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1. Karna P, Sharp SM, Yates C, Prakash S, Aneja R: EM011 activates a survivin-dependent apoptotic program in human non-small cell lung cancer cells. Mol Cancer; 2009 Oct 30;8:93
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  • [Title] EM011 activates a survivin-dependent apoptotic program in human non-small cell lung cancer cells.
  • BACKGROUND: Lung cancer remains a leading cause of cancer death among both men and women in the United States.
  • Treatment modalities available for this malignancy are inadequate and thus new drugs with improved pharmacological profiles and superior therapeutic indices are being continually explored.
  • RESULTS: Here we report that EM011 inhibited proliferation of a comprehensive panel of lung cancer cells with IC(50)'s ranging from 4-50 microM.
  • In A549 human non-small cell lung cancer cells, the antiproliferative activity was mediated through blockage of cell-cycle progression by induction of a transient but robust mitotic arrest accompanied by activation of the spindle assembly checkpoint.
  • The mitotically-arrested A549 cells then override the activated mitotic checkpoint and aberrantly exit mitosis without cytokinesis resulting in pseudo G1-like multinucleated cells that either succumb directly to apoptosis or continue another round of the cell-cycle.
  • The accumulated enormous DNA perhaps acts as genotoxic stress to trigger cell death.
  • EM011-induced apoptotic cell death in A549 cells was associated with a decrease of the Bcl2/BAX ratio, activation of caspase-3 and cleavage of PARP.
  • Furthermore, EM011 induced downregulation of survivin expression over time of treatment.
  • Abrogation of survivin led to an increase of cell death whereas, overexpression caused decreased apoptosis.
  • CONCLUSION: These in vitro data suggest that EM011 mediates antiproliferative and proapoptotic activity in non-small cell A549 lung cancer cells by impeding cell-cycle progression and attenuating antiapoptotic signaling circuitries (viz.
  • The study provides evidence for the potential usefulness of EM011 in chemotherapy of lung cancer.

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  • (PMID = 19878573.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K99 CA131489; United States / NCI NIH HHS / CA / 1K99CA131489
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Dioxoles; 0 / EM011 compound; 0 / Inhibitor of Apoptosis Proteins; 0 / Isoquinolines; 0 / Microtubule-Associated Proteins; 0 / RNA, Small Interfering; 0 / bcl-2-Associated X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ PMC2776016
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2. Cappell KM, Larson B, Sciaky N, Whitehurst AW: Symplekin specifies mitotic fidelity by supporting microtubule dynamics. Mol Cell Biol; 2010 Nov;30(21):5135-44
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  • Using a pangenomic loss-of-function screening strategy, we have previously identified 76 potent modulators of paclitaxel responsiveness in non-small-cell lung cancer.
  • We find that symplekin supports faithful mitosis by contributing to the formation of a bipolar spindle apparatus.
  • Depletion of additional members of the polyadenylation complex induces similar phenotypes, suggesting that polyadenylation machinery is intimately coupled to microtubule function and thus mitotic spindle formation.
  • These results demonstrate a critical connection between the polyadenylation machinery and mitosis and suggest that tumor cells have an enhanced dependency on these components for spindle assembly.

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  • (PMID = 20823274.001).
  • [ISSN] 1098-5549
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA071341-14; United States / NIGMS NIH HHS / GM / GM008719; United States / NCI NIH HHS / CA / CA128926; United States / NCI NIH HHS / CA / R01 CA154699; United States / NCI NIH HHS / CA / R00 CA128926; United States / NCI NIH HHS / CA / T32 CA071341; United States / NCI NIH HHS / CA / K99 CA128926; United States / NIGMS NIH HHS / GM / T32 GM008719
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CKAP5 protein, human; 0 / CKAP5 protein, mouse; 0 / Microtubule-Associated Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / SYMPK protein, human; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC2953045
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3. Hong JY, Choi MK, Uhm JE, Park MJ, Lee J, Park YH, Ahn JS, Park K, Han JH, Ahn MJ: The role of palliative chemotherapy for advanced pulmonary pleomorphic carcinoma. Med Oncol; 2009;26(3):287-91
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  • [Title] The role of palliative chemotherapy for advanced pulmonary pleomorphic carcinoma.
  • Pulmonary pleomorphic carcinoma is an uncommon malignant tumor of the lung, which has the dual cell components of spindle or giant cells and epithelial cells.
  • The objective of this study was to investigate the clinical course and efficacy of palliative chemotherapy in patients with advanced pulmonary pleomorphic carcinoma.
  • Twelve patients were diagnosed with advanced pulmonary pleomorphic carcinoma and received palliative chemotherapy from February 2000 to December 2007.
  • Among the 12 patients, five patients received gemcitabine/cisplatin, three patients received gemcitabine/carboplatin, two patients received paclitaxel/carboplatin, one patient received paclitaxel/cisplatin, and one patient received docetaxel/cisplatin as first-line chemotherapy.
  • After treatment with first-line palliative chemotherapy, seven patients (58%) had progressive disease, three patients (25%) had stable disease, and only two patients (17%) had a partial response.
  • The median overall survival from the day of initiation of first-line chemotherapy was only 8 months (95% CI, 6-10) with median follow-up of 26 months.
  • These results showed the dismal prognosis and the poor response to chemotherapy of advanced pulmonary pleomorphic carcinoma.
  • Further studies are needed to investigate whether the current strategy of palliative chemotherapy for the treatment of advanced pulmonary pleomorphic carcinoma can be justified or not.
  • Moreover, additional novel treatment approaches are required.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lung Neoplasms / drug therapy. Palliative Care / methods

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  • (PMID = 18989796.001).
  • [ISSN] 1357-0560
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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4. Sakuma T, Nomizu T, Miyamoto K, Ogino A, Yamada M, Katagata N, Watanabe F, Yamaguchi Y: Locally advanced and metastatic breast cancer with cartilaginous and/or osseous metaplasia showing excellent response to chemotherapy. Breast Cancer; 2004;11(4):401-8
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  • [Title] Locally advanced and metastatic breast cancer with cartilaginous and/or osseous metaplasia showing excellent response to chemotherapy.
  • We report a case of breast cancer with cartilaginous and/or osseous metaplasia that was StageIV,(T4bN0M1b (PUL)), on the basis of the Japanese General Rules for Clinical and Pathological Recording of Breast Cancer, which responded well to chemotherapy.
  • Chest computed tomography (CT) demonstrated multiple lung metastases.
  • Histology of the biopsy specimens revealed a spindle-shaped cell carcinoma.
  • CAF was given to the patient as preoperative chemotherapy.
  • Five cycles of treatment yielded improvement at the primary site and improvement of the metastatic lung lesions, which was judged as a partial response.
  • The final pathological diagnosis was a rare type of breast cancer with cartilaginous and/or osseous metaplasia.
  • Preoperative chemotherapy had caused necrosis in most of the tumor cells, and the efficacy was judged as Grade 2.
  • Six months after the operation, the multiple lung metastases were completely eliminated and new metastasis to liver or bone or local recurrence have not been observed.
  • [MeSH-major] Breast Neoplasms / diagnosis. Lung Neoplasms / diagnosis. Sarcoma / diagnosis
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Mastectomy. Middle Aged. Neoadjuvant Therapy. Neoplasm Metastasis. Neoplasm Staging. Tomography, X-Ray Computed


5. Huang CH, Treat J: New advances in lung cancer chemotherapy: topotecan and the role of topoisomerase I inhibitors. Oncology; 2001;61 Suppl 1:14-24
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  • [Title] New advances in lung cancer chemotherapy: topotecan and the role of topoisomerase I inhibitors.
  • Objective tumor responses and survival rates with standard chemotherapy options for small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC) have been disappointing.
  • However, several promising new classes of agents have emerged in recent years, including the taxanes, mitotic spindle inhibitors, antimetabolites, and topoisomerase I and II inhibitors.
  • Inhibition of this enzyme by drugs such as topotecan and irinotecan leads to cell death and is the basis for their anticancer activity.
  • The process of DNA replication is halted by the covalent binding of the drug in a topoisomerase I drug/DNA ternary reaction intermediate.
  • The pharmacokinetics of the approved regimen--a 30-min infusion daily for 5 days at 21-day intervals--are well defined, with proportional increases in the area under the plasma concentration-time curve, peak plasma concentration, and steady state concentration following application of higher doses.
  • Topotecan is well tolerated and has demonstrated good efficacy in patients with relapsed SCLC when administered as monotherapy or in combination regimens as first-line or second-line therapy.
  • Preliminary trials also indicate that topotecan is well tolerated and has activity in the first-line treatment of NSCLC.
  • In this article an overview of new agents in lung cancer chemotherapy is provided, with particular attention paid to the topoisomerase I inhibitors.
  • A review of topotecan--the first topoisomerase I inhibitor to be approved for second-line therapy in SCLC--is presented as an illustration of the promise these new agents hold for the treatment of SCLC and NSCLC.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Small Cell / drug therapy. Enzyme Inhibitors / administration & dosage. Lung Neoplasms / drug therapy. Topotecan / administration & dosage
  • [MeSH-minor] Clinical Trials as Topic. DNA Topoisomerases, Type I / drug effects. Female. Humans. Male. Prognosis. Survival Analysis. Treatment Outcome

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  • [Copyright] Copyright 2001 S. Karger AG, Basel
  • (PMID = 11598410.001).
  • [ISSN] 0030-2414
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 7M7YKX2N15 / Topotecan; EC 5.99.1.2 / DNA Topoisomerases, Type I
  • [Number-of-references] 74
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6. Kojima K, Nakashima F, Boku A, Muroishi Y, Nakanishi I, Oda Y: Clinicopathological study of involvement of granulocyte colony stimulating factor and granulocyte-macrophage colony stimulating factor in non-lymphohematopoietic malignant tumors accompanied by leukocytosis. Histol Histopathol; 2002 10;17(4):1005-16

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  • Among 1,778 autopsy cases in the last 20 years, 485 lesions of 439 cases with non-lymphohematopoietic malignant tumors accompanied by leukocytosis with a white blood cell count of 10,000/mm3 or greater during the course were immunohistologically examined for G-CSF and GM-CSF.
  • GM-CSF mRNA was confirmed by using non-fixed cryopreserved tumor tissues in one case positive for GM-CSF.
  • G-CSF-positive cases were large cell carcinoma of the lung, adenocarcinoma of the colon, and adenocarcinoma of the stomach, and GM-CSF-positive cases were spindle cell carcinoma of the lung and malignant thymoma.
  • In the case with stomach carcinoma, the primary lesion showing moderately differentiated adenocarcinoma was negative, but the lung metastatic lesion showing less differentiated adenocarcinoma was G-CSF-positive.
  • The highest white blood cell count in five CSF-positive cases was markedly elevated: 29,400-103,500/mm3 (mean: 59,700/mm3).
  • In four cases, excluding one case which may have been markedly affected by chemotherapy, the bone marrow showed hyperplasia, and the number of the granulocyte series cells significantly increased.

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  • (PMID = 12371127.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / DNA Primers; 0 / RNA, Messenger; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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7. Saijo T, Ishii G, Ochiai A, Yoh K, Goto K, Nagai K, Kato H, Nishiwaki Y, Saijo N: Eg5 expression is closely correlated with the response of advanced non-small cell lung cancer to antimitotic agents combined with platinum chemotherapy. Lung Cancer; 2006 Nov;54(2):217-25
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  • [Title] Eg5 expression is closely correlated with the response of advanced non-small cell lung cancer to antimitotic agents combined with platinum chemotherapy.
  • BACKGROUND: Eg5 is a microtubule motor protein that functions in bipolar spindle assembly.
  • We investigated the relationship between Eg5 expression and the response to chemotherapy of patients with advanced non-small cell lung cancer (NSCLC).
  • All patients received antimitotic agents combined with platinum chemotherapy.
  • The response to chemotherapy was compared in relation to Eg5 and cyclin B1 expression and in relation to clinicopathological factors.
  • RESULTS: The response rate to chemotherapy of patients with Eg5-positive tumors was 37%, as opposed to 10% for patients with Eg5-negative tumors, and Eg5 expression was significantly associated with the response to chemotherapy (P=0.002).
  • A multivariate analysis confirmed Eg5 status to be an independent variable related to response to chemotherapy (P=0.008).
  • CONCLUSIONS: Eg5 expression can predict a response to antimitotic agents combined with platinum chemotherapy among patients with advanced NSCLC.
  • [MeSH-major] Antimitotic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols. Carboplatin / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Cisplatin / therapeutic use. Kinesin / metabolism. Lung Neoplasms / drug therapy

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  • (PMID = 16934364.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antimitotic Agents; 0 / CCNB1 protein, human; 0 / Cyclin B; 0 / Cyclin B1; 0 / KIF11 protein, human; BG3F62OND5 / Carboplatin; EC 3.6.1.- / Kinesin; Q20Q21Q62J / Cisplatin
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8. Mainwaring MG, Poor C, Zander DS, Harman E: Complete remission of pulmonary spindle cell carcinoma after treatment with oral germanium sesquioxide. Chest; 2000 Feb;117(2):591-3
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  • [Title] Complete remission of pulmonary spindle cell carcinoma after treatment with oral germanium sesquioxide.
  • Spindle cell carcinoma (SCC) is a rare form of lung cancer representing 0.2 to 0.3% of all primary pulmonary malignancies.
  • Even with combined surgery, chemotherapy, and radiation therapy, these tumors are associated with a poor prognosis and only 10% of patients survive 2 years after diagnosis.
  • We describe a patient with an unresectable SCC who, following no response to conventional treatment with combined modality therapy, chose to medicate herself with daily doses of germanium obtained in a health food store.
  • She noted prompt symptomatic improvement and remains clinically and radiographically free of disease 42 months after starting her alternative therapy.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma / drug therapy. Complementary Therapies. Germanium / administration & dosage. Lung Neoplasms / drug therapy
  • [MeSH-minor] Female. Follow-Up Studies. Humans. Lung / radiography. Middle Aged. Self Medication. Tomography, X-Ray Computed

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  • [CommentIn] Chest. 2000 Feb;117(2):307-8 [10669667.001]
  • (PMID = 10669709.001).
  • [ISSN] 0012-3692
  • [Journal-full-title] Chest
  • [ISO-abbreviation] Chest
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 00072J7XWS / Germanium
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9. Terada T: Primary small cell carcinoma of the pleura: a case report with immunohistochemical and molecular genetic analyses of KIT and PDGFRA genes. Med Oncol; 2010 Dec;27(4):1119-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary small cell carcinoma of the pleura: a case report with immunohistochemical and molecular genetic analyses of KIT and PDGFRA genes.
  • An extremely rare case of primary small cell carcinoma of the pleura with an emphasis on KIT and platelet-derived growth factor receptor-α (PDGFRA) genes is reported here.
  • The tumor was immunohistochemically shown to be diffuse large B-cell lymphoma.
  • The patient was treated with chemotherapy and radiation and followed up in our hospital.
  • Eight years after the orchiectomy, the patient (75 years old) developed left pleural tumor and pleural effusion, and a biopsy was performed.
  • The biopsy revealed a medullary malignant tumor consisting of small round and spindle cells.
  • The following three possibilities were considered: recurrent lymphoma, mesothelioma, and small cell carcinoma.
  • Therefore, a diagnosis of pleural small cell carcinoma was made.
  • The patient was treated with chemotherapy (cisplatin) and radiation (50 Gray).
  • The present case is the first reported case of primary small cell carcinoma of the pleura with an examination of KIT and PDGFRA expressions and KIT and PDGFRA gene mutations.
  • [MeSH-major] Pleural Neoplasms / pathology. Proto-Oncogene Proteins c-kit / genetics. Receptor, Platelet-Derived Growth Factor alpha / genetics. Small Cell Lung Carcinoma / pathology
  • [MeSH-minor] Aged. Humans. Immunoenzyme Techniques. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large B-Cell, Diffuse / therapy. Male. Mutation / genetics. Orchiectomy. Testicular Neoplasms / metabolism. Testicular Neoplasms / pathology. Testicular Neoplasms / surgery

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  • (PMID = 19859843.001).
  • [ISSN] 1559-131X
  • [Journal-full-title] Medical oncology (Northwood, London, England)
  • [ISO-abbreviation] Med. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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10. Masi G, Fornaro L, Cupini S, Loupakis F, Vasile E, Baldi GG, Stasi I, Salvatore L, Falcone A: Refractory neuroendocrine tumor-response to liposomal doxorubicin and capecitabine. Nat Rev Clin Oncol; 2009 Nov;6(11):670-4
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  • BACKGROUND: A 61-year-old patient with no relevant medical or family history presented with a 2 month history of refractory dry cough that led to the diagnosis of typical carcinoid tumor of the lung metastatic to the mediastinal lymph nodes and liver.
  • She initially received a long-acting somatostatin analog (octreotide) and chemotherapy with cisplatin and etoposide, which was ineffective.
  • INVESTIGATIONS: Physical examination, laboratory test, chromogranin A test, CT scan, (111)In-diethylenetriaminepentaacetic acid (DTPA)-octreotide scan, (18)F-FDG-PET scan, fine-needle and tissue core liver biopsies.
  • DIAGNOSIS: Pulmonary spindle-cell carcinoid tumor with metastases to mediastinal lymph nodes and liver.
  • MANAGEMENT: Systemic treatment with oral capecitabine (1,500 mg/m(2) daily from day 1 to day 21) and intravenous liposomal doxorubicin (10 mg/m(2) on days 1, 8 and 15), both repeated every 4 weeks, administered concomitantly with long-acting octreotide 30 mg every 3 weeks.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Neuroendocrine / drug therapy
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Antineoplastic Agents, Phytogenic / therapeutic use. Capecitabine. Cisplatin / therapeutic use. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Doxorubicin / administration & dosage. Etoposide / therapeutic use. Female. Fluorouracil / administration & dosage. Fluorouracil / analogs & derivatives. Humans. Lymphatic Metastasis / pathology. Middle Aged. Octreotide / therapeutic use. Treatment Outcome

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  • (PMID = 19861994.001).
  • [ISSN] 1759-4782
  • [Journal-full-title] Nature reviews. Clinical oncology
  • [ISO-abbreviation] Nat Rev Clin Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; RWM8CCW8GP / Octreotide; U3P01618RT / Fluorouracil
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11. Yangui I, Smaoui M, Khabir A, Ayoub A, Boudawara T: [A rare primary pulmonary tumor: pleomorphic carcinoma]. Presse Med; 2007 Feb;36(2 Pt 1):243-6
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  • [Title] [A rare primary pulmonary tumor: pleomorphic carcinoma].
  • INTRODUCTION: Pleomorphic carcinoma is a rare malignancy in the family of non-small cell lung cancers.
  • Computed tomography showed a peripheral tumor of the right upper lobe, and the radiography showed signs of malignancy.
  • Pathologic examination of the transparietal biopsy confirmed the tumor diagnosis, classifying it as stage III A.
  • The patient underwent 2 cycles of induction chemotherapy that combined gemcitabine and cisplatin.
  • The patient died 4 months after diagnosis.
  • DISCUSSION: Pleomorphic carcinoma is identified by purely histologic criteria: the concomitant presence of malignant epithelial and homologous sarcomatoid spindle-cell components.
  • Like the other non-small cell lung cancers, treatment is primarily surgical, and the invasive character of this tumor makes it very difficult.
  • Pleomorphic carcinoma has a poorer prognosis than conventional non-small cell lung cancers despite surgery, irradiation and chemotherapy, because relapse occurs early.
  • [MeSH-major] Carcinoma / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Radiography, Thoracic. Treatment Outcome

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  • (PMID = 17259034.001).
  • [ISSN] 0755-4982
  • [Journal-full-title] Presse medicale (Paris, France : 1983)
  • [ISO-abbreviation] Presse Med
  • [Language] fre
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
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12. Nosaka S, Murayama M, Beppu T, Katsuda K, Nakao M, Enomoto M: [Pleomorphic carcinoma of the lung; report of a case]. Kyobu Geka; 2008 Jun;61(6):512-5
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  • [Title] [Pleomorphic carcinoma of the lung; report of a case].
  • Chest radiography and computed tomography (CT) showed a tumor mass near the right hilum and atelectasis of the middle lobe.
  • Histological findings showed adenocarcinoma comprised of spindle cell component, finally diagnosing as pleomorphic carcinoma of the lung.
  • After the operation, systemic chemotherapy, including paclitaxel and carboplatin was performed.
  • [MeSH-major] Carcinoma / surgery. Lung Neoplasms / surgery
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / secondary. Carboplatin / administration & dosage. Chemotherapy, Adjuvant. Fatal Outcome. Female. Humans. Lymph Node Excision. Paclitaxel / administration & dosage. Pneumonectomy. Treatment Outcome

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  • (PMID = 18536305.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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13. Krzakowski M: Systemic therapy options in malignant bone diseases. Ortop Traumatol Rehabil; 2005 Oct 30;7(5):567-72

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systemic therapy options in malignant bone diseases.
  • Bone metastases (secondary bone neoplasms) represent a more significant epidemiological problem than primary bone neoplasms.
  • The differing histogenesis of primary and secondary malignant bone neoplasms (respectively, mesenchymal and epithelial origin) influences the variability of activity and indications for systemic therapy.
  • A common response is the use of systemic therapy within a multidisciplinary therapeutic approach.
  • The principles of chemotherapy used for primary bone neoplasms are essentially similar in spindle-cell and small-cell sarcomas.
  • Initial multi-drug chemotherapy should be administered in all stages.
  • Chemotherapy may also be used following local treatment, although the role of adjuvant chemotherapy is better defined in small-cell sarcomas.
  • Chemotherapy is also applied in the palliative management of disseminated sarcomas.
  • Systemic therapy plays an essential role in the management of patients with bone metastases during the course of breast and prostate carcinoma.
  • The use of hormonal therapy is based on endocrine dependency of both malignancies.
  • Chemotherapy represents a treatment of choice in several clinical situations due to high chemosensitivity of the underlying malignancy (e. g., small-cell lung cancer or lymphoma).
  • The use of bisphosphonates is most justified in patients with breast cancer, multiple myeloma, and prostate carcinoma.

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  • (PMID = 17611451.001).
  • [ISSN] 1509-3492
  • [Journal-full-title] Ortopedia, traumatologia, rehabilitacja
  • [ISO-abbreviation] Ortop Traumatol Rehabil
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
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14. Gotoh M, Yamamoto Y, Huang CL, Yokomise H: A combined small cell carcinoma of the lung containing three components: small cell, spindle cell and squamous cell carcinoma. Eur J Cardiothorac Surg; 2004 Nov;26(5):1047-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A combined small cell carcinoma of the lung containing three components: small cell, spindle cell and squamous cell carcinoma.
  • The mass was diagnosed as pure small cell carcinoma by CT-guided needle biopsy, and the patient underwent chemotherapy.
  • Postoperatively, the mass was diagnosed as small cell carcinoma combined with small cell, spindle cell and squamous cell carcinoma.
  • We report this case in view of the rarity of this combination of morphologic patterns in a primary bronchogenic carcinoma.
  • [MeSH-major] Carcinoma / pathology. Carcinoma, Small Cell / pathology. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology

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  • [CommentIn] Eur J Cardiothorac Surg. 2005 Apr;27(4):734; author reply 735 [15784404.001]
  • (PMID = 15519208.001).
  • [ISSN] 1010-7940
  • [Journal-full-title] European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
  • [ISO-abbreviation] Eur J Cardiothorac Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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15. Rosell R, Taron M, Camps C, López-Vivanco G: Influence of genetic markers on survival in non-small cell lung cancer. Drugs Today (Barc); 2003 Oct;39(10):775-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Influence of genetic markers on survival in non-small cell lung cancer.
  • Cisplatin or carboplatin is commonly used with gemcitabine, docetaxel, paclitaxel or vinorelbine as chemotherapy doublets in the treatment of advanced non-small cell lung cancer.
  • This lack of evidence for improvement in survival with any chemotherapy regimen has created a tabula rasa in which no more large randomized trials should be conducted with out including a genetic analysis.
  • Patients see survival as their major concern, and other considerations, such as cost of treatment and qualify of life, are relegated to lower positions.
  • For a long time, ERCC1 mRNA levels have been known to correlate with DNA repair capacity in various tissues.
  • Levels of DNA cisplatin adducts in peripheral blood and buccal mucosa cells predict chemotherapy response, and high ERCC1 mRNA levels have been related to chemoresistance in ovarian cancer and in malignant lymphocytes from chronic lymphocytic leukemia.
  • Overexpression of ERCC1 correlates with poor survival gemcitabine/cisplatin-treated non-small cell lung cancer patients.
  • An ongoing customized ERCC1-based chemotherapy trial has been established on this knowledge.
  • At the preclinical level, ERCC1 and XPD mRNA expression correlate with each other, and overexpression of XPD causes selective cisplatin resistance in human tumor cell lines.
  • In our experience, time to disease progression is significantly higher in gemcitabine/cisplatin-treated patients with the Lys751Gln genotype (9.6 months) than in those with the Lys751Lys genotype (4.2 months; p = 0.03).
  • This highlights the possibilities of individually tailored chemotherapy.
  • Patients with Lys751Lys had a longer time to progression.
  • At least 50% of non-small cell lung cancer patients harbor Lys751Lys and can benefit from docetaxel/ cisplatin treatment.
  • Genes involved in spindle formation, centrosome functions and mRNA transport along the microtubule tracks should provide further information on potential markers of docetaxel resistance.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / mortality. DNA Helicases. DNA-Binding Proteins. Deoxycytidine / analogs & derivatives. Lung Neoplasms / genetics. Lung Neoplasms / mortality. Transcription Factors
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cisplatin / pharmacology. Cisplatin / therapeutic use. Clinical Trials as Topic. DNA Adducts / metabolism. DNA Repair. Drug Resistance, Neoplasm / genetics. Genetic Markers. Humans. Polymorphism, Genetic. Proteins / genetics. Ribonucleotide Reductases / genetics. Survival Rate. Xeroderma Pigmentosum Group D Protein

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  • (PMID = 14668933.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA Adducts; 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / Proteins; 0 / Transcription Factors; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / Ribonucleotide Reductases; EC 3.6.4.- / DNA Helicases; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human; Q20Q21Q62J / Cisplatin
  • [Number-of-references] 54
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16. Sone S, Nakayama T, Honda T, Tsushima K, Li F, Haniuda M, Takahashi Y, Hanaoka T, Takayama F, Koizumi T, Kubo K, Yamanda T, Kondo R, Fushimi H, Suzuki T: CT findings of early-stage small cell lung cancer in a low-dose CT screening programme. Lung Cancer; 2007 May;56(2):207-15
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  • [Title] CT findings of early-stage small cell lung cancer in a low-dose CT screening programme.
  • The survival of patients with small cell lung cancer (SCLC) is related to T, N, M components, and early diagnosis and treatment of limited stage SCLC may improve survival.
  • The objective of this study was to review the initial and annual repeat screening computed tomography (CT) images of all five patients with SCLC, encountered in our 1996-1998 population-based screening for lung cancer, to clarify any subtle, characteristic CT findings of early-stage small cell lung cancer.
  • We identified characteristic CT features of SCLC in the lung periphery, which were related to gross pathologic findings with longitudinal spread along the bronchial wall: a small spindle-shaped or pyramidal lesion was found as a subtle CT finding of SCLC, and irregularly shaped nodular lesions (vermiform, pine-cone-like or tandem-like nodular lesions) appeared at a more advanced stage.
  • Tumour volume doubling time of the cases ranged from 38 days to 217 days.
  • All five patients were male smokers: four patients underwent surgery and adjuvant chemotherapy; three of them remain alive, while the remaining patient, an interval case, died of lung cancer.
  • One patient refused treatment and died of a cause other than lung cancer.
  • Annual repeat CT screening was useful for detecting SCLC cases mostly at a curable stage, and information about CT features, presented here, should help physicians identify SCLC at an earlier-stage and lead to a more successful treatment of the disease.
  • [MeSH-major] Carcinoma, Small Cell / radiography. Lung Neoplasms / radiography. Mass Screening. Tomography, X-Ray Computed

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  • (PMID = 17258349.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
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17. Kawamura S, Nakamura T, Oya T, Ishizawa S, Sakai Y, Tanaka T, Saito S, Fukuoka J: Advanced malignant solitary fibrous tumor in pelvis responding to radiation therapy. Pathol Int; 2007 Apr;57(4):213-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Advanced malignant solitary fibrous tumor in pelvis responding to radiation therapy.
  • Solitary fibrous tumor (SFT) is a rare spindle cell neoplasm that is benign in most cases.
  • Along with massive invasion to adjacent organs and multiple lung metastases detected on radiography, biopsy from the tumor through the vaginal wall showed malignant looking spindle-cell neoplasm with increased cellularity, areas of necrosis, and high mitotic activity (5/10 high-power fields).
  • Based on pathological features and clinical presentation, diagnosis of malignant SFT was made.
  • The patient received systemic and the intra-arterial chemotherapy followed by whole pelvic radiation therapy (50 Gy).
  • Afterwards, improvement was observed radiologically and pathologically in the 12 months' follow up after the radiation therapy.
  • This is the first report related to therapeutic remarks on advanced malignant SFT.
  • [MeSH-major] Carcinoma / radiotherapy. Neoplasms, Fibrous Tissue / radiotherapy. Pelvic Neoplasms / radiotherapy

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  • (PMID = 17316417.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
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18. Morawietz L, Kuhnen C, Katenkamp D, Le Coutre P, Ladhoff A, Petersen I: Unusual sarcomatoid neoplasm of the lung suggesting a myofibrosarcoma. Virchows Arch; 2005 Dec;447(6):990-5
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  • [Title] Unusual sarcomatoid neoplasm of the lung suggesting a myofibrosarcoma.
  • Clinically suggestive for a lung carcinoma, the tumor showed typical features of a myofibrosarcoma.
  • A major spindle cell component was observed being positive for smooth-muscle actin, calponin, and vimentin, while stainings for desmin, h-caldesmon, alkaline phosphatase (ALK), and extensively studied cytokeratins were negative.
  • Shortly after resection of the primary tumor, the patient showed multiple distant metastases in the contralateral lung, the mediastinal lymph nodes, the left adrenal gland, and the pectoral and deltoid muscle, which responded well to chemotherapy.
  • The case report will discuss the evidence for the final diagnosis of a primary pulmonary myofibrosarcoma and the differential diagnosis of sarcomatoid tumors of the lung.
  • [MeSH-major] Fibrosarcoma / pathology. Lung Neoplasms / pathology. Myosarcoma / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male. Middle Aged. Nucleic Acid Hybridization. Pneumonectomy. Sarcoma / pathology

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  • (PMID = 16158184.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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19. Inomata M, Kawagishi Y, Yamada T, Miwa T, Hayashi R, Kashii T, Matsui S, Fukuoka J, Tobe K: [Two cases of pulmonary sarcomatoid carcinoma mimicking malignant mesothelioma]. Nihon Kokyuki Gakkai Zasshi; 2010 Jan;48(1):33-8
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  • [Title] [Two cases of pulmonary sarcomatoid carcinoma mimicking malignant mesothelioma].
  • We report 2 cases of pulmonary sarcomatoid carcinoma mimicking malignant mesothelioma.
  • Histological findings of specimens obtained from a percutaneous biopsy revealed spindle tumor cells, and the immunohistochemistry showed that the tumor cells were positive for CK-7, AE1/AE3, and vimentin and negative for calretinin, D2-40, and WT-1.
  • We diagnosed pulmonary sarcomatoid carcinoma and started chemotherapy with carboplatin and paclitaxel, but it was ineffective.
  • Histological findings showed necrosis and spindle tumor cells which were positive for AE1/AE3 and vimentin, and negative for calretinin, D2-40, and WT-1.
  • We diagnosed pulmonary sarcomatoid carcinoma and started chemotherapy with carboplatin and paclitaxel.
  • The pulmonary sarcomatoid carcinoma was reported to have spred to the pleural and chest wall.
  • The present two cases showed prominent chest wall and pleural tumors with obscure primary lung tumors.
  • Therefore, we needed to differentiate sarcomatoid carcinoma from malignant pleural mesothelioma.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / diagnosis. Lung Neoplasms / diagnosis. Mesothelioma / diagnosis
  • [MeSH-minor] Aged. Diagnosis, Differential. Histocytochemistry. Humans. Male

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  • (PMID = 20163019.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Number-of-references] 19
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20. Franklin WA: Diagnosis of lung cancer: pathology of invasive and preinvasive neoplasia. Chest; 2000 Apr;117(4 Suppl 1):80S-89S
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  • [Title] Diagnosis of lung cancer: pathology of invasive and preinvasive neoplasia.
  • The histopathologic appearance of lung carcinoma remains an important guide to prognosis and treatment.
  • The newly revised World Health Organization classification retains the broadest pathologic categories of the older classification but includes several revisions, including the elimination of the small cell, intermediate cell type category; the addition of large cell neuroendocrine and spindle/giant cell categories; and an extended consideration of preneoplastic lesions.
  • The histopathologic classification of lung cancer is expected to continue to change as clinical practice and biological understanding of these tumors change.
  • The significance of expression of neuroendocrine markers, histologic grading of response to chemotherapy, and delineation of morphologic changes preceding the occurrence of invasive carcinoma are all areas where understanding microscopic cellular changes in the airways will be critical for clinical advance.
  • [MeSH-major] Lung / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Algorithms. Diagnosis, Differential. Humans. Mesothelioma / pathology. Neoplasm Invasiveness. Neuroendocrine Tumors / pathology. Precancerous Conditions / pathology. World Health Organization

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  • (PMID = 10777460.001).
  • [ISSN] 0012-3692
  • [Journal-full-title] Chest
  • [ISO-abbreviation] Chest
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Number-of-references] 24
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21. Trepp R, Padberg BC, Varga Z, Cathomas R, Inauen R, Reinhart WH: Extensive extranodal metastases of basal-like breast cancer with predominant myoepithelial spindle cell differentiation. Pathol Res Pract; 2010 May 15;206(5):334-7
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  • [Title] Extensive extranodal metastases of basal-like breast cancer with predominant myoepithelial spindle cell differentiation.
  • A differentiation towards myoepithelial cells has been demonstrated in several types of lesions in the breast.
  • These include multifocal myoepitheliomatosis, the rare mixed tumor or pleomorphic adenoma, adenoid cystic carcinoma, adenomyoepithelioma and myoepithelial carcinoma (malignant myoepithelioma).
  • Myoepithelial carcinoma is the only lesion purely composed of myoepithelial cells.
  • The presented case of a breast carcinoma with dominant myoepithelial/spindle cell differentiation in a 58-year-old woman is an excellent example to document the highly aggressive biological behavior of this tumor phenotype.
  • Despite an extensive chemotherapy and radiotherapy, the tumor was rapidly progressive, forming a finally exulcerating local tumor relapse and widespread metastases to the myocardium, lungs, liver, kidneys and skin.
  • Similarities in morphology and biological behavior compared to patients with "triple-negative" (hormone receptor and Her2) monophasic sarcomatoid carcinomas and pure spindle cell sarcomas are discussed.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma / secondary. Kidney Neoplasms / secondary. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Skin Neoplasms / secondary
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic / pathology. Fatal Outcome. Female. Humans. Middle Aged


22. Suzuki-Uematsu S, Shiraishi K, Ito T, Adachi N, Inage Y, Taeda Y, Ueki H, Ohtani H: Malignant phyllodes tumor composed almost exclusively of a fibrosarcomatous component: a case report and review of malignant phyllodes tumors with metastases. Breast Cancer; 2010 Jul;17(3):218-24
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  • On admission, multiple lung metastases were detected by imaging.
  • Microscopically, the tumor showed proliferation of atypical ovoid- or spindle-shaped cells in a myxoid matrix.
  • Multiple sectioning revealed that the tumor had only focal occurrence of elongated tubular structures, and the occurrence of a small component of benign phyllodes tumor, leading to the aforementioned final diagnosis.
  • Spindle cell carcinoma was excluded on the basis of the HE findings and the lack of immunoreactivity for cytokeratin when using a broad spectrum antibody mixture.
  • Although the patient received adjuvant chemotherapy, no responsiveness was obtained.
  • The estimated 2.2-year survival rate following detection of metastasis was 11%, thus confirming the aggressiveness of the disease.
  • [MeSH-major] Breast Neoplasms / pathology. Fibrosarcoma / pathology. Lung Neoplasms / secondary. Phyllodes Tumor / secondary
  • [MeSH-minor] Female. Humans. Mastectomy, Simple. Middle Aged. Tomography, X-Ray Computed

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  • (PMID = 19350353.001).
  • [ISSN] 1880-4233
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Japan
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23. Ikeda S, Takabe K, Suzuki K: Expression of ERCC1 and class IIIbeta tubulin for predicting effect of carboplatin/paclitaxel in patients with advanced inoperable non-small cell lung cancer. Pathol Int; 2009 Dec;59(12):863-7
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  • [Title] Expression of ERCC1 and class IIIbeta tubulin for predicting effect of carboplatin/paclitaxel in patients with advanced inoperable non-small cell lung cancer.
  • It was recently reported that expression of excision repair cross-complementation group 1 (ERCC1), a DNA repair protein, predicts sensitivity to platinum-based chemotherapy drugs.
  • Microtubule inhibitors such as paclitaxel demonstrate anticancer effects by inhibiting spindle fibers during mitosis; and class IIIbeta tubulin (IIIbeta tubulin), a microtubule component, is thought to be resistant to microtubule inhibitors.
  • The purpose of the present study was to examine the correlation between prognosis and expression of these proteins using biopsy tissues obtained from 40 patients with advanced inoperable non-small cell lung cancer who had been treated with carboplatin plus Taxol.
  • It was concluded that determination of the expression of these proteins is useful to predict the effects of platinum-based anticancer drugs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm / genetics. Endonucleases / genetics. Lung Neoplasms / genetics. Tubulin / genetics

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  • [ErratumIn] Pathol Int. 2010 Feb;60(2):148
  • (PMID = 20021611.001).
  • [ISSN] 1440-1827
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / TUBB3 protein, human; 0 / Tubulin; BG3F62OND5 / Carboplatin; EC 3.1.- / ERCC1 protein, human; EC 3.1.- / Endonucleases; P88XT4IS4D / Paclitaxel
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24. Kakegawa S, Kawashima O, Sugano M, Nagashima T, Morishita Y: [Pleomorphic lung cancer; a clinicopathologic study]. Kyobu Geka; 2006 Feb;59(2):110-3
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  • [Title] [Pleomorphic lung cancer; a clinicopathologic study].
  • Pulmonary pleomorphic carcinoma is a comparatively rare histologic type of lung carcinoma, and the incidence among all lung carcinomas has been reported to be 0.4%.
  • We reported our experience with 8 patients who had been diagnosed as pulmonary pleomorphic carcinoma, and discussed clinicopathologically the preoperative diagnosis and treatment.
  • In 2 of 8 patients, preoperative transbronchial lung biopsy revealed spindle cell component, highly suggesting pulmonary pleomorphic carcinoma.
  • All patients underwent surgical treatment and 2 of then had incomplete resections because of intrathoracic disseminations or carcinomatous pericarditis.
  • Although the preoperative diagnosis of biphasic tumor such as pulmonary pleomorphic carcinoma is difficult, it is possible to suspect the diagnosis when sarcomatous components were detected by preoperative biopsy.
  • The efficacy of chemotherapy and radiotherapy have not been established yet, and thus we would like to emphasize that surgery might be the treatment of choice.
  • [MeSH-major] Lung Neoplasms / pathology. Neoplasms, Multiple Primary

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  • (PMID = 16482903.001).
  • [ISSN] 0021-5252
  • [Journal-full-title] Kyobu geka. The Japanese journal of thoracic surgery
  • [ISO-abbreviation] Kyobu Geka
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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25. Raveglia F, Mezzetti M, Panigalli T, Furia S, Giuliani L, Conforti S, Meda S: Personal experience in surgical management of pulmonary pleomorphic carcinoma. Ann Thorac Surg; 2004 Nov;78(5):1742-7
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  • [Title] Personal experience in surgical management of pulmonary pleomorphic carcinoma.
  • BACKGROUND: Pleomorphic carcinoma is a rare epithelial malignant tumor.
  • Pulmonary pleomorphic carcinoma was introduced by the 1999 World Health Organization classification as a new peculiar type of lung carcinoma showing concurrent malignant epithelial and sarcomatoid spindle cell elements.
  • My colleagues and I report a series of patients surgically treated for pulmonary pleomorphic carcinoma to describe our experience with this malignant neoplasm.
  • METHODS: Twenty cases of pleomorphic pulmonary carcinoma were collected and studied clinicopathologically.
  • Histologic diagnosis was established by using light microscopic examination and immunohistochemistry.
  • RESULTS: We postoperatively diagnosed 20 cases of pleomorphic carcinoma: 14 cases were exclusively spindle and giant-cell carcinomas, 2 cases were spindle and giant-cell carcinoma combined with adenocarcinoma, 2 were combined with squamous cell carcinoma, and 2 were combined with large cell carcinoma.
  • CONCLUSIONS: The prognosis of patients with pleomorphic carcinoma was poor, despite surgery and adjuvant chemotherapy, because of early relapse of disease.
  • In case of preoperatively proven pulmonary pleomorphic carcinoma, surgery should be recommended to N0 patients.
  • [MeSH-major] Carcinoma / surgery. Lung Neoplasms / surgery
  • [MeSH-minor] Adenocarcinoma / mortality. Adenocarcinoma / pathology. Adenocarcinoma / surgery. Adult. Aged. Carcinoma, Giant Cell / mortality. Carcinoma, Giant Cell / pathology. Carcinoma, Giant Cell / surgery. Cell Differentiation. Disease-Free Survival. Female. Follow-Up Studies. Humans. Life Tables. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 15511465.001).
  • [ISSN] 1552-6259
  • [Journal-full-title] The Annals of thoracic surgery
  • [ISO-abbreviation] Ann. Thorac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 20
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26. Boroumand N, Raja V, Jones DV, Haque AK: SYT-SSX2 variant of primary pulmonary synovial sarcoma with focal expression of CD117 (c-Kit) protein and a poor clinical outcome. Arch Pathol Lab Med; 2003 Apr;127(4):e201-4
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  • [Title] SYT-SSX2 variant of primary pulmonary synovial sarcoma with focal expression of CD117 (c-Kit) protein and a poor clinical outcome.
  • We report a case of primary pulmonary synovial sarcoma with the SYT-SSX2 phenotype and a rapidly progressive downhill course.
  • Previous reports have suggested that the soft tissue synovial sarcomas with SYT-SSX2 phenotype have a favorable clinical outcome.
  • A 45-year-old woman presented with left chest pain and was found to have a left lower lobe tumor that was originally diagnosed as a sarcomatoid carcinoma.
  • After the patient underwent chemotherapy and brachytherapy, the specimen from a left pneumonectomy showed a large spindle cell tumor, which was reclassified as a synovial sarcoma based on the results of immunophenotyping and molecular genetic studies.
  • Differentiation between sarcoma and carcinosarcoma is crucial for implementing appropriate therapy.
  • Furthermore, if the tumor expresses c-Kit, it may respond to target-based therapy.
  • [MeSH-major] Genetic Variation / genetics. Lung Neoplasms / diagnosis. Lung Neoplasms / genetics. Oncogene Proteins, Fusion / genetics. Proto-Oncogene Proteins c-kit / biosynthesis. Sarcoma, Synovial / diagnosis. Sarcoma, Synovial / genetics

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  • (PMID = 12683902.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Oncogene Proteins, Fusion; 0 / SYT-SSX fusion protein; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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27. Tonai K, Kitasato Y, Kawakami T, Kondo H, Koga T, Takata S, Katafuchi R, Kawasaki M: [Autopsy case of rapidly progressive pulmonary spindle cell carcinoma with multiple metastases to the brain and pancreas]. Nihon Kokyuki Gakkai Zasshi; 2009 Sep;47(9):828-32
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  • [Title] [Autopsy case of rapidly progressive pulmonary spindle cell carcinoma with multiple metastases to the brain and pancreas].
  • A 53-year-old man was admitted to our hospital because of an abnormal lung shadow on his chest X-ray film.
  • Chest X-ray and computed tomography showed a large mass lesion in the right lower lobe of the lung.
  • We diagnosed primary non-small cell lung cancer; cT3N1M1 stage IV.
  • Systemic chemotherapy using carboplatin and paclitaxcel was performed.
  • However, the treatment had no effect and he died two months after admission.
  • An autopsy showed pulmonary spindle cell carcinoma, with multiple metastases to the brain, pancreas, etc.
  • Pulmonary spindle cell carcinoma had been recognized as a variant of the squamous cell carcinoma for years, however, in the recent WHO and Japanese classification of lung tumors, it was redefined as an independent histological type.
  • It is a rare form of lung cancer, representing 0.2 to 0.3% of all primary pulmonary malignancies and seems to have poor prognosis.
  • We need to pay more attention to this type of lung cancer.
  • [MeSH-major] Autopsy. Brain Neoplasms / secondary. Carcinoma / secondary. Lung Neoplasms / pathology. Pancreatic Neoplasms / secondary

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  • (PMID = 19827589.001).
  • [ISSN] 1343-3490
  • [Journal-full-title] Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society
  • [ISO-abbreviation] Nihon Kokyuki Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
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28. Hirano H, Yoshida T, Sakamoto T, Yoshimura H, Fukuoka M, Tachibana S, Saito H, Ohkubo E, Nakasho K, Nishigami T: Pulmonary pleomorphic carcinoma producing hCG. Pathol Int; 2007 Oct;57(10):698-702
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  • [Title] Pulmonary pleomorphic carcinoma producing hCG.
  • An 80-year-old woman with a pleomorphic carcinoma (PC) producing hCG was admitted to Nippon Steel Hirohata Hospital because of an abnormal shadow on CT seen during a follow-up examination after surgery for breast cancer.
  • On histology the tumor consisted mostly of intermingled spindle and polygonal cells, while evidence of poorly differentiated adenocarcinoma was seen in a few areas.
  • A diagnosis of PC was made due to hCG expression in approximately 20% of the spindle and polygonal cells on immunohistology.
  • The patient died due to metastases 1 year after the operation, even though the patient had been at stage 1B at the time of the operation and appropriate chemotherapy had been given.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Carcinosarcoma / metabolism. Chorionic Gonadotropin / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Aged, 80 and over. Combined Modality Therapy. Fatal Outcome. Female. Humans. Radiography, Thoracic. Tomography, X-Ray Computed

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  • (PMID = 17803660.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin
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29. Platta CS, Greenblatt DY, Kunnimalaiyaan M, Chen H: The HDAC inhibitor trichostatin A inhibits growth of small cell lung cancer cells. J Surg Res; 2007 Oct;142(2):219-26
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  • [Title] The HDAC inhibitor trichostatin A inhibits growth of small cell lung cancer cells.
  • BACKGROUND: An estimated 162,460 people will die of lung cancer in the United States in 2006, making it the leading cause of cancer deaths.
  • Small cell lung cancer (SCLC) accounts for 20% of all lung cancers and exhibits aggressive behavior with early metastases.
  • Current treatments yield five-year survival rates of 5 to 10%, indicating a need for novel therapeutic approaches.
  • Light microscopy was used to assess changes in cell morphology.
  • The effect of TSA treatment on cellular growth was measured by the MTT assay.
  • Finally, levels of BCL-2, cleaved poly(ADP-ribose) polymerase, p21, and p27 proteins were measured to look for induction of cell cycle arrest and/or apoptosis.
  • RESULTS: DMS53 cells treated with TSA underwent dramatic changes in cell appearance.
  • Treated cells assumed round and spindle shapes with distinct cellular borders.
  • TSA treatment resulted in a dose-dependent inhibition of growth.
  • CONCLUSIONS: TSA causes morphological differentiation and dose-dependent inhibition of cell growth via cell cycle arrest and subsequent apoptosis.
  • This suggests that TSA and other HDACIs may represent a new potential therapy for patients with SCLC.
  • [MeSH-major] Carcinoma, Small Cell / drug therapy. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Lung Neoplasms / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Cell Cycle / drug effects. Cell Division / drug effects. Cell Line, Tumor. Humans

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  • (PMID = 17612559.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / T35 DK062709; United States / NIDDK NIH HHS / DK / T35 DK062709
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 3X2S926L3Z / trichostatin A
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30. Vitale I, Antoccia A, Cenciarelli C, Crateri P, Meschini S, Arancia G, Pisano C, Tanzarella C: Combretastatin CA-4 and combretastatin derivative induce mitotic catastrophe dependent on spindle checkpoint and caspase-3 activation in non-small cell lung cancer cells. Apoptosis; 2007 Jan;12(1):155-66
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  • [Title] Combretastatin CA-4 and combretastatin derivative induce mitotic catastrophe dependent on spindle checkpoint and caspase-3 activation in non-small cell lung cancer cells.
  • We investigated the molecular mechanisms leading to cell death in non-small cell lung cancer H460 cells induced by natural (CA-4) and synthetic stilbenoids (ST2151) structurally related to CA-4.
  • We found that both compounds induced depolymerization and rearrangement of spindle microtubules, as well as an increasingly aberrant organization of metaphase chromosomes in a dose- and time-dependent manner.
  • H460 cells were arrested at a pro-metaphase stage, with condensed chromosomes and a triggered spindle assembly checkpoint, as evaluated by kinetochore localization of Bub1 and Mad1 antibodies.
  • On the other hand, caspase-2, and -8 were not activated by the drug treatment.
  • In conclusion, we believe that discovery of new agents able to trigger mitotic catastrophe cell death as a result of mitotic block and prolonged spindle checkpoint activation is particularly worthwhile, considering that tumor cells have a high proliferative rate and mitotic failure occurs irrespective of p53 status.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Mitosis / drug effects. Stilbenes / pharmacology
  • [MeSH-minor] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Cytochromes c / metabolism. Enzyme Activation / drug effects. Humans. Microscopy, Electron. Microtubules / drug effects. Mitochondria / drug effects. Spindle Apparatus / drug effects. Spindle Apparatus / pathology

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  • (PMID = 17143747.001).
  • [ISSN] 1360-8185
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Stilbenes; 9007-43-6 / Cytochromes c; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; I5590ES2QZ / fosbretabulin
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31. Rho JK, Choi YJ, Lee JK, Ryoo BY, Na II, Yang SH, Kim CH, Lee JC: Epithelial to mesenchymal transition derived from repeated exposure to gefitinib determines the sensitivity to EGFR inhibitors in A549, a non-small cell lung cancer cell line. Lung Cancer; 2009 Feb;63(2):219-26
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  • [Title] Epithelial to mesenchymal transition derived from repeated exposure to gefitinib determines the sensitivity to EGFR inhibitors in A549, a non-small cell lung cancer cell line.
  • In this study, we established a gefitinib-resistant subline (A549/GR), which was derived from the parental A549 cell line by chronic, repeated exposure to gefitinib.
  • Phenotypic changes such as a spindle-cell shape and increased pseudopodia formation suggesting EMT was present in the A549/GR cells.
  • TGF-beta1 treatment for 72 h also induced EMT in the A549 cells and this transition led to resistance to gefitinib.
  • In conclusion, induction of EMT may contribute to the decreased efficacy of therapy in primary and acquired resistance to gefitinib.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Non-Small-Cell Lung / drug therapy. Epithelium / pathology. Lung Neoplasms / drug therapy. Mesoderm / pathology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Cell Line, Tumor. Cell Movement. Drug Resistance, Neoplasm. Humans. Neoplasm Invasiveness. Proto-Oncogene Proteins c-akt / metabolism. Transforming Growth Factor beta1 / pharmacology

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  • (PMID = 18599154.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / Transforming Growth Factor beta1; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; S65743JHBS / gefitinib
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32. Shen C, Buck A, Polat B, Schmid-Kotsas A, Matuschek C, Gross HJ, Bachem M, Reske SN: Triplex-forming oligodeoxynucleotides targeting survivin inhibit proliferation and induce apoptosis of human lung carcinoma cells. Cancer Gene Ther; 2003 May;10(5):403-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Triplex-forming oligodeoxynucleotides targeting survivin inhibit proliferation and induce apoptosis of human lung carcinoma cells.
  • Survivin is expressed in most cancers but is undetectable in differentiated adult cells, and plays an important role both in the suppression of apoptosis and mitotic spindle checkpoint; thus it has attracted great interest as a potential drug target.
  • In this study, we investigated the antigene and antiproliferative effects of triplex-forming oligodeoxynucleotides (TFO) targeting survivin in human lung carcinoma A549 cells.
  • Treatment of A549 cells with survivin-specific but not control TFOs at a concentration of 400 nM in the presence of uptake-enhancing liposome significantly reduced survivin protein level, inhibited cell proliferation, and induced cell apoptosis as demonstrated by immunoblot, cell number counting, and Annexin V-staining.
  • Our results indicate that targeting survivin is a promising alternative strategy for the development of novel anticancer therapeutics.
  • [MeSH-major] Apoptosis / drug effects. Lung Neoplasms / pathology. Microtubule-Associated Proteins / genetics. Oligodeoxyribonucleotides / pharmacology
  • [MeSH-minor] Annexin A5 / metabolism. Cell Count. Cell Division / drug effects. DNA Primers / chemistry. Electrophoretic Mobility Shift Assay. Humans. Inhibitor of Apoptosis Proteins. Liposomes. Neoplasm Proteins. Nucleic Acid Conformation. Tumor Cells, Cultured

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  • (PMID = 12719710.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / BIRC5 protein, human; 0 / DNA Primers; 0 / Inhibitor of Apoptosis Proteins; 0 / Liposomes; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Oligodeoxyribonucleotides
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33. Li JP, Lin JC, Yang JL: ERK activation in arsenite-treated G1-enriched CL3 cells contributes to survival, DNA repair inhibition, and micronucleus formation. Toxicol Sci; 2006 Jan;89(1):164-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Arsenite also perturbs mitotic spindle and induces G2/M prolongation, leading to genomic instability.
  • In this study, we investigate the roles of ERK activation in survival, micronucleus formation, and nucleotide excision repair (NER) synthesis in arsenite-treated G1-enriched CL3 human non-small-cell lung carcinoma cells.
  • After arsenite exposure, the G1 cells exhibited a marked retard in the formation of binucleated cells when they were cultured in cytochalasin B, an inhibitor of cytokinesis, suggesting that arsenite delays the cell cycle progression.
  • Arsenite activated sustained-ERK signal in G1 cells whose suppression further decreased cell proliferation and survival and could lower the micronucleus induction.
  • [MeSH-major] Arsenites / toxicity. Carcinoma, Non-Small-Cell Lung / drug therapy. DNA Repair / drug effects. DNA, Neoplasm / drug effects. G1 Phase / drug effects. Lung Neoplasms / drug therapy. MAP Kinase Signaling System / drug effects. Micronuclei, Chromosome-Defective / chemically induced
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Dose-Response Relationship, Drug. Humans

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  • (PMID = 16207941.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Arsenites; 0 / DNA, Neoplasm; N5509X556J / arsenite
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34. Whitehurst AW, Bodemann BO, Cardenas J, Ferguson D, Girard L, Peyton M, Minna JD, Michnoff C, Hao W, Roth MG, Xie XJ, White MA: Synthetic lethal screen identification of chemosensitizer loci in cancer cells. Nature; 2007 Apr 12;446(7137):815-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have combined a high-throughput cell-based one-well/one-gene screening platform with a genome-wide synthetic library of chemically synthesized small interfering RNAs for systematic interrogation of the molecular underpinnings of cancer cell chemoresponsiveness.
  • NCI-H1155, a human non-small-cell lung cancer line, was employed in a paclitaxel-dependent synthetic lethal screen designed to identify gene targets that specifically reduce cell viability in the presence of otherwise sublethal concentrations of paclitaxel.
  • Here we show that several of these targets sensitize lung cancer cells to paclitaxel concentrations 1,000-fold lower than otherwise required for a significant response, and we identify mechanistic relationships between cancer-associated aberrant gene expression programmes and the basic cellular machinery required for robust mitotic progression.
  • [MeSH-major] Genes, Lethal / genetics. Lung Neoplasms / genetics. Lung Neoplasms / pathology. Paclitaxel / pharmacology
  • [MeSH-minor] Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Cell Line, Tumor. Cell Survival / drug effects. DNA Mutational Analysis. Dose-Response Relationship, Drug. Humans. Lung / drug effects. Lung / metabolism. Lung / pathology. Microtubules / drug effects. Microtubules / metabolism. Mitosis / drug effects. RNA, Small Interfering / genetics. RNA, Small Interfering / metabolism. Spindle Apparatus / drug effects. Spindle Apparatus / metabolism. Spindle Apparatus / pathology






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