuous control.
  • The patient died after 8 months of this therapy.
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Carcinoma, Squamous Cell / therapy. Humans. Lung Neoplasms / therapy. Male. Medical Errors / instrumentation. Middle Aged. Time. Treatment Outcome

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  • (PMID = 12618930.001).
  • [ISSN] 0941-4355
  • [Journal-full-title] Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
  • [ISO-abbreviation] Support Care Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
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20. D'Andrea MR, Gasparini G: The future of anti-EGFR therapy. Int J Biol Markers; 2007 Jan-Mar;22(1 Suppl 4):S88-93
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  • [Title] The future of anti-EGFR therapy.
  • A critical review of the anti-EGFR therapeutic strategies is also outlined.
  • The chimeric anti- EGFR monoclonal antibody cetuximab has been approved for EGFR-expressing colorectal tumors in patients who progress after irinotecan-based chemotherapy in combination with irinotecan and in squamous cell head and neck carcinomas for patients with locally advanced disease in combination with radiation therapy or after failure of platinum-based chemotherapy in recurrent or metastatic disease (FDA).
  • Cetuximab has the potential to provide an improvement of clinical outcome also in other indications and tumor types, particularly when used as first-line therapy combined with standard chemotherapy for metastatic disease or in the adjuvant setting.
  • (ii) the development of standardized predictive biomarkers as surrogates for early monitoring of drug efficacy; and (iii) adequate study design, statistical analysis and proper end points of efficacy to be applied in future prospective trials.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Biomarkers, Tumor / analysis. Carcinoma, Non-Small-Cell Lung / drug therapy. Cetuximab. Colorectal Neoplasms / drug therapy. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Lung Neoplasms / drug therapy. Predictive Value of Tests

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  • (PMID = 17520586.001).
  • [ISSN] 0393-6155
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
  • [Number-of-references] 49
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21. Miyazu YM, Miyazawa T, Hiyama K, Kurimoto N, Iwamoto Y, Matsuura H, Kanoh K, Kohno N, Nishiyama M, Hiyama E: Telomerase expression in noncancerous bronchial epithelia is a possible marker of early development of lung cancer. Cancer Res; 2005 Nov 1;65(21):9623-7
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  • [Title] Telomerase expression in noncancerous bronchial epithelia is a possible marker of early development of lung cancer.
  • Centrally located lung cancers in smokers frequently associated with subsequent primary tumors.
  • We evaluated the telomerase expression chronologically in noncancerous epithelia as a risk factor of susceptibility to lung cancer development.
  • Telomerase protein expression was examined in situ by immunohistochemistry in 26 noncancerous bronchial epithelia adjacent to centrally located early-stage lung cancers in sequential 23 patients treated by photodynamic therapy or surgery among 206 patients who underwent autofluorescence bronchoscopy from 1997 to 2003.
  • Among the 15 lesions in 12 patients treated by photodynamic therapy alone, 11 lesions achieved complete remission after photodynamic therapy, and none of their noncancerous bronchial epithelia was telomerase positive.
  • On the contrary, in the remaining four lesions, either recurrence or secondary lung cancer developed adjacent to the successfully treated primary cancer within 26 months, and the telomerase protein expression in noncancerous epithelia was detected before the secondary cancer development (P < 0.001).
  • The overall relationship of human telomerase reverse transcriptase positivity in noncancerous epithelia and subsequent lung cancer development, including patients treated by radiation or surgery, showed higher significance (P < 0.0001).
  • Histologically "normal" bronchial epithelia in smokers may unphysiologically express telomerase as a field, and such epithelia are likely susceptible to develop lung cancer.
  • We propose that ectopic expression of telomerase in bronchial epithelia may precede transformation in human lung cancer development and that detection of telomerase protein in noncancerous bronchial epithelia will become a useful marker detecting high-risk patients for lung cancer development.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Bronchi / enzymology. Cell Transformation, Neoplastic / metabolism. Lung Neoplasms / enzymology. Telomerase / biosynthesis
  • [MeSH-minor] Carcinoma in Situ / drug therapy. Carcinoma in Situ / enzymology. Carcinoma in Situ / radiotherapy. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / enzymology. Carcinoma, Squamous Cell / radiotherapy. DNA-Binding Proteins / biosynthesis. Epithelial Cells / enzymology. Humans. Immunohistochemistry. Photochemotherapy

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  • (PMID = 16266979.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; EC 2.7.7.49 / Telomerase
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22. Wu Z, Ma JY, Yang JJ, Zhao YF, Zhang SF: Primary small cell carcinoma of esophagus: report of 9 cases and review of literature. World J Gastroenterol; 2004 Dec 15;10(24):3680-2
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  • [Title] Primary small cell carcinoma of esophagus: report of 9 cases and review of literature.
  • AIM: To analyze the clinical manifestations, pathological features and treatment of primary small cell carcinoma (SCC) of the esophagus and to review the literature on this entity.
  • METHODS: The records of 9 patients with primary esophageal small cell carcinoma were examined and the demographic data, presenting symptoms, methods of tumor diagnosis, and types of treatment given, response to treatment, pathologic findings, and clinical outcome were reviewed.
  • Two patients had a stage IIa disease, five had a stage IIb disease, and the other two had a stage III disease of International Union Contrele Cancer (UICC).
  • Three of the nine resected specimens showed foci of squamous cell carcinoma in situ.
  • They received adjuvant systemic chemotherapy and local radiation therapy after discharge.
  • During follow-up, three patients developed multiple liver, brain, lung and bone metastases and died between 5 and 18 mo after the diagnosis.
  • Three patients developed widespread metastasis disease and died between 18 and 37 mo after the diagnosis.
  • CONCLUSION: Primary small cell carcinoma of the esophagus is a rare but very malignant tumor.
  • Radical resection combined with chemotherapy and radiotherapy is helpful in limited stage cases.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Esophageal Neoplasms / pathology

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  • (PMID = 15534932.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] China
  • [Number-of-references] 18
  • [Other-IDs] NLM/ PMC4612018
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23. Ngan RK, Yiu HH, Cheng HK, Chan JK, Sin VC, Lau WH: Central nervous system metastasis from nasopharyngeal carcinoma: a report of two patients and a review of the literature. Cancer; 2002 Jan 15;94(2):398-405
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  • [Title] Central nervous system metastasis from nasopharyngeal carcinoma: a report of two patients and a review of the literature.
  • BACKGROUND: Central nervous system (CNS) metastasis from nasopharyngeal carcinoma (NPC) is an extremely rare occurrence, although direct intracranial invasion is not infrequent in patients with NPC at a locally advanced stage.
  • RESULTS: Both patients had locally advanced disease at the time of presentation and were treated with neoadjuvant chemotherapy and radical radiotherapy.
  • The patient with brain metastasis died 6 months later of lung metastasis, whereas the other patient is still alive 40 months from the diagnosis of spinal metastasis.
  • After aggressive therapy, the ultimate survival depends on control of extracranial disease.
  • [MeSH-major] Brain Neoplasms / secondary. Carcinoma, Squamous Cell / secondary. Nasopharyngeal Neoplasms / pathology. Spinal Cord Neoplasms / secondary
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Fatal Outcome. Herpesvirus 4, Human / genetics. Herpesvirus 4, Human / metabolism. Humans. In Situ Hybridization. Male. Middle Aged. Prognosis. Radiotherapy, Adjuvant. Survival

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  • (PMID = 11905411.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 22
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24. Perrett CM, McGregor JM, Warwick J, Karran P, Leigh IM, Proby CM, Harwood CA: Treatment of post-transplant premalignant skin disease: a randomized intrapatient comparative study of 5-fluorouracil cream and topical photodynamic therapy. Br J Dermatol; 2007 Feb;156(2):320-8
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of post-transplant premalignant skin disease: a randomized intrapatient comparative study of 5-fluorouracil cream and topical photodynamic therapy.
  • BACKGROUND: Organ transplant recipients (OTR) are at high risk of developing nonmelanoma skin cancer and premalignant epidermal dysplasia (carcinoma in situ/ Bowen's disease and actinic keratoses).
  • Epidermal dysplasia is often widespread and there are few comparative studies of available treatments.
  • OBJECTIVES: To compare topical methylaminolaevulinate (MAL) photodynamic therapy (PDT) with topical 5% fluorouracil (5-FU) cream in the treatment of post-transplant epidermal dysplasia.
  • Treatment with two cycles of topical MAL PDT 1 week apart was randomly assigned to one area of epidermal dysplasia, and 5-FU cream was applied twice daily for 3 weeks to a clinically and histologically comparable area.
  • Patients were reviewed at 1, 3 and 6 months after treatment.
  • The main outcome measures were complete resolution rate (CRR), overall reduction in lesional area, treatment-associated pain and erythema, cosmetic outcome and global patient preference.
  • RESULTS: At all time points evaluated after completion of treatment, PDT was more effective than 5-FU in achieving complete resolution: eight of nine lesional areas cleared with PDT (CRR 89%, 95% CI: 0.52-0.99), compared with one of nine lesional areas treated with 5-FU (CRR 11%, 95% CI: 0.003-0.48) (P = 0.02).
  • CONCLUSIONS: Compared with topical 5-FU, MAL PDT was a more effective and cosmetically acceptable treatment for epidermal dysplasia in OTRs and was preferred by patients.
  • Further studies are now required to confirm these results and to examine the effect of treating epidermal dysplasia with PDT on subsequent development of squamous cell carcinoma in this high risk population.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma in Situ / drug therapy. Fluorouracil / therapeutic use. Photochemotherapy / methods. Precancerous Conditions / drug therapy. Skin Neoplasms / drug therapy. Transplantation / adverse effects
  • [MeSH-minor] Administration, Topical. Aged. Aminolevulinic Acid / administration & dosage. Bowen's Disease / drug therapy. Bowen's Disease / etiology. Double-Blind Method. Female. Humans. Keratosis / drug therapy. Keratosis / etiology. Male. Middle Aged. Risk Factors. Treatment Outcome

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  • (PMID = 17223873.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6695
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 88755TAZ87 / Aminolevulinic Acid; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2423222; NLM/ UKMS1912
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25. Zhang X, Zhang H, Tighiouart M, Lee JE, Shin HJ, Khuri FR, Yang CS, Chen Z', Shin DM: Synergistic inhibition of head and neck tumor growth by green tea (-)-epigallocatechin-3-gallate and EGFR tyrosine kinase inhibitor. Int J Cancer; 2008 Sep 1;123(5):1005-14
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  • We investigated whether combining EGCG with the EGFR-tyrosine kinase inhibitor (EGFR-TKI) erlotinib may augment erlotinib-induced cell growth inhibition of squamous cell carcinoma of the head and neck (SCCHN) in a mouse xenograft model.
  • In vitro studies with 5 head and neck cancer cell lines revealed that synergistic cell growth inhibition by the combination of EGCG and erlotinib was associated with significantly greater inhibition of pEGFR and pAKT, increased activation of caspases 9, 3 and PARP compared to the inhibition induced by EGCG or erlotinib alone.
  • The efficacy of the combination treatment was investigated with nude mice (n = 25) orally gavaged with vehicle control, EGCG, erlotinib or the combination at the same doses for 7 days, followed by subcutaneous injection with Tu212 cells.
  • The combined treatment resulted in significantly greater inhibition of tumor growth and delayed tumor progression as a result of increased apoptosis, decreased cell proliferation and reduced pEGFR and pAKT compared to the single agent treatment groups.
  • Our results suggest a synergistic antitumor effect of a combined treatment with EGCG and erlotinib, and provide a promising regimen for future chemoprevention and treatment of SCCHN.

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  • (PMID = 18546267.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA101244; United States / NCI NIH HHS / CA / U01 CA101244-04; United States / NCI NIH HHS / CA / R01 CA112643-02; United States / NCI NIH HHS / CA / CA128613-010001; United States / NCI NIH HHS / CA / CA128613-02; United States / NCI NIH HHS / CA / R01 CA112643; United States / NCI NIH HHS / CA / CA101244-04; United States / NCI NIH HHS / CA / P50 CA128613-010001; United States / NCI NIH HHS / CA / CA112643-02; United States / NCI NIH HHS / CA / P50 CA128613-02; United States / NCI NIH HHS / CA / P50 CA128613
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Enzyme Inhibitors; 0 / Quinazolines; 8R1V1STN48 / Catechin; BQM438CTEL / epigallocatechin gallate; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ NIHMS64892; NLM/ PMC2555987
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