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1. Vickers JL, Matherne RJ, Allison AW, Wilkerson MG, Tyring SK, Bartlett BL, Rady PL, Kelly BC: Transitional cell neoplasm of the nasolacrimal duct associated with human papillomavirus type 11. J Cutan Pathol; 2010 Jul;37(7):793-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transitional cell neoplasm of the nasolacrimal duct associated with human papillomavirus type 11.
  • BACKGROUND: Tumors of the lacrimal sac are rare but noteworthy because of their significant potential to become malignant or life-threatening if treatment is delayed.
  • Histology of the lesion revealed transitional epithelium in a papillary growth pattern with numerous goblet cells, scattered mitoses and focal full-thickness atypia.
  • The patient was diagnosed with transitional cell neoplasm (inverted papilloma-type) of the nasolacrimal duct.
  • PCR evaluation identified HPV type 11 in the lesion.
  • [MeSH-major] Carcinoma, Transitional Cell / virology. Eye Neoplasms / virology. Nasolacrimal Duct / pathology. Papilloma, Inverted / virology. Papillomavirus Infections / complications

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  • (PMID = 19615034.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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2. Buettner M, Greiner A, Avramidou A, Jäck HM, Niedobitek G: Evidence of abortive plasma cell differentiation in Hodgkin and Reed-Sternberg cells of classical Hodgkin lymphoma. Hematol Oncol; 2005 Sep-Dec;23(3-4):127-32
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  • [Title] Evidence of abortive plasma cell differentiation in Hodgkin and Reed-Sternberg cells of classical Hodgkin lymphoma.
  • Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL) show genotypic features of germinal centre-derived B-cells in most cases.
  • Nevertheless, these cells typically lack expression of B-cell antigens.
  • Previous studies have suggested that plasma cell differentiation may occur in HRS cells and that this may account for the down-regulation of B-cell antigens.
  • We have addressed this question using immunohistochemistry and a panel of antibodies directed against antigens which are differentially expressed during terminal B-cell differentiation.
  • Pax-5, a transcription factor required for B-lineage commitment, and IRF4/Mum1, which is physiologically expressed in germinal centre cells and plasma cells, were consistently detectable in HRS cells.
  • Bcl-6, a transcription factor expressed in germinal centre B-cells, was present in HRS cells of approximately 25% of cHL cases.
  • Expression of the B-lymphocyte-induced maturation protein-1 (Blimp-1), a key regulator of plasma cell differentiation, was observed in HRS cells of 23% of cHL cases.
  • In these cases, Blimp-1 expression was restricted to a small proportion of HRS cells.
  • HRS cells were consistently negative for the plasma cell marker CD138.
  • These results suggest that plasma cell differentiation may be initiated in a small subset of HRS cells but remains abortive.
  • Thus, terminal differentiation is unlikely to explain the lack of B-cell antigen expression in HRS cells.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Gene Expression Regulation, Leukemic. Hodgkin Disease / metabolism. Neoplasm Proteins / biosynthesis. Plasma Cells / metabolism. Reed-Sternberg Cells / metabolism. Transcription Factors / biosynthesis

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  • [Copyright] 2005 John Wiley & Sons, Ltd.
  • (PMID = 16342298.001).
  • [ISSN] 0278-0232
  • [Journal-full-title] Hematological oncology
  • [ISO-abbreviation] Hematol Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Membrane Glycoproteins; 0 / Neoplasm Proteins; 0 / Proteoglycans; 0 / SDC1 protein, human; 0 / Syndecan-1; 0 / Syndecans; 0 / Transcription Factors
  • [Number-of-references] 28
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3. Wong VK, Chiu P, Chung SS, Chow LM, Zhao YZ, Yang BB, Ko BC: Pseudolaric acid B, a novel microtubule-destabilizing agent that circumvents multidrug resistance phenotype and exhibits antitumor activity in vivo. Clin Cancer Res; 2005 Aug 15;11(16):6002-11
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  • EXPERIMENTAL DESIGN: The effect of PAB on cell growth inhibition toward a panel of cancer cell lines was assayed.
  • Cell cycle analysis, Western blotting, immunocytochemistry, and apoptosis analysis were carried out to examine the mechanism of action.
  • A P-glycoprotein-overexpressing cell line was used to evaluate the efficacy of PAB toward multidrug-resistant phenotypes.
  • RESULTS: PAB induces cell cycle arrest at G2-M transition, leading to apoptosis.
  • Furthermore, PAB circumvents the multidrug resistance mechanism, displaying notable potency also in P-glycoprotein-overexpressing cells.
  • [MeSH-major] Diterpenes / pharmacology. Drug Resistance, Multiple / drug effects. Drug Resistance, Neoplasm / drug effects. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Antineoplastic Agents / chemistry. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Apoptosis / drug effects. Binding Sites. Binding, Competitive / drug effects. Blotting, Western. Cell Cycle Proteins / metabolism. Cell Division / drug effects. Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Colchicine / pharmacology. Dose-Response Relationship, Drug. Drugs, Chinese Herbal. G2 Phase / drug effects. HeLa Cells. Humans. Liver Neoplasms / drug therapy. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Microscopy, Fluorescence. Microtubules / metabolism. Molecular Structure. Time Factors. Treatment Outcome. Tubulin / metabolism

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  • (PMID = 16115945.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / Diterpenes; 0 / Drugs, Chinese Herbal; 0 / Tubulin; 82508-31-4 / pseudolaric acid B; SML2Y3J35T / Colchicine
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4. Arepalli SK, Sridhar V, Venkateswara Rao J, Kavin Kennady P, Venkateswarlu Y: Furano-sesquiterpene from soft coral, Sinularia kavarittiensis: induces apoptosis via the mitochondrial-mediated caspase-dependent pathway in THP-1, leukemia cell line. Apoptosis; 2009 May;14(5):729-40
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  • [Title] Furano-sesquiterpene from soft coral, Sinularia kavarittiensis: induces apoptosis via the mitochondrial-mediated caspase-dependent pathway in THP-1, leukemia cell line.
  • The results show that MDTFC could efficiently and selectively inhibit the proliferation of several human cancer cell lines.
  • Among all the cell lines, THP-1 was found to be most sensitive (IC(50) 29.59 microM), whereas the peripheral blood mononuclear cells were least effected (IC(50) 464.16 microM).
  • Induction of apoptosis in THP-1 cells was characterized by cell membrane blebbing, chromatin condensation, DNA fragmentation, and decrease in level of pro-caspases 3, 9 and increase in Bax/Bcl-2 ratio.
  • Moreover, phosphatidyl serine exposure and appearance of sub-G1 peak also demonstrated cell death, when analyzed by flow cytometry.
  • In summary, MDTFC mediated apoptosis involves mitochondria-dependent pathway and the present compound of marine origin might have a therapeutic value against human cancer cell lines and especially on leukemia cells.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Shape / drug effects. Colorimetry. DNA Fragmentation / drug effects. Drug Screening Assays, Antitumor. Flow Cytometry. Humans. Membrane Potential, Mitochondrial / drug effects. Neoplasm Proteins / metabolism. Propidium / metabolism

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  • (PMID = 19283488.001).
  • [ISSN] 1573-675X
  • [Journal-full-title] Apoptosis : an international journal on programmed cell death
  • [ISO-abbreviation] Apoptosis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / Sesquiterpenes; 36015-30-2 / Propidium; EC 3.4.22.- / Caspases
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5. Oh SY, Kim WS, Lee DH, Kim SJ, Kim SH, Ryoo BY, Kang HJ, Choi YJ, Chung JS, Kim HJ, Suh C: Phase II study of gemcitabine for treatment of patients with advanced stage marginal zone B-cell lymphoma: Consortium for Improving Survival of Lymphoma (CISL) trial. Invest New Drugs; 2010 Apr;28(2):171-7
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  • [Title] Phase II study of gemcitabine for treatment of patients with advanced stage marginal zone B-cell lymphoma: Consortium for Improving Survival of Lymphoma (CISL) trial.
  • BACKGROUND: Therapeutic approaches to marginal zone B-cell lymphoma (MZL) continue to evolve.
  • However, MZL manifests as a disseminated disease in one-third of the cases at diagnosis.
  • The treatment was repeated every 3 weeks and continued for 6 cycles until disease progression, withdrawal due to toxicity, or withdrawal of consent.
  • Non-hematologic toxicities were mild and tolerable.
  • CONCLUSION: Gemcitabine as a single agent, in this dosage and at this schedule, evidenced minimal clinical activity in cases of advanced MZL.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Cooperative Behavior. Deoxycytidine / analogs & derivatives. Lymphoma, B-Cell, Marginal Zone / drug therapy. Lymphoma, B-Cell, Marginal Zone / pathology
  • [MeSH-minor] Adult. Aged. Disease Progression. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Neoplasm Staging. Recurrence. Survival Analysis. Time Factors. Treatment Outcome

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  • (PMID = 19421710.001).
  • [ISSN] 1573-0646
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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6. Bidoli P, Zilembo N, Cortinovis D, Mariani L, Isa L, Aitini E, Cullurà D, Pari F, Nova P, Mancin M, Formisano B, Bajetta E: Randomized phase II three-arm trial with three platinum-based doublets in metastatic non-small-cell lung cancer. An Italian Trials in Medical Oncology study. Ann Oncol; 2007 Mar;18(3):461-7
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  • [Title] Randomized phase II three-arm trial with three platinum-based doublets in metastatic non-small-cell lung cancer. An Italian Trials in Medical Oncology study.
  • BACKGROUND: Many patients with advanced non-small-cell lung cancer (NSCLC) do not tolerate cisplatin-based regimens because of its nonhemathological toxicity.

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  • (PMID = 17110590.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 0 / Taxoids; 04ZR38536J / oxaliplatin; 0W860991D6 / Deoxycytidine; 15H5577CQD / docetaxel; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin
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7. Sher YP, Chou CC, Chou RH, Wu HM, Wayne Chang WS, Chen CH, Yang PC, Wu CW, Yu CL, Peck K: Human kallikrein 8 protease confers a favorable clinical outcome in non-small cell lung cancer by suppressing tumor cell invasiveness. Cancer Res; 2006 Dec 15;66(24):11763-70
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  • [Title] Human kallikrein 8 protease confers a favorable clinical outcome in non-small cell lung cancer by suppressing tumor cell invasiveness.
  • We found that overexpressing the KLK8 gene in highly invasive lung cancer cell lines suppresses their invasiveness.
  • This role in invasiveness was further confirmed by the fact that inhibition of endogenous KLK8 expression with a specific short hairpin RNA reduced cancer cell invasiveness.
  • In situ degradation and cell adhesion assays showed that proteins produced from KLK8 splice variants modify the extracellular microenvironment by cleaving fibronectin.
  • DNA microarray experiments and staining of cells for actin filaments revealed that the degradation of fibronectin by hK8 suppresses integrin signaling and retards cancer cell motility by inhibiting actin polymerization.
  • In addition, studies in a mouse model coupled with the detection of circulating tumor cells by quantitative PCR for the human Alu sequence showed that KLK8 suppresses tumor growth and invasion in vivo.
  • Finally, studies of clinical specimens from patients with non-small cell lung cancer showed that the time to postoperative recurrence was longer for early-stage patients (stages I and II) with high KLK8 expression (mean, 49.9 months) than for patients with low KLK8 expression (mean, 22.9 months).
  • Collectively, these findings show that KLK8 expression confers a favorable clinical outcome in non-small cell lung cancer by suppressing tumor cell invasiveness.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / pathology. Kallikreins / genetics. Kallikreins / metabolism. Lung Neoplasms / enzymology. Lung Neoplasms / pathology
  • [MeSH-minor] Base Sequence. Cell Adhesion. DNA Primers. Fibronectins / metabolism. Humans. Molecular Sequence Data. Neoplasm Invasiveness / genetics. Neoplasm Invasiveness / prevention & control. Reverse Transcriptase Polymerase Chain Reaction. Treatment Outcome

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  • (PMID = 17178872.001).
  • [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 / DNA Primers; 0 / Fibronectins; EC 3.4.21.- / KLK8 protein, human; EC 3.4.21.- / Kallikreins
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8. Gariboldi MB, Ravizza R, Molteni R, Osella D, Gabano E, Monti E: Inhibition of Stat3 increases doxorubicin sensitivity in a human metastatic breast cancer cell line. Cancer Lett; 2007 Dec 18;258(2):181-8
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  • [Title] Inhibition of Stat3 increases doxorubicin sensitivity in a human metastatic breast cancer cell line.
  • Metastatic breast cancer is an incurable disease, often characterized by poor response to standard chemotherapy, which is mainly based on anthracyclines and taxanes.
  • Thus, increasing tumor cell sensitivity to these agents is an attractive goal towards improving the clinical management of this disease.
  • The present study investigates the effects of signal transducer and activator of transcription 3 (Stat3) inhibition on the response of the highly metastatic MDA-MB-231 human breast adenocarcinoma cell line to doxorubicin (DOX).
  • Stat3 is a transcription factor often constitutively activated in breast tumors and cancer cell lines, and is thought to contribute to malignant transformation and progression by transactivation of a host of target genes involved in cell proliferation and survival, angiogenesis and invasiveness.
  • Our results indicate that (a) untreated MDA-MB-231 cells express higher baseline levels of (activated) pTyr(705)Stat3, that are further upregulated following exposure to DOX, than the non-metastatic MCF-7 cell line;.
  • (b) inhibiting the Stat3 signaling pathway, by exposure to the tyrphostin AG490 (an inhibitor of the upstream activating Janus kinases), by transfection with a dominant-negative form of Stat3 or by treatment with satraplatin (a tetravalent platinum derivative that inhibits Stat3 activation), increases breast cancer cell response to the proapoptotic effect of DOX (to different extents).
  • Overall, these observations suggest that suppression of Stat3 signaling may provide a potential therapeutic approach to overcoming DOX resistance in metastatic breast cancer cells.
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Line, Tumor. Cell Survival / drug effects. Female. Flow Cytometry. Humans. Immunoblotting. Neoplasm Metastasis. Organoplatinum Compounds / pharmacology. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / metabolism. Transfection

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  • (PMID = 17920763.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 0 / STAT3 Transcription Factor; 0 / Tyrphostins; 0 / alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide; 80168379AG / Doxorubicin; 8D7B37T28G / satraplatin; EC 2.7.10.1 / Protein-Tyrosine Kinases
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9. Olasz L, Orsi E, Markó T, Szalma J: Induction chemotherapy response and recurrence rates in correlation with N0 or N+ stage in oral squamous cell cancer (OSCC). Cancer Metastasis Rev; 2010 Dec;29(4):607-11
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  • [Title] Induction chemotherapy response and recurrence rates in correlation with N0 or N+ stage in oral squamous cell cancer (OSCC).
  • During a 12-year period, 180 consecutive oral squamous cell cancer patients were observed.
  • [MeSH-major] Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Mouth Neoplasms / drug therapy. Mouth Neoplasms / pathology
  • [MeSH-minor] Chemotherapy, Adjuvant. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Prognosis. Remission Induction

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  • (PMID = 20842409.001).
  • [ISSN] 1573-7233
  • [Journal-full-title] Cancer metastasis reviews
  • [ISO-abbreviation] Cancer Metastasis Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
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10. Ivanov V, Tabouret E, Chuto G, Chetaille B, Fezoui H, Coso D, Rey J, Aurran-Schleinitz T, Schiano JM, Stoppa AM, Blaise D, Bouabdallah R: Rituximab-lenalidomide-dexamethasone induces complete and durable remission in relapsed refractory diffuse large B-cell non-Hodgkin lymphoma. Leuk Lymphoma; 2010 Sep;51(9):1758-60
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  • [Title] Rituximab-lenalidomide-dexamethasone induces complete and durable remission in relapsed refractory diffuse large B-cell non-Hodgkin lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Resistance, Neoplasm / drug effects. Lymphoma, Large B-Cell, Diffuse / drug therapy. Neoplasm Recurrence, Local / drug therapy. Salvage Therapy

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  • (PMID = 20629527.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 4Z8R6ORS6L / Thalidomide; 7S5I7G3JQL / Dexamethasone; F0P408N6V4 / lenalidomide
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11. Khan AA, Shergill IS, Hamid R, Gujral SS: Giant nonfunctioning carcinoma of the adrenal cortex mimicking renal cell carcinoma: a diagnostic dilemma. Urology; 2007 Jul;70(1):178.e1-2
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  • [Title] Giant nonfunctioning carcinoma of the adrenal cortex mimicking renal cell carcinoma: a diagnostic dilemma.
  • Adrenocortical carcinoma is a rare, highly malignant neoplasm that originates in the adrenal cortex and is difficult to differentiate from renal cell carcinoma, especially if it is gigantic and nonfunctional.
  • Magnetic resonance imaging revealed that the mass originated from the right kidney and was highly suggestive of renal cell carcinoma.
  • We discuss the obscurity and implications of such a diagnosis.
  • [MeSH-major] Adrenal Cortex Neoplasms / diagnosis. Adrenocortical Carcinoma / diagnosis. Carcinoma, Renal Cell / diagnosis. Diagnostic Errors. Kidney Neoplasms / diagnosis
  • [MeSH-minor] Adult. Diagnosis, Differential. Humans. Male

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  • (PMID = 17656234.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 9
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12. Fúnez R, Pereda T, Rodrigo I, Robles L, González C: Simultaneous chromophobe renal cell carcinoma and squamous renal cell carcinoma. Diagn Pathol; 2007;2:30
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  • [Title] Simultaneous chromophobe renal cell carcinoma and squamous renal cell carcinoma.
  • Chromophobe renal cell carcinoma (CHRC) is a neoplasm of the kidney with clinicopathologic peculiarities that seems to be of better prognosis than conventional renal cell carcinoma.
  • Also, it has been described in association with carcinoma of collecting ducts, conventional renal cell carcinoma and sarcomatoid renal cell carcinoma.
  • Squamous renal carcinoma is a very rare neoplasm with a malignant course.
  • We describe a case of simultaneous chromophobe renal cell carcinoma with squamous cell carcinoma, finding which, to the best of our knowledge, has not previously been reported.

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  • [Cites] Ann Diagn Pathol. 2002 Aug;6(4):244-7 [12170456.001]
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  • (PMID = 17711572.001).
  • [ISSN] 1746-1596
  • [Journal-full-title] Diagnostic pathology
  • [ISO-abbreviation] Diagn Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2045079
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13. Montella L, Caraglia M, Addeo R, Costanzo R, Faiola V, Abbruzzese A, Del Prete S: Atrial fibrillation following chemotherapy for stage IIIE diffuse large B-cell gastric lymphoma in a patient with myotonic dystrophy (Steinert's disease). Ann Hematol; 2005 Mar;84(3):192-3
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  • [Title] Atrial fibrillation following chemotherapy for stage IIIE diffuse large B-cell gastric lymphoma in a patient with myotonic dystrophy (Steinert's disease).
  • The authors describe the unusual association between diffuse B-cell gastric lymphoma and myotonic dystrophy, the most common form of adult muscular dystrophy, and sudden atrial fibrillation following one cycle of doxorubicin-based chemotherapy in the same patient.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Atrial Fibrillation / chemically induced. Lymphoma, Large B-Cell, Diffuse / complications. Myotonic Dystrophy / complications. Stomach Neoplasms / complications
  • [MeSH-minor] Doxorubicin / adverse effects. Humans. Lymphoma, B-Cell / complications. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / pathology. Male. Middle Aged. Neoplasm Staging


14. Plaza JA, Wakely PE Jr, Suster S: Lipoblastic nerve sheath tumors: report of a distinctive variant of neural soft tissue neoplasm with adipocytic differentiation. Am J Surg Pathol; 2006 Mar;30(3):337-44
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  • [Title] Lipoblastic nerve sheath tumors: report of a distinctive variant of neural soft tissue neoplasm with adipocytic differentiation.
  • Benign nerve sheath tumors of soft tissue can occasionally adopt unusual or unfamiliar morphologic appearances that may introduce difficulties for diagnosis, such as multinucleation, bizarre nuclei, intranuclear vacuoles, and other degenerative changes.
  • Tumor cells adopting a signet-ring or lipoblast-like configuration, however, are mostly associated with epithelial malignancies, liposarcoma and melanoma, and have been only rarely observed in spindle cell tumors of soft tissue.
  • We report 5 cases of benign nerve sheath neoplasms that displayed prominent signet-ring cells with lipoblast-like features.
  • Four tumors predominantly showed features of schwannoma and one of neurofibroma; however, intimately admixed with the spindle cell population, there were also numerous scattered mature adipocytes as well as lipoblast-like cells displaying a signet-ring cell appearance.
  • Immunohistochemical studies showed strong S-100 protein positivity in the spindle cells as well as in the signet-ring lipoblast-like cells and the mature adipocytes.
  • The signet-ring cells were negative for mucin stains, cytokeratin, EMA, CEA, and several other differentiation markers.
  • The signet-ring cells contained large cytoplasmic lipid droplets that displaced the nuclei to the periphery, consistent with lipoblastic differentiation, whereas complex, interdigitating cytoplasmic processes covered by basal lamina material characteristic of nerve sheath differentiation could be identified in the spindle cells.
  • The presence of mature fat and signet-ring lipoblast-like cells within a nerve sheath neoplasm is quite rare and may signify a process of aberrant differentiation.
  • Neurogenic tumors should be added in the differential diagnosis of spindle cell tumors capable of displaying prominent signet-ring cell features.
  • [MeSH-minor] Adenocarcinoma / pathology. Adult. Carcinoma, Signet Ring Cell / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Male. Microscopy, Electron, Transmission. Middle Aged

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  • (PMID = 16538053.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Lu RZ, Qiu L, Wang XD, Li XF, Chen LJ, Wang XL, Zhang BL, Ma J: [Arsenic trioxide inhibits cell growth in imatinib-resistant bcr-abl mutant cell lines in vitro]. Zhonghua Xue Ye Xue Za Zhi; 2009 Jan;30(1):13-7
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  • [Title] [Arsenic trioxide inhibits cell growth in imatinib-resistant bcr-abl mutant cell lines in vitro].
  • OBJECTIVE: To explore the effect of arsenic trioxide (As2O3) on the growth inhibition of imatinib (IM)-resistant bcr-abl mutant cell lines in vitro.
  • METHODS: Cell growth of one IM-sensitive cell line, 32Dp210 and 15 IM-resistant cell lines including T315I and other 14 bcr-abl mutants were detected by MTT assay after treatment with IM and As2O3.
  • The cell lines with 5 frequently observed mutants in CML patients were analyzed for apoptosis by flow cytometry with Annexin V and PI staining as well as the expression of bcr-abl fusion protein, phosphorylated CRKL protein and apoptosis-related proteins by Western blot.
  • RESULTS: The fifty percent inhibition concentration (IC50) values of As2O3 for 15 IM-resistant cell lines were 2.6-5.3 fold lower than that for IM-sensitive cell line.
  • Coincidently, the cell apoptosis was induced through caspase-3, 8 and 9 pathways.
  • CONCLUSION: As2O3 remarkably inhibits cell growth and induces apoptosis of IM-resistant bcr-abl mutant cell lines in vitro, suggesting that it might be a potential therapeutic agent for IM-resistant CML patients.
  • [MeSH-major] Apoptosis / drug effects. Arsenicals / pharmacology. Cell Proliferation / drug effects. Fusion Proteins, bcr-abl / genetics. Oxides / pharmacology. Piperazines / pharmacology. Pyrimidines / pharmacology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / metabolism. Benzamides. Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Mutation. Nuclear Proteins / metabolism

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  • (PMID = 19563028.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Arsenicals; 0 / Benzamides; 0 / CRKL protein; 0 / Nuclear Proteins; 0 / Oxides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl; S7V92P67HO / arsenic trioxide
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16. Sagulenko V, Muth D, Sagulenko E, Paffhausen T, Schwab M, Westermann F: Cathepsin D protects human neuroblastoma cells from doxorubicin-induced cell death. Carcinogenesis; 2008 Oct;29(10):1869-77
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  • [Title] Cathepsin D protects human neuroblastoma cells from doxorubicin-induced cell death.
  • We have reported previously that ectopic MYCN expression promotes proliferation of neuroblastoma Tet21N cells and simultaneously sensitizes them to the drug-induced apoptosis.
  • Downregulation of cathepsin D expression by RNA interference or inhibition of its enzymatic activity increased sensitivity of MYCN-expressing Tet21N cells to doxorubicin.
  • Overexpression of cathepsin D in Tet21N cells attenuated doxorubicin-induced apoptosis.
  • It was accompanied by activation of protein kinase B (Akt) and persistent antiapoptotic activity of Bcl-2.
  • We further show that neuroblastoma cells can secrete mitogenic procathepsin D and that MYCN expression and especially doxorubicin treatment promote procathepsin D secretion.
  • Extracellular exogenous cathepsin D induces Akt-1 phosphorylation and doxorubicin resistance in sensitive cells.
  • These results demonstrate an important role of cathepsin D in antiapoptotic signaling in neuroblastoma cells and suggest a novel mechanism for the development of chemotherapy resistance in neuroblastoma.
  • [MeSH-minor] Apoptosis Regulatory Proteins / physiology. Cell Line, Tumor. Drug Resistance, Neoplasm. Enzyme Precursors / secretion. Humans. Nuclear Proteins / genetics. Oncogene Proteins / genetics. Phosphatidylinositol 3-Kinases / physiology. Proto-Oncogene Proteins c-akt / physiology. Ribosomal Proteins / physiology. Signal Transduction

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  • (PMID = 18566016.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Apoptosis Regulatory Proteins; 0 / DAP3 protein, human; 0 / Enzyme Precursors; 0 / MYCN protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins; 0 / Ribosomal Proteins; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.23.- / procathepsin D; EC 3.4.23.5 / Cathepsin D
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17. Ozawa S, Kato Y, Kubota E, Hata R: BRAK/CXCL14 expression in oral carcinoma cells completely suppresses tumor cell xenografts in SCID mouse. Biomed Res; 2009 Oct;30(5):315-8
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  • [Title] BRAK/CXCL14 expression in oral carcinoma cells completely suppresses tumor cell xenografts in SCID mouse.
  • SCID mice are a model of human severe combined immunodeficiency disease and are deficient in B cell function in addition to T cell function.
  • We previously reported that the chemokine BRAK/CXCL14 is expressed in normal cells but its expression is down regulated in an in vitro cancer progression model, suggesting that it has the potential for antitumor activity.
  • Here we report that the growth of BRAK/CXCL14 expression vector-transfected oral cancer cells was completely (100%) suppressed in SCID mouse xenografts even though mock-vector introduced control tumor cells grew well with 100% of animals developing tumors.
  • In addition, suppression of xenografts was much faster and the rate was much higher in SCID mice than in T cell function-deficient nude mice.
  • These data indicate the possibility that BRAK expression inhibits tumor cell establishment by regulating interactions between tumor stem cells and NK cells and/or suppressing formation of tumor microvessels.
  • [MeSH-minor] Animals. Female. Humans. Mice. Mice, Nude / immunology. Neoplasm Transplantation

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  • (PMID = 19887729.001).
  • [ISSN] 1880-313X
  • [Journal-full-title] Biomedical research (Tokyo, Japan)
  • [ISO-abbreviation] Biomed. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CXCL14 protein, mouse; 0 / Chemokines, CXC
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18. Huynh E, Sigal D, Saven A: Cladribine in the treatment of hairy cell leukemia: initial and subsequent results. Leuk Lymphoma; 2009 Oct;50 Suppl 1:12-7
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  • [Title] Cladribine in the treatment of hairy cell leukemia: initial and subsequent results.
  • Hairy cell leukemia (HCL) is a chronic B-cell lymphoproliferative disorder associated with pancytopenia, splenomegaly, and recurrent infections.
  • Although interferon alpha and pentostatin were initially found to be effective in this disease, cladribine has emerged as the preferred initial therapy.
  • Although both complications are postulated to be related to therapy, they may also be due to the duration and burden of the disease.
  • Minimal residual disease detected on bone marrow biopsy is thought to predict for future relapse.
  • [MeSH-major] Cladribine / therapeutic use. Leukemia, Hairy Cell / drug therapy
  • [MeSH-minor] Algorithms. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. Models, Biological. Neoplasm, Residual. Purines / therapeutic use

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  • (PMID = 19814692.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Purines; 47M74X9YT5 / Cladribine
  • [Number-of-references] 27
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19. Véronèse L, Tournilhac O, Verrelle P, Davi F, Dighiero G, Chautard E, Veyrat-Masson R, Kwiatkowski F, Goumy C, Vago P, Travade P, Tchirkov A: Low MCL-1 mRNA expression correlates with prolonged survival in B-cell chronic lymphocytic leukemia. Leukemia; 2008 Jun;22(6):1291-3
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  • [Title] Low MCL-1 mRNA expression correlates with prolonged survival in B-cell chronic lymphocytic leukemia.
  • [MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / mortality. Neoplasm Proteins / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / genetics
  • [MeSH-minor] Cohort Studies. Flow Cytometry. Humans. Lymphocyte Subsets. Myeloid Cell Leukemia Sequence 1 Protein. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction. Survival Rate. Time Factors

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  • (PMID = 18046444.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger
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20. Sun W, McGregor DK, Ordonez NG, Ayala AG, Caraway NP: Fine needle aspiration cytology of a low grade myxoid renal epithelial neoplasm: a case report. Acta Cytol; 2005 Sep-Oct;49(5):525-9
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  • [Title] Fine needle aspiration cytology of a low grade myxoid renal epithelial neoplasm: a case report.
  • BACKGROUND: Recently, several case reports have described a rare but distinct subtype of renal tumor, referred to as a "low grade renal epithelial neoplasm," that appears to have a better prognosis than conventional renal cell carcinoma does.
  • CASE: A 53-year-old woman with a history of lymphoma had a renal mass incidentally discovered on an abdominal computed tomographic scan performed for lymphoma restaging.
  • Results of an FNA biopsy showed relatively uniform, medium-sized tumor cells with moderate amounts of finely vacuolated or wispy cytoplasm and indistinct cell borders.
  • In the cell block preparation, the tumor cells showed a tubular architecture and an abundant myxoid matrix.
  • CONCLUSION: This unusual kidney tumor appears to have distinctive cytomorphologic features, including a uniform population of epithelial cells with round nuclei, an abundant myxoid matrix and tubular architecture.
  • [MeSH-major] Carcinoma / pathology. Epithelial Cells / pathology. Kidney / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Antigens, CD15 / metabolism. Biopsy, Fine-Needle. Cell Nucleus / pathology. Cell Nucleus / ultrastructure. Female. Humans. Keratins / metabolism. Microscopy, Electron, Transmission. Microvilli / pathology. Microvilli / ultrastructure. Middle Aged. Nephrectomy. Prognosis. Tomography, X-Ray Computed. Vimentin / metabolism

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  • (PMID = 16334030.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD15; 0 / Vimentin; 68238-35-7 / Keratins
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21. Ribera JM, Oriol A, Morgades M, González-Barca E, Miralles P, López-Guillermo A, Gardella S, López A, Abella E, García M, PETHEMA, GELTAMO, GELCAB and GESIDA Groups: Safety and efficacy of cyclophosphamide, adriamycin, vincristine, prednisone and rituximab in patients with human immunodeficiency virus-associated diffuse large B-cell lymphoma: results of a phase II trial. Br J Haematol; 2008 Feb;140(4):411-9
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  • [Title] Safety and efficacy of cyclophosphamide, adriamycin, vincristine, prednisone and rituximab in patients with human immunodeficiency virus-associated diffuse large B-cell lymphoma: results of a phase II trial.
  • Immunochemotherapy with cyclophosphamide, adriamycin, vincristine, prednisone and rituximab (R-CHOP) is the standard treatment in non-immunosuppressed patients with diffuse large B-cell lymphoma (DLBCL), but its adequacy has not been definitively established in patients with human immunodeficiency virus (HIV)-related lymphoma.
  • Complete response was achieved in 55 (69%) patients, with an estimated 3-year disease-free survival of 77% and 3-year overall survival of 56%.
  • The prognosis depends on lymphoma-related parameters and on the response to HAART.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Lymphoma, AIDS-Related / drug therapy. Lymphoma, Large B-Cell, Diffuse / drug therapy
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / adverse effects. Antibodies, Monoclonal, Murine-Derived. Antiretroviral Therapy, Highly Active. CD4 Lymphocyte Count. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prednisone / administration & dosage. Prednisone / adverse effects. Prognosis. Rituximab. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage. Vincristine / adverse effects. Viral Load

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  • (PMID = 18162120.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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22. Wang Z, Song W, Aboukameel A, Mohammad M, Wang G, Banerjee S, Kong D, Wang S, Sarkar FH, Mohammad RM: TW-37, a small-molecule inhibitor of Bcl-2, inhibits cell growth and invasion in pancreatic cancer. Int J Cancer; 2008 08 15;123(4):958-66
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  • [Title] TW-37, a small-molecule inhibitor of Bcl-2, inhibits cell growth and invasion in pancreatic cancer.
  • Bcl-2 family of proteins plays critical roles in human cancers, including pancreatic cancer, suggesting that the discovery of specific agents targeting Bcl-2 family proteins would be extremely valuable for pancreatic cancer therapy.
  • We have previously reported the synthesis and characterization of TW-37, which seems to be a negative regulator of Bcl-2.
  • In this investigation, we tested our hypothesis whether TW-37 could be an effective inhibitor of cell growth, invasion and angiogenesis in pancreatic cancer cells.
  • Using multiple cellular and molecular approaches such as MTT assay, apoptosis enzyme-linked immunosorbent assay, real-time reverse transcription-polymerase chain reaction, Western blotting, electrophoretic mobility shift assay for measuring DNA binding activity of NF-kappaB, migration, invasion and angiogenesis assays, we found that TW-37, in nanomolar concentrations, inhibited cell growth in a dose- and time-dependent manner.
  • This was accompanied by increased apoptosis and concomitant attenuation of NF-kappaB, and downregulation of NF-kappaB downstream genes such as MMP-9 and VEGF, resulting in the inhibition of pancreatic cancer cell migration, invasion and angiogenesis in vitro and caused antitumor activity in vivo.
  • From these results, we conclude that TW-37 is a potent inhibitor of progression of pancreatic cancer cells, which could be due to attenuation of Bcl-2 cellular signaling processes.
  • Our findings provide evidence showing that TW-37 could act as a small-molecule Bcl-2 inhibitor on well-characterized pancreatic cancer cells in culture as well as when grown as tumor in a xenograft model.
  • [MeSH-major] Benzamides / pharmacology. Pancreatic Neoplasms / drug therapy. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Sulfones / pharmacology
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Endothelial Cells / cytology. Endothelial Cells / drug effects. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. I-kappa B Kinase / biosynthesis. I-kappa B Kinase / genetics. I-kappa B Proteins / metabolism. Matrix Metalloproteinase 9 / biosynthesis. Matrix Metalloproteinase 9 / genetics. Mice. Mice, Inbred ICR. Mice, SCID. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Neoplasm Invasiveness. Neovascularization, Pathologic / drug therapy. Phosphorylation / drug effects. Transcription, Genetic. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics. Xenograft Model Antitumor Assays

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 18528859.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109389; United States / NCI NIH HHS / CA / U19CA11317; United States / NCI NIH HHS / CA / P30CA22453; United States / NCI NIH HHS / CA / 5R01CA101870; United States / NCI NIH HHS / CA / R01CA109389; United States / NCI NIH HHS / CA / P30 CA022453; United States / NCI NIH HHS / CA / R01 CA101870
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Retracted Publication
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / I kappa B beta protein; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Sulfones; 0 / TW-37 compound; 0 / Vascular Endothelial Growth Factor A; EC 2.7.11.10 / I-kappa B Kinase; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ NIHMS511242; NLM/ PMC3766317
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23. Minchin RF, Knight S, Arulpragasam A, Fogel-Petrovic M: Concentration-dependent effects of N1, N11-diethylnorspermine on melanoma cell proliferation. Int J Cancer; 2006 Jan 15;118(2):509-12
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  • [Title] Concentration-dependent effects of N1, N11-diethylnorspermine on melanoma cell proliferation.
  • During our studies into the causes of this variation, we observed a consistent increase in cell proliferation at low drug concentrations (<10 microM) in human melanoma cells resistant to the drug.
  • At higher concentrations, growth inhibition was seen in all cell lines, with IC50 values ranging 2-180 microM.
  • We hypothesized that DENSPM may mimic endogenous polyamines at low concentrations, supporting cell growth in resistant lines.
  • We also observed that DENSPM downregulated polyamine transport in a manner similar to that for spermidine, a finding that confirms previous reports.
  • Finally, DENSPM could rescue cells from growth arrest by the ornithine decarboxylase inhibitor difluoromethylornithine, which depletes intracellular polyamines.
  • Taken together, these results suggest that DENSPM, at clinically relevant concentrations, can mimic endogenous polyamines and induce proliferation in resistant human melanoma cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Proliferation / drug effects. Melanoma / pathology. Skin Neoplasms / pathology. Spermine / analogs & derivatives
  • [MeSH-minor] Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Humans. Ornithine Decarboxylase / metabolism. Ornithine Decarboxylase Inhibitors. Polyamines. Tumor Cells, Cultured

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  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • (PMID = 16052528.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ornithine Decarboxylase Inhibitors; 0 / Polyamines; 121749-39-1 / N(1),N(11)-diethylnorspermine; 2FZ7Y3VOQX / Spermine; EC 4.1.1.17 / Ornithine Decarboxylase
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24. Corapçioglu F, Basar EZ, Demirel A, Inan N, Babaoğlu K, Karakurt H, Kus E, Aksu G: Granulomatous reaction in mediastinal B-cell non-Hodgkin lymphoma and intracardiac thrombosis. Pediatr Hematol Oncol; 2008 Apr-May;25(3):217-26
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  • [Title] Granulomatous reaction in mediastinal B-cell non-Hodgkin lymphoma and intracardiac thrombosis.
  • Epithelioid cell granulomas may be associated with several neoplasms.
  • Lymphomas may mimic or are associated with epithelioid granulomas.
  • In this article the authors report a child with granulomatous reaction in B cell non-Hodgkin lymphoma and intracardiac thrombosis.
  • Although cancer alone is a risk factor for thromboembolism, thrombosis is a multifactorial disorder with both hereditary and acquired risk factors.
  • This is the first reported case of intracardiac thrombosis with MTHFR A1298C and factor XIII V34L mutations together with granulomatous reaction in non-Hodgkin lymphoma.
  • [MeSH-major] Granuloma / complications. Heart Diseases / etiology. Lymphoma, B-Cell / complications. Mediastinal Neoplasms / complications. Thrombosis / etiology


25. Landriscina M, Altamura SA, Roca L, Gigante M, Piscazzi A, Cavalcanti E, Costantino E, Barone C, Cignarelli M, Gesualdo L, Ranieri E: Reverse transcriptase inhibitors induce cell differentiation and enhance the immunogenic phenotype in human renal clear-cell carcinoma. Int J Cancer; 2008 Jun 15;122(12):2842-50
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  • [Title] Reverse transcriptase inhibitors induce cell differentiation and enhance the immunogenic phenotype in human renal clear-cell carcinoma.
  • Reverse transcriptase (RT) inhibitors are emerging as a novel class of anticancer differentiating agents, active in several human tumor cell models, such as melanoma and prostate, thyroid and colon carcinoma.
  • Indeed, much evidence suggests that they may act by inhibiting endogenous RT, a gene highly expressed in undifferentiated and transformed cells.
  • We therefore evaluated whether endogenous RT may represent a new molecular target in the treatment of human renal clear-cell carcinoma, a neoplasm with very low sensitivity to standard pharmacological therapies.
  • Efavirenz and nevirapine, 2 non-nucleosidic RT inhibitors commonly used in HIV patients, either induced a reversible downregulation of cell proliferation or enhanced cell differentiation in primary cultures of human renal carcinoma cells characterized by high levels of endogenous RT activity.
  • Both agents upregulated the expression of the vitamin D receptor and calbindin 28k genes, which are constitutively expressed in renal tubular cells, and induced vitamin D signaling by enhancing the ability of tumor cells to upregulate the vitamin D-dependent gene, CYP24.
  • Furthermore, efavirenz- and nevirapine-differentiated tumor cells exhibited an immunogenic phenotype with an increased expression of HLA-I and CD40 antigens and an enhanced ability to elicit a specific T-cell response in mixed lymphocyte/tumor-cell cultures.
  • Indeed, renal carcinoma cells exposed to efavirenz induced a CD8(+)CCR7-CD45RA(-) effector memory T-cell phenotype, whereas untreated RCC cells induced a CD8(+)CCR7(+)CD45RA(-) central memory T-cell phenotype.
  • These data suggest that RT inhibitors may be a novel tool in the treatment of human renal clear-cell carcinoma, potentially able to enhance the immunogenic potential of tumor cell.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. Kidney Neoplasms / pathology. Reverse Transcriptase Inhibitors / pharmacology
  • [MeSH-minor] Cell Line, Tumor. DNA Primers. Fluorescent Antibody Technique, Indirect. Humans. Microscopy, Confocal. Phenotype. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18351578.001).
  • [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 / Antineoplastic Agents; 0 / DNA Primers; 0 / Reverse Transcriptase Inhibitors
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26. Sim HG, Lange PH, Lin DW: Role of post-chemotherapy surgery in germ cell tumors. Urol Clin North Am; 2007 May;34(2):199-217; abstract ix
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  • [Title] Role of post-chemotherapy surgery in germ cell tumors.
  • The clinical outcome is strongly influenced by patient selection and extent of extirpative surgery.
  • Although extensive predictive modeling has attempted to define appropriate post-chemotherapy surgical candidates based on various clinical and pathologic parameters, the accuracy of these models remains controversial.
  • Complete removal of all post-chemotherapy residual masses in nonseminomatous germ cell tumors remains the standard of care and allows for improved prognostication of the long-term oncologic and functional outcome.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasms, Germ Cell and Embryonal. Testicular Neoplasms
  • [MeSH-minor] Chemotherapy, Adjuvant. Clinical Trials as Topic. Drug Therapy, Combination. Humans. Male. Neoplasm Staging. Treatment Outcome

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  • (PMID = 17484925.001).
  • [ISSN] 0094-0143
  • [Journal-full-title] The Urologic clinics of North America
  • [ISO-abbreviation] Urol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 95
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27. Yu JB, Zuo Z, Tang Y, Zhao S, Zhang YC, Bi CF, Wang WY, Zhang WY, Wang L, Liu WP: Extranodal nasal-type natural killer/T-cell lymphoma of the skin: a clinicopathologic study of 16 cases in China. Hum Pathol; 2009 Jun;40(6):807-16
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extranodal nasal-type natural killer/T-cell lymphoma of the skin: a clinicopathologic study of 16 cases in China.
  • Extranodal nasal-type natural killer/T-cell lymphoma presenting in skin, either primary or secondary, is relatively rare in China, accounting for about 4.1% of tumors.
  • The clinicopathologic features of the neoplasm are still poorly understood.
  • Sixteen Chinese cases of cutaneous natural killer/T-cell lymphomas were investigated retrospectively by pathology, immunophenotype, genotype, Epstein-Barr virus status, and survival analysis.
  • The neoplastic cells of all 16 cases were positive for CD3varepsilon/CD45RO and granzyme B and negative for CD4, CD5, CD8, and CD20; 87.5% of the tumors expressed CD56.
  • Thirteen of 15 patients received chemotherapy; a partial response was achieved in 10 patients; 10 (66.7%) of 15 patients died of the disease, and the average survival time was 6.6 months.
  • In conclusion, both primary and secondary cutaneous natural killer/T-cell lymphomas are highly aggressive.
  • [MeSH-major] Lymphoma, T-Cell / pathology. Nose / pathology. Nose Neoplasms / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. China / epidemiology. Female. Humans. Killer Cells, Natural / pathology. Male. Middle Aged. Retrospective Studies

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  • (PMID = 19200574.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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28. Jain R, Gramigna V, Sanchez-Marull R, Perez-Ordoñez B: Composite intestinal-type adenocarcinoma and small cell carcinoma of sinonasal tract. J Clin Pathol; 2009 Jul;62(7):634-7
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  • [Title] Composite intestinal-type adenocarcinoma and small cell carcinoma of sinonasal tract.
  • BACKGROUND AND AIMS: Sinonasal intestinal-type adenocarcinomas (ITACs) are rare neoplasms resembling intestinal adenocarcinomas.
  • Although several studies have documented neuroendocrine differentiation in ITACs, the combination of ITAC and small cell carcinoma has not been previously described in detail.
  • The aim of this report is to detail the histopathological and immunohistochemical characteristics of two cases of composite ITAC with small cell carcinoma.
  • METHODS: Two cases of composite ITAC with small cell carcinoma were routinely processed, and representative sections were stained with CAM5.2, AE1:AE3, keratin 7, keratin 20, keratin 19, CDX-2, p63, villin, chromogranin, synaptophysin and CD56.
  • RESULTS: One tumour consisted of a mixed-type ITAC showing colonic-type and poorly differentiated adenocarcinoma with foci of "signet-ring" cells combined with small cell carcinoma.
  • Both components stained positively with CAM5.2, AE1:AE3, CK7, CK20 and CK19, whereas only the small cell carcinoma expressed synaptophysin and CD56.
  • The "signet-ring" cells stained positively with chromogranin and synaptophysin.
  • The second tumour showed a papillary-type ITAC combined with a small cell carcinoma.
  • The adenocarcinoma and small cell carcinoma stained positively with CAM5.2, AE1:AE3, CK7, CK19 and CK20.
  • Only the adenocarcinoma was CDX-2 positive, whereas the small cell carcinoma expressed CD56 and synaptophysin.
  • CONCLUSIONS: The two components of the combined ITACs and neuroendocrine small cell carcinoma show significant immunohistochemical overlap, supporting a common origin.
  • [MeSH-major] Adenocarcinoma, Papillary / pathology. Carcinoma, Small Cell / pathology. Neoplasms, Multiple Primary / pathology. Paranasal Sinus Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / metabolism. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism

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  • (PMID = 19321468.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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29. Liu Y, Dai B, Fu L, Jia J, Mei C: Rosiglitazone inhibits cell proliferation by inducing G1 cell cycle arrest and apoptosis in ADPKD cyst-lining epithelia cells. Basic Clin Pharmacol Toxicol; 2010 Jun;106(6):523-30
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  • [Title] Rosiglitazone inhibits cell proliferation by inducing G1 cell cycle arrest and apoptosis in ADPKD cyst-lining epithelia cells.
  • Abnormal proliferation is an important pathological feature of autosomal dominant polycystic kidney disease (ADPKD).
  • Many drugs inhibiting cell proliferation have been proved to be effective in slowing the disease progression in ADPKD.
  • Recent evidence has suggested that peroxisome proliferator-activated receptor gamma (PPARgamma) ligands have anti-neoplasm effects through inhibiting cell growth and inducing cell apoptosis in various cancer cells.
  • In the present study, we examined the expression of PPARgamma in human ADPKD kidney tissues and cyst-lining epithelial cell line, and found that the expression of PPARgamma was greater in ADPKD kidney tissues and cyst-lining epithelial cell line than in normal kidney tissues and human kidney cortex (HKC) cell line.
  • Rosiglitazone inhibited significantly proliferation of cyst-lining epithelial cells in a concentration- and time-dependent manner.
  • Cell cycle analysis showed a G0/G1 arrest in human ADPKD cyst-lining epithelial cells with rosiglitazone treatment.
  • Analysis of cell cycle regulatory proteins revealed that rosiglitazone decreased the protein levels of proliferating cell nuclear antigen, pRb, cyclin D1, cyclin D2 and Cdk4 but increased the levels of p21 and p27 in a dose-dependent manner.
  • Rosiglitazone also induced apoptosis in cyst-lining epithelial cells, which was correlated with increased bax expression and decreased bcl-2 expression.
  • [MeSH-minor] Cell Line. Cell Proliferation / drug effects. Cells, Cultured. Dose-Response Relationship, Drug. Epithelial Cells / drug effects. Epithelial Cells / pathology. G0 Phase / drug effects. G1 Phase / drug effects. Humans. Kidney / cytology. Kidney / drug effects. Kidney / metabolism. Time Factors

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  • (PMID = 20210794.001).
  • [ISSN] 1742-7843
  • [Journal-full-title] Basic & clinical pharmacology & toxicology
  • [ISO-abbreviation] Basic Clin. Pharmacol. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone
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30. Childs-Sanford SE, Peters RM, Morrisey JK, Alcaraz A: Sarcomatoid renal cell carcinoma in a binturong (Arctictis binturong). J Zoo Wildl Med; 2005 Jun;36(2):308-12
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  • [Title] Sarcomatoid renal cell carcinoma in a binturong (Arctictis binturong).
  • Diagnostic investigations, including radiographs, abdominal ultrasound, clinical laboratory findings, and a fine-needle aspirate of the mass, were suggestive of a sarcoma with metastasis.
  • Necropsy and histopathologic findings confirmed a widely disseminated sarcomatoid variant of a renal cell carcinoma, likely originating in the left kidney, with metastasis to the right kidney, spleen, pancreas, liver, mesenteric lymph nodes, and lungs.
  • This is the first report of this neoplasm in a binturong and only the second report in the veterinary literature.
  • Sarcomatoid renal cell carcinoma is a rare histologic variant of renal cell carcinoma that is aggressive, commonly metastatic, and associated with a very poor prognosis in humans.
  • Accurate antemortem diagnosis of this tumor may be complicated by its biphasic morphology, which may resemble carcinoma or sarcoma (or both), often necessitating the use of immunohistochemical techniques.
  • [MeSH-major] Carcinoma, Renal Cell / veterinary. Carnivora. Kidney Neoplasms / veterinary. Sarcoma / veterinary
  • [MeSH-minor] Animals. Animals, Zoo. Fatal Outcome. Female. Immunohistochemistry / veterinary. Neoplasm Metastasis / pathology

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  • (PMID = 17323574.001).
  • [ISSN] 1042-7260
  • [Journal-full-title] Journal of zoo and wildlife medicine : official publication of the American Association of Zoo Veterinarians
  • [ISO-abbreviation] J. Zoo Wildl. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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31. Connor J, Ashton-Key M: Gastric and intestinal diffuse large B-cell lymphomas are clinically and immunophenotypically different. An immunohistochemical and clinical study. Histopathology; 2007 Nov;51(5):697-703
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  • [Title] Gastric and intestinal diffuse large B-cell lymphomas are clinically and immunophenotypically different. An immunohistochemical and clinical study.
  • AIMS: To determine the immunophenotype of gastric and intestinal diffuse large B-cell lymphomas and investigate the clinical significance of patterns of antigen expression.
  • METHODS AND RESULTS: Immunohistochemistry was performed for detection of CD10, Bcl-6, Bcl-2, MUM1 and p53 in paraffin-embedded tissue from 29 patients with primary diffuse large B-cell lymphoma of the stomach and intestine.
  • Thirteen of the 29 cases were of germinal centre phenotype (CD10+ or CD10-, Bcl-6+ and MUM1-).
  • Sixteen were of activated B-cell phenotype (all CD10- and either Bcl-6-, or Bcl-6+ and MUM1+).
  • Sixteen cases showed Bcl-2 expression.
  • There was a statistically significant difference (P < 0.05) in immunophenotype of the neoplastic cells relating to tumour site.
  • Of 15 gastric lymphomas, 11 were of activated B-cell phenotype and 9/14 intestinal tumours were of germinal centre phenotype.
  • CONCLUSIONS: Primary gastric and intestinal large cell lymphomas appear to show different patterns of antigen expression.
  • Gastric diffuse large B-cell lymphomas are usually of activated B-cell phenotype that may reflect a relationship with low-grade gastric lymphomas of marginal zone type.
  • Intestinal diffuse large B-cell lymphomas usually show a germinal centre phenotype, suggesting an origin from germinal centre B cells.
  • [MeSH-major] Intestinal Neoplasms / classification. Intestinal Neoplasms / mortality. Lymphoma, Large B-Cell, Diffuse / classification. Lymphoma, Large B-Cell, Diffuse / mortality. Stomach Neoplasms / classification. Stomach Neoplasms / mortality

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  • (PMID = 17927592.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers
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32. Wang W, Guo Q, You Q, Zhang K, Yang Y, Yu J, Liu W, Zhao L, Gu H, Hu Y, Tan Z, Wang X: Involvement of bax/bcl-2 in wogonin-induced apoptosis of human hepatoma cell line SMMC-7721. Anticancer Drugs; 2006 Aug;17(7):797-805
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  • [Title] Involvement of bax/bcl-2 in wogonin-induced apoptosis of human hepatoma cell line SMMC-7721.
  • The molecular mechanisms of wogonin-induced apoptosis of human hepatoma SMMC-7721 cells are reported.
  • Wogonin treatment resulted in significant inhibition of SMMC-7721 cells in a time-dependent and concentration-dependent manner.
  • Typical morphological changes and apoptotic blebbing in SMMC-7721 cells were observed after treatment with 1x10(-4) mol/l wogonin for a period of 0-48 h.
  • Flow cytometry and Annexin-V/propidium iodide double-staining experiments revealed a dramatic increase in the number of apoptotic and G0/G1 phase cells after wogonin treatment.
  • The proapoptotic activity of wogonin is attributed to its ability to modulate the expression of bcl-2 and bax proteins.
  • It is observed that the expression of bax protein is dramatically increased whereas the synthesis of bc1-2 protein is significantly decreased when cells are treated with wogonin.
  • [MeSH-major] Apoptosis / physiology. Carcinoma, Hepatocellular / pathology. Flavanones / pharmacology. Proto-Oncogene Proteins c-bcl-2 / physiology. bcl-2-Associated X Protein / physiology
  • [MeSH-minor] Annexin A5 / metabolism. Blotting, Western. Cell Cycle / drug effects. Cell Line, Tumor. Cell Shape. Colorimetry. DNA Fragmentation. DNA, Neoplasm / biosynthesis. DNA, Neoplasm / genetics. Humans. Propidium. Reverse Transcriptase Polymerase Chain Reaction. Tetrazolium Salts. Thiazoles

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  • (PMID = 16926629.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / S06GM-008205
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Annexin A5; 0 / DNA, Neoplasm; 0 / Flavanones; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / bcl-2-Associated X Protein; 298-93-1 / thiazolyl blue; 36015-30-2 / Propidium; 632-85-9 / wogonin
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33. Leitner L, Shaposhnikov D, Descot A, Hoffmann R, Posern G: Epithelial Protein Lost in Neoplasm alpha (Eplin-alpha) is transcriptionally regulated by G-actin and MAL/MRTF coactivators. Mol Cancer; 2010;9:60
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  • [Title] Epithelial Protein Lost in Neoplasm alpha (Eplin-alpha) is transcriptionally regulated by G-actin and MAL/MRTF coactivators.
  • Epithelial Protein Lost in Neoplasm alpha is a novel cytoskeleton-associated tumor suppressor whose expression inversely correlates with cell growth, motility, invasion and cancer mortality.
  • [MeSH-minor] Animals. Mice. Mutation / genetics. NIH 3T3 Cells. Promoter Regions, Genetic / genetics. Protein Binding. Serum Response Factor / metabolism. Signal Transduction

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  • (PMID = 20236507.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Actins; 0 / Cytoskeletal Proteins; 0 / D15Ertd366e protein, mouse; 0 / MKL1 protein, mouse; 0 / Serum Response Factor; 0 / Trans-Activators
  • [Other-IDs] NLM/ PMC2848193
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34. Zhang LP, Cheng YF, Liu GL, Lu AD, Liu YR, Wang H: [The clinical significance of detecting minimal residual disease in acute childhood B-cell lymphoblastic leukemia with flow cytometry]. Zhonghua Er Ke Za Zhi; 2005 Jul;43(7):481-5
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  • [Title] [The clinical significance of detecting minimal residual disease in acute childhood B-cell lymphoblastic leukemia with flow cytometry].
  • OBJECTIVE: Flow cytometry may be used to detect minimal residual disease (MRD) in acute lymphoblastic leukemia because leukemic cells often display aberrant phenotypes when compared to normal cells.
  • The present study was designed to establish a flow cytometric method for detecting MRD in children with B-ALL and evaluate its clinical prognostic value.
  • The authors detected MRD in 6 cases without effective antibody combinations by the four-color antibody combinations consisting of CD(45)/CD(19)/CD(10)/CD(34) and CD(45)/CD(19)/CD(20)/CD(22) and detected the aberrance of the minor subsets of CD(19)(+) cells. RESULTS:.
  • The sensitivity of this method was 0.01%. (2) Patients with MRD levels > or = 0.01% at 9 and 12 months of therapy had significantly low disease-free survival compared with patients with MRD levels < 0.01%. (3) Six out of seven patients with recurrence in the BM had MRD levels > or = 0.1% prior to recurrence.
  • Patients with MRD levels > or = 0.1% during chemotherapy had significantly low disease-free survival as compared with patients with MRD values < 0.1%. (4) Two out of seven patients with recurrence had positive results of the qualitative PCR prior to recurrence. (5) Five patients with recurrence had no shift of antigen expression at relapse except that a patient missed CD(13). (6) Detectable MRD was not found in six patients without effective antibody combinations.
  • [MeSH-major] B-Lymphocyte Subsets / immunology. Flow Cytometry. Immunophenotyping. Neoplasm, Residual / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis
  • [MeSH-minor] Adolescent. Child. Child, Preschool. China. Disease-Free Survival. Female. Humans. Male. Sensitivity and Specificity. Treatment Outcome


35. Gesundheit B, Shapira MY, Resnick IB, Amar A, Kristt D, Dray L, Budowski E, Or R: Successful cell-mediated cytokine-activated immunotherapy for relapsed acute myeloid leukemia after hematopoietic stem cell transplantation. Am J Hematol; 2009 Mar;84(3):188-90
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  • [Title] Successful cell-mediated cytokine-activated immunotherapy for relapsed acute myeloid leukemia after hematopoietic stem cell transplantation.
  • Acute myeloid leukemia (AML) is an extremely aggressive disease with a high relapse rate even after allogeneic hematopoietic stem cell transplantation (HSCT).
  • We report the successful outcome of cell-mediated cytokine-activated immunotherapy in a high-risk pediatric AML patient who relapsed shortly after allogeneic HSCT.
  • Donor lymphocyte infusion along with interferon induced a graft-versus-leukemia effect, presenting as a reversible episode of graft-versus-host disease, which led to stable complete donor chimerism and total eradication of AML for over 24 months, at the time of this report.
  • [MeSH-major] Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Lymphocyte Transfusion. Neoplasm Recurrence, Local / immunology. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Child. Graft vs Host Disease. Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Humans. Immunologic Factors / administration & dosage. Immunotherapy. Interferon-alpha / administration & dosage. Male. Recombinant Proteins

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  • (PMID = 19105234.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interferon-alpha; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a
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36. Danielides V, Katotomichelakis M, Homsioglou E, Koukourakis MI, Giatromanolaki A, Sivridis E: Squamous cell nose and a synchronous in-situ vocal cord carcinoma: a case report. B-ENT; 2007;3(1):45-8
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  • [Title] Squamous cell nose and a synchronous in-situ vocal cord carcinoma: a case report.
  • However, most of these tumours are either metachronous primary or secondary tumours of the same histopathological type.
  • The development of a synchronous primary squamous cell skin cancer of the nose and an in-situ vocal cord carcinoma is something unusual.
  • We present the case of a patient with a primary neoplasm along the lateral side of the nose up to the bone of the pyramid, including the skin of the inner side of the nose and an infiltration of the inferior nasal concha on the right side, together with a small synchronous primary lesion of the left vocal cord.
  • To the best of our knowledge the case described is the first in the English medical literature and we discuss the complete management of synchronous head and neck malignancies, emphasising the importance of panendoscopy in the prevention of pitfalls in diagnosis and the therapeutic procedure.
  • [MeSH-major] Carcinoma in Situ / diagnosis. Laryngeal Neoplasms / diagnosis. Neoplasms, Multiple Primary / diagnosis. Nose Neoplasms / diagnosis. Skin Neoplasms / diagnosis. Vocal Cords
  • [MeSH-minor] Combined Modality Therapy. Endoscopy. Humans. Laryngoscopy. Male. Middle Aged. Neoplasm Staging. Radiotherapy, Adjuvant


37. Miller AA, Wang XF, Gu L, Hoffman P, Khatri J, Dunphy F, Edelman MJ, Bolger M, Vokes EE, Green MR, Cancer and Leukemia Group B (CALGB): Phase II randomized study of dose-dense docetaxel and cisplatin every 2 weeks with pegfilgrastim and darbepoetin alfa with and without the chemoprotector BNP7787 in patients with advanced non-small cell lung cancer (CALGB 30303). J Thorac Oncol; 2008 Oct;3(10):1159-65
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  • [Title] Phase II randomized study of dose-dense docetaxel and cisplatin every 2 weeks with pegfilgrastim and darbepoetin alfa with and without the chemoprotector BNP7787 in patients with advanced non-small cell lung cancer (CALGB 30303).
  • INTRODUCTION: We investigated dose-dense docetaxel and cisplatin in patients with measurable non-small cell lung cancer in a randomized phase II study without [A] or with [B] a putative chemoprotective agent, BNP7787.
  • Its further investigation in the curative setting in non-small cell lung cancer should be considered.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Erythropoietin / analogs & derivatives. Granulocyte Colony-Stimulating Factor / therapeutic use. Lung Neoplasms / drug therapy. Mesna / analogs & derivatives
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / secondary. Adenocarcinoma, Bronchiolo-Alveolar / drug therapy. Adenocarcinoma, Bronchiolo-Alveolar / secondary. Adult. Aged. Anemia / drug therapy. Brain Neoplasms / drug therapy. Brain Neoplasms / secondary. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / secondary. Cisplatin / administration & dosage. Darbepoetin alfa. Dose-Response Relationship, Drug. Drug Therapy, Combination. Feasibility Studies. Female. Filgrastim. Hematinics / therapeutic use. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Staging. Neutropenia / drug therapy. Prognosis. Recombinant Proteins. Survival Rate. Taxoids / administration & dosage

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  • (PMID = 18827613.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA03927; United States / NCI NIH HHS / CA / CA114558-02; United States / NCI NIH HHS / CA / CA21060; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA31983; United States / NCI NIH HHS / CA / CA33601; United States / NCI NIH HHS / CA / CA35113; United States / NCI NIH HHS / CA / CA35421; United States / NCI NIH HHS / CA / CA37447; United States / NCI NIH HHS / CA / CA41287; United States / NCI NIH HHS / CA / CA45389; United States / NCI NIH HHS / CA / CA45418; United States / NCI NIH HHS / CA / CA45564; United States / NCI NIH HHS / CA / CA45808; United States / NCI NIH HHS / CA / CA47559; United States / NCI NIH HHS / CA / CA47577; United States / NCI NIH HHS / CA / CA47642; United States / NCI NIH HHS / CA / CA74811; United States / NCI NIH HHS / CA / CA77298; United States / NCI NIH HHS / CA / CA77440
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hematinics; 0 / Recombinant Proteins; 0 / Taxoids; 11096-26-7 / Erythropoietin; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 15H5577CQD / docetaxel; 15UQ94PT4P / Darbepoetin alfa; 3A58010674 / pegfilgrastim; 45127-11-5 / 2,2'-dithiodiethanesulfonic acid; NR7O1405Q9 / Mesna; PVI5M0M1GW / Filgrastim; Q20Q21Q62J / Cisplatin
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38. Edwards PC, Fantasia JE, Saini T, Rosenberg TJ, Sachs SA, Ruggiero S: Clinically aggressive central giant cell granulomas in two patients with neurofibromatosis 1. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2006 Dec;102(6):765-72
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  • [Title] Clinically aggressive central giant cell granulomas in two patients with neurofibromatosis 1.
  • BACKGROUND: Neurofibromatosis 1 (NF1) is an autosomal dominantly inherited disorder caused by a spectrum of mutations affecting the Nf1 gene.
  • Affected patients develop benign and malignant tumors at an increased frequency.
  • Clinical findings include multiple cutaneous café-au-lait pigmentations, neurofibromas, axillary freckling, optic gliomas, benign iris hamartomas (Lisch nodules), scoliosis, and poorly defined soft tissue lesions of the skeleton.
  • Kerl first reported an association of NF1 with multiple central giant cell granulomas (CGCGs) of the jaws.
  • CLINICAL CASES: We report on 2 patients who presented with NF1 and aggressive CGCGs of the jaws.
  • In both cases, the clinical course was characterized by numerous recurrences despite mechanical curettage and surgical resection.
  • Alternatively, the CGCG in NF1 patients could represent a true neoplasm, resulting from additional, as of yet unidentified, genetic alterations to Nf1-haploinsufficient bone.
  • [MeSH-major] Granuloma, Giant Cell / complications. Jaw Diseases / complications. Neurofibromatosis 1 / complications


39. Osman I, Dai J, Mikhail M, Navarro D, Taneja SS, Lee P, Christos P, Shen R, Nanus DM: Loss of neutral endopeptidase and activation of protein kinase B (Akt) is associated with prostate cancer progression. Cancer; 2006 Dec 1;107(11):2628-36
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  • BACKGROUND: Neutral endopeptidase (NEP) is a cell-surface peptidase that can regulate the activation of Akt kinase through catalytic-dependent and independent mechanisms.
  • The authors investigated whether NEP loss in vivo would result in Akt phosphorylation and potentially contribute to prostate cancer progression by examining the interaction of NEP, Akt, and phosphatase and tensin homolog (PTEN) in a prostate xenograft model and in clinical specimens from patients with prostate cancer.
  • The clinical relevance of NEP, phosphorylated Akt, and PTEN protein expression also was investigated in 204 patients who had undergone radical prostatectomy.
  • In the study cohort, loss of PTEN protein expression did not correlated significantly with phosphorylated Akt or with patients' clinical outcome.
  • CONCLUSIONS: The findings from this investigation demonstrated that NEP loss leads to Akt activation and contributes to the clinical progression of prostate cancer.
  • [MeSH-minor] Animals. Disease Progression. Enzyme Activation. Humans. Immunohistochemistry. Male. Mice. Neoplasm Recurrence, Local / enzymology. Neoplasm Recurrence, Local / pathology. Neoplasm Transplantation. Phosphorylation. Prospective Studies. Prostate-Specific Antigen. Prostatectomy. Transplantation, Heterologous


40. Moore TV, Lyons GE, Brasic N, Roszkowski JJ, Voelkl S, Mackensen A, Kast WM, Le Poole IC, Nishimura MI: Relationship between CD8-dependent antigen recognition, T cell functional avidity, and tumor cell recognition. Cancer Immunol Immunother; 2009 May;58(5):719-28
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  • [Title] Relationship between CD8-dependent antigen recognition, T cell functional avidity, and tumor cell recognition.
  • Effective immunotherapy using T cell receptor (TCR) gene-modified T cells requires an understanding of the relationship between TCR affinity and functional avidity of T cells.
  • In this study, we evaluate the relative affinity of two TCRs isolated from HLA-A2-restricted, gp100-reactive T cell clones with extremely high functional avidity.
  • Furthermore, one of these T cell clones, was CD4- CD8- indicating that antigen recognition by this clone was CD8 independent.
  • However, when these TCRs were expressed in CD8- Jurkat cells, the resulting Jurkat cells recognized gp100:209-217 peptide loaded T2 cells and had high functional avidity, but could not recognize HLA-A2+ melanoma cells expressing gp100.
  • Tumor cell recognition by Jurkat cells expressing these TCRs could not be induced by exogenously loading the tumor cells with the native gp100:209-217 peptide.
  • These results indicate that functional avidity of a T cell does not necessarily correlate with TCR affinity and CD8-independent antigen recognition by a T cell does not always mean its TCR will transfer CD8-independence to other effector cells.
  • The implications of these findings are that T cells can modulate their functional avidity independent of the affinity of their TCRs.

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  • (PMID = 18836717.001).
  • [ISSN] 1432-0851
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA090873; United States / NCI NIH HHS / CA / CA 109536; United States / NCI NIH HHS / CA / CA 104947; United States / NCI NIH HHS / CA / P01 CA097296; United States / NCI NIH HHS / CA / CA104947-02; United States / NCI NIH HHS / CA / R01 CA102280; United States / NCI NIH HHS / CA / CA 102280; United States / NCI NIH HHS / CA / CA102280-06; United States / NCI NIH HHS / CA / CA 90873; United States / NCI NIH HHS / CA / R01 CA102280-06; United States / NCI NIH HHS / CA / R01 CA104947; United States / NCI NIH HHS / CA / R01 CA109536; United States / NCI NIH HHS / CA / CA 97296; United States / NCI NIH HHS / CA / R01 CA104947-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Epitopes, T-Lymphocyte; 0 / HLA-A2 Antigen; 0 / Membrane Glycoproteins; 0 / PMEL protein, human; 0 / Receptors, Antigen, T-Cell, alpha-beta; 0 / Recombinant Fusion Proteins; 0 / gp100 Melanoma Antigen
  • [Other-IDs] NLM/ NIHMS109713; NLM/ PMC2773431
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41. Bhalme MD, Levison SE, Banait GS: Paraneoplastic oesophageal dysmotility-renal cell carcinoma presenting as dysphagia: a case report. Cases J; 2009;2:8170
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  • [Title] Paraneoplastic oesophageal dysmotility-renal cell carcinoma presenting as dysphagia: a case report.
  • CASE PRESENTATION: We present a case report of dysphagia secondary to oesophageal dysmotility attributed to a paraneoplastic manifestation of an occult renal cell carcinoma.
  • CONCLUSION: We believe this patient's dysphagia was a paraneoplastic manifestation of the renal cell tumour, an association that has never been previously reported.
  • Importantly, this must include the consideration of a paraneoplastic process secondary to an occult neoplasm.

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  • (PMID = 19830056.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2740017
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42. Distel LV, Fickenscher R, Dietel K, Hung A, Iro H, Zenk J, Nkenke E, Büttner M, Niedobitek G, Grabenbauer GG: Tumour infiltrating lymphocytes in squamous cell carcinoma of the oro- and hypopharynx: prognostic impact may depend on type of treatment and stage of disease. Oral Oncol; 2009 Oct;45(10):e167-74
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  • [Title] Tumour infiltrating lymphocytes in squamous cell carcinoma of the oro- and hypopharynx: prognostic impact may depend on type of treatment and stage of disease.
  • he purpose of this study was to evaluate the prognostic influence of various subtypes of tumour infiltrating lymphocytes (TIL) in head and neck cancer, in particular the potential influence of regulatory T cells (Treg) in relation to different treatment modalities was addressed.
  • A total of 115 patients with squamous cell carcinoma of the oro- and hypopharynx were selected.
  • A low-risk group of 62 patients with early disease was treated by primary surgery followed by external radiotherapy.
  • A high-risk group of 53 inoperable patients with advanced disease was treated by primary radiochemotherapy.
  • The impact of TIL on prognosis in patients with head and neck cancer may be affected by type of treatment and stage of disease.
  • This finding will influence future studies on the role of TIL in human cancers.
  • [MeSH-major] Carcinoma, Squamous Cell / immunology. Hypopharyngeal Neoplasms / immunology. Lymphocytes, Tumor-Infiltrating / immunology. Oropharyngeal Neoplasms / immunology
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Risk Factors. T-Lymphocytes, Regulatory / immunology

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  • (PMID = 19576838.001).
  • [ISSN] 1879-0593
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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43. Michal M, Kazakov DV, Síma R, Vanecek T: Primitive small cell tumor with epithelial, gangliocytic, neuroendocrine, and mesenchymal differentiation: report of 2 cases. Int J Surg Pathol; 2007 Oct;15(4):429-36
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  • [Title] Primitive small cell tumor with epithelial, gangliocytic, neuroendocrine, and mesenchymal differentiation: report of 2 cases.
  • The predominant cell type was small round to fusiform dark blue cells.
  • The dark blue cells formed distinct epithelial cords with gland-like formations with mucicarmine-positive mucus.
  • The mesenchymal areas appeared benign and could be likened to a fibroma having a densely collagenous stroma, or they had spindle cells set in the myxoid background, rendering a myxoma-like appearance.
  • Another distinctive feature was ganglion cell differentiation.
  • Mitotic figures, including atypical forms, were found only in the small cell component.
  • All cells were immunohistochemically negative for actin, calponin, desmin, HMB45, neurofilament protein, CD99/MIC2, Melan A, tyrosinase, serotonin, CD56, Melan A, GFAP, and S-100 protein.
  • Cytokeratin, synaptophysin, FLI1 protein, and chromogranin antibodies reacted only in the primitive small round cells, while all the other components were cytokeratin negative.
  • Ultrastructurally, the cells were endowed with well-formed intercellular desmosomes membrane-bound secretory in the cytoplasm.
  • We suggest the name "primitive small cell tumor with epithelial, gangliocytic, neuroendocrine, and mesenchymal differentiation" for this neoplasm.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Neuroendocrine Tumors / pathology. Sarcoma, Small Cell / pathology. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Aneuploidy. Biomarkers, Tumor / metabolism. Cell Transformation, Neoplastic. Child, Preschool. Chromosomes, Human, Pair 12. Combined Modality Therapy. Desmosomes / ultrastructure. Epithelial Cells / metabolism. Epithelial Cells / pathology. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Microscopy, Electron, Transmission. Secretory Vesicles / ultrastructure

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  • (PMID = 17913955.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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44. McCluggage WG, Aydin NE, Wong NA, Cooper K: Low-grade epithelial-myoepithelial carcinoma of bartholin gland: report of 2 cases of a distinctive neoplasm arising in the vulvovaginal region. Int J Gynecol Pathol; 2009 May;28(3):286-91
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  • [Title] Low-grade epithelial-myoepithelial carcinoma of bartholin gland: report of 2 cases of a distinctive neoplasm arising in the vulvovaginal region.
  • We report 2 cases of a distinctive neoplasm arising from Bartholin gland and presenting as a vulval or vaginal mass.
  • They were composed of tubular, trabecular, or insular arrangements with a double layer of inner cuboidal cells with round nuclei and outer cells with ovoid nuclei and clear cytoplasm, corresponding to epithelial and myoepithelial cells, respectively.
  • In both cases, a minor proportion of the neoplasm consisted of cribriform arrangements, creating an appearance reminiscent of adenoid cystic carcinoma, although the overall morphology was not typical of that lesion.
  • Immunohistochemically, the inner cells were positive with epithelial markers, including broad-spectrum cytokeratins and epithelial membrane antigen, and the outer cell layer was positive with myoepithelial markers p63, calponin, and alpha-smooth muscle actin.
  • Both neoplasms exhibited diffuse strong immunoreactivity of the epithelial cells with c-kit.
  • We believe this represents a low-grade carcinoma arising from Bartholin gland composed of a dual population of epithelial and myoepithelial cells and closely resembling the salivary gland neoplasm termed epithelial-myoepithelial carcinoma.


45. Joshi SS, Mittal AK, Wang P, Joshi AD, Vu E, Wang X: Differential gene expression in murine large cell B-cell lymphoma metastatic variants. Int Immunopharmacol; 2008 Sep;8(9):1257-63
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  • [Title] Differential gene expression in murine large cell B-cell lymphoma metastatic variants.
  • Previous studies from this laboratory have characterized RAW117-P murine large cell B-cell lymphoma and its in vivo selected highly malignant and liver metastatic RAW117-H10 subline for their biological and biochemical properties.
  • In this study, to understand the molecular basis of low and high metastatic behavior of these variant sublines, we have investigated the molecular phenotypes of these cells using differential display techniques and cDNA array analysis.
  • Differential display analysis indicated a significant difference in expression of several genes between these two metastatic variant lymphoma cells.
  • Further analyses of these cells using microarray showed an increased expression of several genes including uPAR1, CRE-BP1, Chop-10, IGF, insulin-like growth factor-IA, STAT6, Cyclin-D1, Cyclin-E, ERBB-3, Alpha NGF, Kruppel-like factor LKLF, (P)19INK4 in metastatic RAW117-H10 cells compared to parental RAW117-P cells.
  • On the other hand, MIP1beta, CD14 antigen, Cathepsin B and MOD are expressed more in RAW117-P cells compared to RAW117-H10 cells.
  • The combination of plasminogen activator and its receptor and IGF-like growth factors, cell cycle regulatory molecules and transcription factors might provide an ideal environment for RAW117-H10 cells to metastasize to distant organs and colonize.
  • Thus these results identify certain differentially expressed genes that are involved in the metastatic properties of these lymphoma cells and lay foundation for further in depth analyses to use this information to develop therapy for metastatic lymphoma.
  • [MeSH-major] Gene Expression Regulation, Neoplastic / genetics. Lymphoma, B-Cell / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Cells, Cultured. DNA Primers. DNA, Complementary / biosynthesis. DNA, Complementary / genetics. Mice. Neoplasm Metastasis / genetics. Neoplasm Metastasis / pathology. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction


46. Périé S, Hugentobler A, Susini B, Balogova S, Grahek D, Kerrou K, Montravers F, Chater PE, St Guily JL, Talbot JN: Impact of FDG-PET to detect recurrence of head and neck squamous cell carcinoma. Otolaryngol Head Neck Surg; 2007 Oct;137(4):647-53
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  • [Title] Impact of FDG-PET to detect recurrence of head and neck squamous cell carcinoma.
  • OBJECTIVE: Prospectively evaluate the impact of fluorodeoxyglucose-fluorine-18 positron emission tomography (FDG-PET) in the management of recurrence of advanced head and neck squamous cell carcinoma during the first year after treatment.
  • Systematic FDG-PET had a significantly lesser impact in comparison with FDG-PET motivated by clinical suspicion.
  • [MeSH-major] Carcinoma, Squamous Cell / radionuclide imaging. Fluorodeoxyglucose F18. Head and Neck Neoplasms / radionuclide imaging. Neoplasm Recurrence, Local / radionuclide imaging. Positron-Emission Tomography / methods. Radiopharmaceuticals

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  • (PMID = 17903585.001).
  • [ISSN] 0194-5998
  • [Journal-full-title] Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
  • [ISO-abbreviation] Otolaryngol Head Neck Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 0Z5B2CJX4D / Fluorodeoxyglucose F18
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47. Hotchkiss KA, Basile CM, Spring SC, Bonuccelli G, Lisanti MP, Terman BI: TEM8 expression stimulates endothelial cell adhesion and migration by regulating cell-matrix interactions on collagen. Exp Cell Res; 2005 Apr 15;305(1):133-44
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  • [Title] TEM8 expression stimulates endothelial cell adhesion and migration by regulating cell-matrix interactions on collagen.
  • The TEM8 gene is selectively expressed in tumor versus normal blood vessels, though its function in endothelial cell biology is not known.
  • Towards the goal of clarifying this function, we tested whether TEM8 overexpression, or blocking TEM8's function with a dominant negative protein, would modulate endothelial cell activities.
  • We found that TEM8-expressing endothelial cells migrated at a rate 3-fold greater than control cells in a monolayer denudation assay.
  • Taken together, these results indicate that TEM8 plays a positive role in endothelial cell activities related to angiogenesis.
  • [MeSH-major] Cell Adhesion / physiology. Cell Movement / physiology. Endothelium, Vascular / physiology. Extracellular Matrix / physiology. Receptors, Cell Surface / genetics
  • [MeSH-minor] Adipose Tissue / blood supply. Animals. Base Sequence. Cells, Cultured. Chemotaxis. Cloning, Molecular. Collagen / metabolism. DNA Primers. Epididymis. Humans. Male. Membrane Proteins. Neoplasm Proteins. Neovascularization, Physiologic. Polymerase Chain Reaction. Rats. Transfection. Umbilical Veins

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  • (PMID = 15777794.001).
  • [ISSN] 0014-4827
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA86289; United States / NHLBI NIH HHS / HL / HL067019
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANTXR1 protein, human; 0 / DNA Primers; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Receptors, Cell Surface; 9007-34-5 / Collagen
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48. Park SR, Baek JY, Kim DW, Im SA, Kim TY, Bang YJ, Kim NK, Jeon YK, Kim CW, Heo DS: Primary systemic anaplastic large cell lymphoma in a single Korean institution: clinical characteristics and treatment outcome. J Korean Med Sci; 2006 Aug;21(4):633-8
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  • [Title] Primary systemic anaplastic large cell lymphoma in a single Korean institution: clinical characteristics and treatment outcome.
  • Despite advances in the characterization of anaplastic large cell lymphoma (ALCL), little data is available on Asian patients.
  • We report here upon single Korean institution's experience regarding the clinical characteristics and outcomes of ALCL.
  • Ann Arbor stage III-IV, B symptoms, high-intermediate/ high International Prognostic Index (IPI), and extranodal disease at diagnosis were present in 56%, 44%, 41%, and 63%, respectively.
  • The staining results for anaplastic lymphoma kinase were positive in 6 (33%) of 18 cases available.
  • Age, performance status, lactate dehydrogenase, extranodal disease sites number, and IPI were correlated with treatment response and survival.
  • [MeSH-major] Lymphoma, Large-Cell, Anaplastic / drug therapy. Lymphoma, Large-Cell, Anaplastic / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antigens, CD30 / analysis. Female. Humans. Korea. Male. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 16891805.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antigens, CD30
  • [Other-IDs] NLM/ PMC2729883
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49. Villella J, Herrmann FR, Kaul S, Lele S, Marchetti D, Natiella J, Odunsi K, Mhawech-Fauceglia P: Clinical and pathological predictive factors in women with adult-type granulosa cell tumor of the ovary. Int J Gynecol Pathol; 2007 Apr;26(2):154-9
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  • [Title] Clinical and pathological predictive factors in women with adult-type granulosa cell tumor of the ovary.
  • Granulosa cell tumor (GCT) is a rare neoplasm hallmarked by a very indolent course and late recurrences.
  • Although numerous clinical and pathological parameters have been implicated as prognostic factors for GCT, their role remains controversial.
  • Demographic and clinical course information was recorded from the medical record.
  • [MeSH-major] Granulosa Cell Tumor / diagnosis. Granulosa Cell Tumor / pathology. Ovarian Neoplasms / diagnosis. Ovarian Neoplasms / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. DNA, Neoplasm / genetics. Female. Humans. Kaplan-Meier Estimate. Ki-67 Antigen. Middle Aged. Mitotic Index. Ploidies. Predictive Value of Tests. Prognosis. Retrospective Studies

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  • (PMID = 17413982.001).
  • [ISSN] 0277-1691
  • [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] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Ki-67 Antigen
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50. Yodkeeree S, Garbisa S, Limtrakul P: Tetrahydrocurcumin inhibits HT1080 cell migration and invasion via downregulation of MMPs and uPA. Acta Pharmacol Sin; 2008 Jul;29(7):853-60
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  • [Title] Tetrahydrocurcumin inhibits HT1080 cell migration and invasion via downregulation of MMPs and uPA.
  • The proteases that participate in extracellular matrix (ECM) degradation are involved in cancer cell metastasis.
  • The present study investigates the effect of an ultimate metabolite of curcumin, THC, on the invasion and motility of highly-metastatic HT1080 human fibrosarcoma cells.
  • METHODS: The effect of THC on HT1080 cell invasion and migration was determined using Boyden chamber assay.
  • Cell-adhesion assay was used for examining the binding of cells to ECM molecules.
  • Zymography assay was used to analyze the effect of THC on matrix metalloproteinase (MMP)-2, MMP-9, and urokinase plasminogen activator (uPA) secretion from HT1080 cells.
  • Tissue inhibitor of metalloproteinase (TIMP)-2 and membrane-type 1 matrix metalloproteinase (MT1-MMP) proteins levels were analyzed by Western blotting.
  • RESULTS: Treatment with THC reduced HT1080 cell invasion and migration in a dose-dependent manner.
  • THC also decreased the cell adhesion to Matrigel and laminin-coated plates.
  • CONCLUSION: Our findings revealed that THC reduced HT1080 cell invasion and migration.
  • The inhibition of cancer cell invasion is associated with the downregulation of ECM degradation enzymes and the inhibition of cell adhesion to ECM proteins.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Cell Movement / drug effects. Curcumin / analogs & derivatives. Matrix Metalloproteinases / biosynthesis. Urokinase-Type Plasminogen Activator / biosynthesis
  • [MeSH-minor] Animals. Cell Line, Tumor. Down-Regulation / drug effects. Humans. Mice. NIH 3T3 Cells. Neoplasm Invasiveness / pathology

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  • (PMID = 18565284.001).
  • [ISSN] 1745-7254
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 00U0645U03 / tetrahydrocurcumin; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.24.- / Matrix Metalloproteinases; IT942ZTH98 / Curcumin
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51. Emadi Baygi M, Soheili ZS, Schmitz I, Sameie S, Schulz WA: Snail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines. Cell Biol Toxicol; 2010 Dec;26(6):553-67
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  • [Title] Snail regulates cell survival and inhibits cellular senescence in human metastatic prostate cancer cell lines.
  • Snail, a master regulator of EMT, has been recently proposed to act additionally as a cell survival factor and inducer of motility.
  • We have investigated the function of Snail (SNAI1) in prostate cancer cells by downregulating its expression via short (21-mer) interfering RNA (siRNA) and measuring the consequences on EMT markers, cell viability, death, cell cycle, senescence, attachment, and invasivity.
  • Of eight carcinoma cell lines, the prostate carcinoma cell lines LNCaP and PC-3 showed the highest and moderate expression of SNAI1 mRNA, respectively, as measured by quantitative RT-PCR.
  • Long-term knockdown of Snail induced a severe decline in cell numbers in LNCaP and PC-3 and caspase activity was accordingly enhanced in both cell lines.
  • In addition, suppression of Snail expression induced senescence in LNCaP cells.
  • SNAI1-siRNA-treated cells did not tolerate detachment from the extracellular matrix, probably due to downregulation of integrin α6.
  • Invasiveness of PC-3 cells was not significantly diminished by Snail knockdown.
  • Our data suggest that Snail acts primarily as a survival factor and inhibitor of cellular senescence in prostate cancer cell lines.
  • [MeSH-major] Cell Aging / genetics. Prostatic Neoplasms / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Survival / genetics. Down-Regulation. Epithelial-Mesenchymal Transition / genetics. Gene Expression Regulation, Neoplastic. Humans. Integrin alpha6 / metabolism. Male. Neoplasm Metastasis. RNA, Messenger / metabolism

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  • (PMID = 20397042.001).
  • [ISSN] 1573-6822
  • [Journal-full-title] Cell biology and toxicology
  • [ISO-abbreviation] Cell Biol. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Integrin alpha6; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / snail family transcription factors
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52. Lodillinsky C, Rodriguez V, Vauthay L, Sandes E, Casabé A, Eiján AM: Novel invasive orthotopic bladder cancer model with high cathepsin B activity resembling human bladder cancer. J Urol; 2009 Aug;182(2):749-55
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  • MATERIAL AND METHODS: The MB49-I invasive bladder tumor cell line was obtained after 13 consecutive in vivo passages of primary tumor obtained by subcutaneous inoculation of MB49 bladder tumor cells in C57Bl/6J male mice.
  • In vitro the MB49-I cell line showed higher invasive properties associated with an increase in cathepsin B, metalloproteinase 9 and urokinase-type plasminogen activator proteolytic activities.
  • Orthotopic bladder tumors induced by electrocautery of the bladder wall and subsequent instillation of MB49 and MB49-I bladder cancer cells generated superficial and invasive bladder tumors, respectively.
  • CONCLUSIONS: The new murine bladder model described resembles human bladder disease, making it a useful tool for studying the molecular mechanisms of tumor progression and metastasis, and assaying antimetastatic and anti-invasive agents.
  • [MeSH-major] Cathepsin B / physiology. Disease Models, Animal. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Animals. Cell Line, Tumor. Male. Mice. Mice, Inbred C57BL. Neoplasm Invasiveness

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  • (PMID = 19539312.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.22.1 / Cathepsin B
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53. Berridge MV, Herst PM, Tan AS: Metabolic flexibility and cell hierarchy in metastatic cancer. Mitochondrion; 2010 Nov;10(6):584-8
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  • [Title] Metabolic flexibility and cell hierarchy in metastatic cancer.
  • Cancer is characterized by disturbed homeostasis of self-renewing cell populations, and their ability to seed and grow in multiple microenvironments.
  • This overarching cellular property of metastatic cancer emerges from the contentious cancer stem cell hypothesis that underpins the more generic hallmarks of cancer (Hanahan and Weinberg, 2000) and its subsequent add-ons.
  • Metabolic flexibility may circumvent limitations inherent in the increasingly popular but erroneous view that aerobic glycolysis is a universal property of cancer cells.
  • Integrated approaches that address cancer cell hierarchy and complexity, and how cancer cells adapt their metabolism according to their changing environment are now beginning to emerge, and these approaches promise to address the poor mortality statistics of metastatic cancer.
  • [MeSH-major] Mitochondria / metabolism. Neoplasm Metastasis / pathology. Neoplasm Metastasis / physiopathology. Neoplasms / pathology. Neoplasms / physiopathology

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  • [Copyright] Copyright © 2010 Mitochondria Research Society. Published by Elsevier B.V. All rights reserved.
  • (PMID = 20709626.001).
  • [ISSN] 1872-8278
  • [Journal-full-title] Mitochondrion
  • [ISO-abbreviation] Mitochondrion
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
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54. Carlsson B, Sadeghi A, Bengtsson M, Wagenius G, Tötterman TH: Effector T cell analysis of melanoma tumor-infiltrating lymphocyte cultures using HLA-ABC semimatched melanoma cell lines. J Immunother; 2008 Sep;31(7):633-43
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  • [Title] Effector T cell analysis of melanoma tumor-infiltrating lymphocyte cultures using HLA-ABC semimatched melanoma cell lines.
  • The generation of T cells with specific reactivity against tumor-associated antigens is prerequisite for adoptive transfer therapy.
  • Cultures were analyzed for the presence of interferon gamma (IFNgamma)-producing cells upon stimulation with a panel of HLA-ABC semimatched melanoma cell lines.
  • We sought to find whether such cell lines could be used to analyze TIL reactivity.
  • Cell lines were used as stimulators to circumvent the need for autologous primary tumor cells.
  • Ninety-one of 318 cultures (28.6%) contained IFNgamma-producing cells after stimulation.
  • All but one HLA-A*0201 patient had MART-1/Melan-A27-35-directed TILs, with frequencies ranging from 0.1% to 90% of CD8 cells.
  • Overall, surgical material generated more cultures positive for T cells.
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm / chemistry. Antigens, Neoplasm / immunology. Cell Line, Tumor. Cell Proliferation. Drug Resistance, Neoplasm. Female. Humans. Interferon-gamma / immunology. Interferon-gamma / secretion. Lymphocyte Activation / drug effects. Lymphocyte Activation / immunology. Lymphocytes, Tumor-Infiltrating / immunology. Lymphocytes, Tumor-Infiltrating / pathology. Male. Melanoma-Specific Antigens. Middle Aged. Neoplasm Proteins / chemistry. Neoplasm Proteins / immunology. Peptides / chemical synthesis. Peptides / immunology. Peptides / pharmacology. Protein Binding. T-Lymphocyte Subsets / immunology. T-Lymphocyte Subsets / pathology. T-Lymphocytes, Cytotoxic / immunology. T-Lymphocytes, Cytotoxic / pathology

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  • (PMID = 18600181.001).
  • [ISSN] 1537-4513
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / HLA Antigens; 0 / Melanoma-Specific Antigens; 0 / Neoplasm Proteins; 0 / Peptides; 82115-62-6 / Interferon-gamma
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55. Liu YR, Wang H, Chang Y, Cheng YF, Fu JY, Zhang LP, Liu GL, Chen SS: [Detection of minimal residual disease in B lineage acute lymphoblastic leukemia by 4-color flow cytometry]. Zhonghua Xue Ye Xue Za Zhi; 2005 Jun;26(6):327-31
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  • [Title] [Detection of minimal residual disease in B lineage acute lymphoblastic leukemia by 4-color flow cytometry].
  • OBJECTIVE: To evaluate the method and value of detecting bone marrow minimal residual disease (MRD) in B lineage acute lymphoblastic leukemia (B-ALL) by multiparameter flow cytometry (FCM).
  • The immunophenotype of leukemia cells of B-ALL was also detected by four to six antibodies combination of 4-color CD45/SSC gating FCM.
  • The CD19, CD10, CD34 fluorescence intensity of B-cell precursors in normal and leukemic bone marrow was compared by relatively quantitative method.
  • RESULTS: Twelve patients were MRD positive (MRD(+)) among 50 patients during MRD monitoring, the percentages of residual leukemia cells were 0.06% to 7.73%.
  • The percentages of leukemia cells in all the 4 patients were over 0.1%.
  • [MeSH-major] Flow Cytometry / methods. Leukemia, B-Cell / diagnosis. Neoplasm, Residual / diagnosis

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  • (PMID = 16185473.001).
  • [ISSN] 0253-2727
  • [Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi
  • [ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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56. Binyamin L, Alpaugh RK, Hughes TL, Lutz CT, Campbell KS, Weiner LM: Blocking NK cell inhibitory self-recognition promotes antibody-dependent cellular cytotoxicity in a model of anti-lymphoma therapy. J Immunol; 2008 May 1;180(9):6392-401
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  • [Title] Blocking NK cell inhibitory self-recognition promotes antibody-dependent cellular cytotoxicity in a model of anti-lymphoma therapy.
  • Human NK cells lyse Ab-coated target cells through the process of Ab-dependent cellular cytotoxicity (ADCC).
  • NK cell inhibitory receptors, such as killer cell Ig-like receptors, engage with MHC class I molecules on self-cells to block NK cell activation.
  • Accordingly, we enhanced ADCC responses by blocking NK cell inhibitory receptors, thus perturbing induction of the self-recognition signal.
  • In a cell line model of anti-lymphoma therapy, the combination of rituximab with an Ab that blocks inhibitory self-recognition yielded increased NK cell-mediated target cell lysis when compared with rituximab alone.
  • To validate this proof-of-concept, we then used a more representative approach in which an individual's fresh primary NK cells encountered autologous, EBV-transformed B cells.
  • In this system, rituximab and a combination of Abs that block NK cell inhibitory receptors yielded improved NK cell-mediated lysis over rituximab alone.

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  • (PMID = 18424763.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 06927; United States / NCI NIH HHS / CA / CA 50633; United States / NCI NIH HHS / CA / R01 CA050633; United States / NCI NIH HHS / CA / CA050633-19A1; United States / NIAID NIH HHS / AI / R01 AI050656; United States / NCI NIH HHS / CA / R01 CA050633-19A1; United States / NCI NIH HHS / CA / R01 CA083859; United States / NCI NIH HHS / CA / CA 083859; United States / NIAID NIH HHS / AI / AI 050656; United States / NCI NIH HHS / CA / P30 CA006927
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Receptors, KIR; 4F4X42SYQ6 / Rituximab
  • [Other-IDs] NLM/ NIHMS163662; NLM/ PMC2810560
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57. Du Z, Chen J, Zhou X, Zhang T, Chen B, Tang F: Composite lymphoma with relapse of enteropathy-type T-cell lymphoma. Leuk Lymphoma; 2009 May;50(5):749-56
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  • [Title] Composite lymphoma with relapse of enteropathy-type T-cell lymphoma.
  • We describe an unusual case of with de novo composite diffuse large B-cell lymphoma and enteropathy-type T-cell lymphoma involving the duodenum in a 65-year-old man with celiac disease.
  • The coexistence of two malignancies was confirmed by immunohistochemical and molecular biologic analysis, which revealed clonal T-cell receptor gamma and immunoglobulin heavy chain gene rearrangements.
  • Epstein-Barr virus was not detected in the B- and T-cell components.
  • After chemotherapy, the patient experienced two relapses of enteropathy-type T-cell lymphoma only.
  • We review the medical literature on composite B- and T-cell lymphomas and discuss their diagnosis, pathogenesis, prognosis and treatment.
  • [MeSH-major] Intestinal Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, T-Cell / pathology
  • [MeSH-minor] Aged. Duodenal Neoplasms / pathology. Duodenum / pathology. Humans. Male. Neoplasm Invasiveness. Neoplasms, Second Primary. Recurrence. Treatment Outcome

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  • (PMID = 19330653.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 41
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58. Tan TL, Fang N, Neo TL, Singh P, Zhang J, Zhou R, Koh CG, Chan V, Lim SG, Chen WN: Rac1 GTPase is activated by hepatitis B virus replication--involvement of HBX. Biochim Biophys Acta; 2008 Mar;1783(3):360-74
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  • Understanding its interactions with cellular proteins is critical in the elucidation of the mechanisms of disease progression.
  • Using a cell-based HBV replication system, we showed that HBV replication in HepG2 cells resulted in a cellular morphological changes displaying membrane rufflings and lamellipodia like structures reminiscent of cells expressing constitutively activated Rac1.
  • HBV replication specifically activated wild type Rac1, but not Cdc42.
  • The smallest HBV viral protein, HBX, was able to activate the endogenous Rac1 and induce membrane ruffling when transfected into cells.
  • Taken together, we have shown the interaction of HBV with the Rho GTPase, affecting cell morphology through the Rac1 activation pathway.
  • [MeSH-minor] Carcinoma, Hepatocellular / pathology. Cell Cycle Proteins / metabolism. Cell Shape / genetics. Cells, Cultured. Disease Progression. Enzyme Activation. Guanine Nucleotide Exchange Factors / metabolism. Humans. Liver Neoplasms / pathology. Models, Biological. Neoplasm Metastasis. Protein Binding. Rho Guanine Nucleotide Exchange Factors. Trans-Activators. Transfection. cdc42 GTP-Binding Protein / physiology. src Homology Domains

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  • (PMID = 18086571.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Guanine Nucleotide Exchange Factors; 0 / Rho Guanine Nucleotide Exchange Factors; 0 / Trans-Activators; 0 / Viral Regulatory and Accessory Proteins; 0 / hepatitis B virus X protein; EC 3.6.5.2 / cdc42 GTP-Binding Protein; EC 3.6.5.2 / rac1 GTP-Binding Protein
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59. Mingoli A, Brachini G, Petroni R, Antoniozzi A, Cavaliere F, Simonelli L, Chirletti P, Modini C: Squamous and adenosquamous cell carcinomas of the gallbladder. J Exp Clin Cancer Res; 2005 Mar;24(1):143-50
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  • [Title] Squamous and adenosquamous cell carcinomas of the gallbladder.
  • Squamous and adenosquamous cell carcinomas (ASC and SCC) are rare subtypes of gallbladder cancer, traditionally considered more aggressive and with a poorer prognosis than adenocarcinoma.
  • We report about two patients affected by an advanced squamous cell carcinoma of the gallbladder.
  • Natural history, clinical findings, prognosis and outcome of this rare gallbladder tumour are discussed on the basis of a review of the English literature.
  • In conclusion, an aggressive and radical surgical treatment of advanced squamous and adenosquamous cell gallbladder carcinomas seems to be indicated for their low proclivity to distant spreading.
  • [MeSH-major] Carcinoma, Adenosquamous / pathology. Carcinoma, Squamous Cell / pathology. Gallbladder Neoplasms / pathology
  • [MeSH-minor] Aged. Female. Humans. Neoplasm Staging. Survival Rate. Tomography Scanners, X-Ray Computed

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  • (PMID = 15943044.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 50
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60. Kerr JP, Turner M, Ashton-Key M, Mead GM, Johnson PW: Intestinal strictures: a new complication of treatment for primary gastrointestinal diffuse large B-cell lymphoma. Br J Haematol; 2008 Mar;140(6):712-4
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  • [Title] Intestinal strictures: a new complication of treatment for primary gastrointestinal diffuse large B-cell lymphoma.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Gastrointestinal Neoplasms / drug therapy. Intestinal Obstruction / chemically induced. Lymphoma, Large B-Cell, Diffuse / drug therapy
  • [MeSH-minor] Adult. Aged. Diagnosis, Differential. Humans. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Tomography, X-Ray Computed

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  • (PMID = 18218049.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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61. Lin P, Medeiros LJ: High-grade B-cell lymphoma/leukemia associated with t(14;18) and 8q24/MYC rearrangement: a neoplasm of germinal center immunophenotype with poor prognosis. Haematologica; 2007 Oct;92(10):1297-301
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  • [Title] High-grade B-cell lymphoma/leukemia associated with t(14;18) and 8q24/MYC rearrangement: a neoplasm of germinal center immunophenotype with poor prognosis.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Germinal Center / metabolism. Leukemia / genetics. Leukemia / pathology. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / pathology. Proto-Oncogene Proteins c-myc / genetics

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  • [CommentOn] Haematologica. 2007 Oct;92(10):1335-42 [18024371.001]
  • (PMID = 18024366.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Comment; Editorial
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-myc
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62. Rittenbach J, Cao JD, Weiss LM, Rowsell EH, Chick W, Wang J: Primary diffuse large B-cell lymphoma of the uterus presenting solely as an endometrial polyp. Int J Gynecol Pathol; 2005 Oct;24(4):347-51
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  • [Title] Primary diffuse large B-cell lymphoma of the uterus presenting solely as an endometrial polyp.
  • We report a primary diffuse large B-cell lymphoma of endometrial polyp in a 44-year-old woman who presented with irregular vaginal spotting and was found to have a polyp protruding from the cervical os.
  • Histology of the polyp showed an atypical diffuse infiltration by large, mononuclear cells within the stroma and between endometrial glands in one of the polypoid fragments.
  • Immunohistochemistry and testing for immunoglobulin heavy chain gene rearrangement showed a B-cell lineage, consistent with diffuse large B-cell lymphoma.
  • Staging procedures including detailed gynecology examination, body computed tomography scan, and bone marrow examination, as well as total hysterectomy, showed no evidence of lymphoma outside of the polyp.
  • To our knowledge, this represents the first well-documented instance of primary lymphoma of the uterus presenting as an endometrial polyp.
  • The differential diagnosis of endometrial biopsies containing an atypical lymphoid infiltrate should include the rather rare possibility of primary uterine lymphoma arising in an endometrial polyp.
  • Immunohistochemistry and/or molecular analysis for antigen receptor gene rearrangements are critical in arriving at the correct diagnosis.
  • [MeSH-major] Endometrial Neoplasms / pathology. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology. Polyps / pathology. Uterine Neoplasms / pathology
  • [MeSH-minor] Adult. Bone Marrow / pathology. Diagnosis, Differential. Female. Gene Rearrangement, B-Lymphocyte, Heavy Chain / genetics. Humans. Hysterectomy. Immunohistochemistry. Neoplasm Staging. Polymerase Chain Reaction

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  • (PMID = 16175080.001).
  • [ISSN] 0277-1691
  • [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
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63. Pérez-Galán P, Roué G, Villamor N, Campo E, Colomer D: The BH3-mimetic GX15-070 synergizes with bortezomib in mantle cell lymphoma by enhancing Noxa-mediated activation of Bak. Blood; 2007 May 15;109(10):4441-9
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  • [Title] The BH3-mimetic GX15-070 synergizes with bortezomib in mantle cell lymphoma by enhancing Noxa-mediated activation of Bak.
  • Mantle cell lymphoma (MCL) is an aggressive B-cell lymphoma resistant to conventional chemotherapy.
  • The Bcl-2 pathway is deregulated in these tumors and may represent an interesting target for new therapeutic strategies.
  • The new small-molecule pan-Bcl-2 inhibitor GX15-070 mimics BH3-only proteins by binding to multiple antiapoptotic Bcl-2 members.
  • Here we show that GX15-070 induced apoptosis in vitro in MCL cell lines and primary cells from patients with MCL by releasing Bak from Mcl-1 and Bcl-X(L) at short incubation times and low micromolar doses.
  • GX15-070 was effective in cells bearing defective DNA damage-sensor genes or cell-cycle regulators, inducing Bax and Bak conformational changes, mitochondrial depolarization, phosphatidylserine exposure, and caspase-3 activation.
  • Furthermore, GX15-070 synergized with bortezomib, sensitizing MCL cells to low doses of this proteasome inhibitor, by neutralizing bortezomib-induced Mcl-1 accumulation and cooperating with Noxa to induce Bak displacement from this protein.
  • Importantly, GX15-070 alone or in combination with bortezomib showed no significant cytotoxic effect in peripheral blood mononuclear cells from healthy donors.
  • [MeSH-major] Boronic Acids / pharmacology. Lymphoma, Mantle-Cell / drug therapy. Proto-Oncogene Proteins c-bcl-2 / metabolism. Pyrazines / pharmacology. Pyrroles / pharmacology. bcl-2 Homologous Antagonist-Killer Protein / metabolism
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Bortezomib. Drug Synergism. Gene Expression Regulation, Neoplastic. Humans. Molecular Mimicry. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / metabolism. Peptide Fragments / chemistry. Peptide Fragments / pharmacology. Protein Binding. Proto-Oncogene Proteins / chemistry. Proto-Oncogene Proteins / pharmacology. Tumor Cells, Cultured. bcl-X Protein / metabolism

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  • (PMID = 17227835.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAK1 protein, human; 0 / BCL2L1 protein, human; 0 / Bax protein (53-86); 0 / Boronic Acids; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / PMAIP1 protein, human; 0 / Peptide Fragments; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Pyrroles; 0 / bcl-2 Homologous Antagonist-Killer Protein; 0 / bcl-X Protein; 0 / obatoclax; 69G8BD63PP / Bortezomib
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64. Xie Q, Gao CF, Shinomiya N, Sausville E, Hay R, Gustafson M, Shen Y, Wenkert D, Vande Woude GF: Geldanamycins exquisitely inhibit HGF/SF-mediated tumor cell invasion. Oncogene; 2005 May 26;24(23):3697-707
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  • [Title] Geldanamycins exquisitely inhibit HGF/SF-mediated tumor cell invasion.
  • Induction of the urokinase-type plasminogen activator (uPA) by hepatocyte growth factor/scatter factor (HGF/SF) plays an important role in tumor cell invasion and metastasis that is mediated through the Met receptor tyrosine kinase.
  • Previously, we have shown that a subset of GA derivatives exhibit exquisite potency, inhibiting HGF/SF-induced uPA-plasmin activation at femtomolar concentrations (fM-GAi) in canine MDCK cells.
  • Here, we report that (1) inhibition of HGF/SF-induced uPA activity by fM-GAi is not uncommon, in that several human tumor glioblastoma cell lines (DBTRG, U373 and SNB19), as well as SK-LMS-1 human leiomyosarcoma cells are also sensitive to fM-GAi;.
  • (2) fM-GAi drugs only display inhibitory activity against HGF/SF-induced uPA activity (rather than basal activity), and only when the observed magnitude of uPA activity induction by HGF/SF is at least 1.5 times basal uPA activity; and (3) not only do fM-GAi derivatives strongly inhibit uPA activity but they also block MDCK cell scattering and in vitro invasion of human glioblastoma cells at similarly low drug concentrations.
  • These effects of fM-GAi drugs on the Met-activated signaling pathway occur at concentrations well below those required to measurably affect Met expression or cell proliferation.
  • Thus, we show that certain GA drugs (fM-GAi) in an HGF/SF-dependent manner block uPA-plasmin activation in tumor cells at femtomolar levels.
  • Our findings also provide strong circumstantial evidence for a novel non-HSP90 molecular target that is involved in HGF/SF-mediated tumor cell invasion.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Hepatocyte Growth Factor / antagonists & inhibitors. Quinones / pharmacology. Urokinase-Type Plasminogen Activator / antagonists & inhibitors
  • [MeSH-minor] Animals. Benzoquinones. Cell Line. Dogs. HSP90 Heat-Shock Proteins / metabolism. Humans. Lactams, Macrocyclic. Neoplasm Invasiveness. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-met. Receptors, Growth Factor / metabolism

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  • (PMID = 15782129.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Proto-Oncogene Proteins; 0 / Quinones; 0 / Receptors, Growth Factor; 67256-21-7 / Hepatocyte Growth Factor; 73341-73-8 / macbecin II; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; Z3K3VJ16KU / geldanamycin
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65. Kimby E: Management of advanced-stage peripheral T-cell lymphomas. Curr Hematol Malig Rep; 2007 Oct;2(4):242-8
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  • [Title] Management of advanced-stage peripheral T-cell lymphomas.
  • Peripheral T-cell lymphomas (PTCLs), several entities with great clinical, histologic, and biologic heterogeneity, represent 8% to 15% of all malignant lymphomas.
  • Outcome is poorer with PTCL than with aggressive B-cell lymphoma because of more frequent adverse clinical features at diagnosis, a lower response rate to chemotherapy, and a higher incidence of relapses, but it is also known that the T-cell phenotype itself is associated with a poor prognosis independent of other prognostic factors.
  • In fit elderly patients, standard therapy is still six cycles of CHOP-14, but up-front consolidation with intensive chemotherapy and autologous stem cell transplantation are often used in younger patients.
  • The humanized CD52 monoclonal antibody alemtuzumab has shown activity in some T-cell malignancies; with appropriate antibiotic and virostatic prophylaxis, its use seems feasible for PTCL, both as a single agent and in conjunction with chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, T-Cell, Peripheral / drug therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antibodies, Neoplasm / therapeutic use. Antigens, CD / immunology. Antigens, Neoplasm / immunology. Clinical Trials as Topic. Combined Modality Therapy. Drugs, Investigational / therapeutic use. Folic Acid Antagonists / therapeutic use. Glycoproteins / immunology. Histone Deacetylase Inhibitors / therapeutic use. Humans. Immunologic Factors / therapeutic use. Immunotherapy. Mice. Mice, Nude. Multicenter Studies as Topic. Retrospective Studies. Stem Cell Transplantation. Xenograft Model Antitumor Assays

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  • (PMID = 20425376.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / CD52 antigen; 0 / Drugs, Investigational; 0 / Folic Acid Antagonists; 0 / Glycoproteins; 0 / Histone Deacetylase Inhibitors; 0 / Immunologic Factors; 3A189DH42V / alemtuzumab
  • [Number-of-references] 53
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66. Griffiths RW, Suvarna SK, Stone J: Do basal cell carcinomas recur after complete conventional surgical excision? Br J Plast Surg; 2005 Sep;58(6):795-805
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  • [Title] Do basal cell carcinomas recur after complete conventional surgical excision?
  • For 1378 patients treated in the 11 years 1988-1998 by conventional excision of 1635 basal cell carcinomas, 1516 first index lesions were histologically completely excised.
  • Two thirds of possible and probable recurrences occurred in the temple and forehead, although these sites represented only 22% of all lesions, which may rather suggest new lesions in an area of field change as opposed to residual disease.
  • These figures indicate there is a low order of probability for the incidence of recurrent basal cell carcinoma during minimum 5 years follow period after conventional surgical excision and conventional histological assessment of tumour resection margins.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Neoplasm Recurrence, Local / pathology. Skin Neoplasms / pathology

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  • [CommentIn] J Plast Reconstr Aesthet Surg. 2007;60(4):451-3 [17349608.001]
  • [CommentIn] J Plast Reconstr Aesthet Surg. 2006;59(11):1247 [17046636.001]
  • (PMID = 16086990.001).
  • [ISSN] 0007-1226
  • [Journal-full-title] British journal of plastic surgery
  • [ISO-abbreviation] Br J Plast Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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67. Ikuerowo SO, Kuczyk MA, Mengel M, van der Heyde E, Shittu OB, Vaske B, Jonas U, Machtens S, Serth J: Alteration of subcellular and cellular expression patterns of cyclin B1 in renal cell carcinoma is significantly related to clinical progression and survival of patients. Int J Cancer; 2006 Aug 15;119(4):867-74
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  • [Title] Alteration of subcellular and cellular expression patterns of cyclin B1 in renal cell carcinoma is significantly related to clinical progression and survival of patients.
  • Cyclin B1, identified as a regulator of late cell cycle, is involved in the development and progression of a variety of human malignancies.
  • To clarify the role of cyclin B1 in the pathogenesis and prognosis of renal cell carcinoma (RCC), protein expression was compared with clinicopathological characteristics of patients as well as the long-term survival after surgical therapy.
  • Immunopositivity within the primary tumors was significantly associated with tumor stage (pT) (p < 0.01), lymph node status (pN) (p < 0.01) as well as the presence of systemic metastatic disease (p = 0.01).
  • Subcellular expression in the cytoplasm of tumor cells significantly correlated with pT (p = 0.02) and pN (p = 0.03).
  • When peritumoral tissue samples exhibited a relative amount of <10% of positively reacting epithelial cells, cyclin B positivity was identified to predict long-term survival of patients in univariate analysis (p < 0.01) whereas borderline significance was observed in multivariate statistical analysis (p = 0.05).
  • Increased intratumoral cyclin B1 positivity and aberrant localization of signals within the cytoplasm of tumor cells is positively correlated with the tendency towards tumor progression, indicating the significant role of cyclin B1 in the development and pathogenesis of RCC.
  • [MeSH-major] Carcinoma, Renal Cell / metabolism. Carcinoma, Renal Cell / pathology. Cyclin B / metabolism. Gene Expression Regulation, Neoplastic
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cyclin B1. Disease Progression. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness / pathology. Subcellular Fractions / metabolism. Survival Rate

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 16557593.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCNB1 protein, human; 0 / Cyclin B; 0 / Cyclin B1
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68. Shimizu Y, Tanae K, Takahashi N, Kohri M, Arai E, Bessho M, Niitsu N: Primary cutaneous anaplastic large-cell lymphoma presenting with hemophagocytic syndrome: a case report and review of the literature. Leuk Res; 2010 Feb;34(2):263-6
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  • [Title] Primary cutaneous anaplastic large-cell lymphoma presenting with hemophagocytic syndrome: a case report and review of the literature.
  • Primary cutaneous anaplastic large-cell lymphoma (C-ALCL) is a rare entity of lymphoma.
  • Histopathological examination of the skin biopsy specimens showed non-epidermotropic infiltrates with cohesive sheets of large tumor cells.
  • The tumor cells showed CD4-, CD8+, CD30+, CD56-, ALK-, TIA-1+, and granzyme B+.
  • C-ALCL is generally a disorder that progresses slowly and has a good prognosis.
  • [MeSH-major] Lymphohistiocytosis, Hemophagocytic / etiology. Lymphoma, Large-Cell, Anaplastic / complications. Skin Ulcer / etiology
  • [MeSH-minor] Adult. Disease-Free Survival. Humans. Immunohistochemistry. Male. Neoplasm Invasiveness. Skin Neoplasms / etiology. Skin Neoplasms / pathology

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  • [Copyright] Copyright 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19640585.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 12
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69. Nikolova DA, Asangani IA, Nelson LD, Hughes DP, Siwak DR, Mills GB, Harms A, Buchholz E, Pilz LR, Manegold C, Allgayer H: Cetuximab attenuates metastasis and u-PAR expression in non-small cell lung cancer: u-PAR and E-cadherin are novel biomarkers of cetuximab sensitivity. Cancer Res; 2009 Mar 15;69(6):2461-70
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  • [Title] Cetuximab attenuates metastasis and u-PAR expression in non-small cell lung cancer: u-PAR and E-cadherin are novel biomarkers of cetuximab sensitivity.
  • Cetuximab, which blocks ligand binding to epidermal growth factor receptor (EGFR), is currently being studied as a novel treatment for non-small cell lung cancer (NSCLC).
  • (b) investigate urokinase-type plasminogen activator receptor (u-PAR), a major molecule promoting invasion and metastasis, as a target molecule;.
  • Cetuximab treatment resulted in reduced growth and Matrigel invasion of H1395 and A549 NSCLC cell lines, in parallel with reduced u-PAR mRNA and protein. u-PAR down-regulation was brought about by suppressing the binding of JunD and c-Jun to u-PAR promoter motif -190/-171 in vivo, and an inhibition of MAP/ERK kinase signaling.
  • Low E-cadherin and high u-PAR, but not EGFR, was associated with resistance to Cetuximab in seven NSCLC cell lines.

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  • (PMID = 19276367.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA118730-04; United States / NCI NIH HHS / CA / P50 CA098258; United States / NCI NIH HHS / CA / K08 CA118730-04; United States / NCI NIH HHS / CA / K08 CA118730
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Proto-Oncogene Proteins c-jun; 0 / Receptors, Urokinase Plasminogen Activator; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; PQX0D8J21J / Cetuximab
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70. Ji H, Zhang WY, Liu WP, Li GD, Li L: [Mediastinal (thymic) large B-cell lymphoma: three cases reports]. Zhonghua Bing Li Xue Za Zhi; 2005 May;34(5):315-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Mediastinal (thymic) large B-cell lymphoma: three cases reports].
  • [MeSH-major] Lymphoma, B-Cell / pathology. Mediastinal Neoplasms / pathology
  • [MeSH-minor] Adolescent. Aged. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Cyclophosphamide / administration & dosage. Diagnosis, Differential. Doxorubicin / administration & dosage. Female. Hodgkin Disease / pathology. Humans. Lung Neoplasms / pathology. Male. Mediastinum / surgery. Neoplasm Invasiveness. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Prednisone / administration & dosage. Thymoma / pathology. Thymus Neoplasms / pathology. Vincristine / administration & dosage

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  • (PMID = 16181560.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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71. Müller-Richter UD, Dowejko A, Reuther T, Kleinheinz J, Reichert TE, Driemel O: Analysis of expression profiles of MAGE-A antigens in oral squamous cell carcinoma cell lines. Head Face Med; 2009;5:10
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  • [Title] Analysis of expression profiles of MAGE-A antigens in oral squamous cell carcinoma cell lines.
  • Their differential expression profiles also modulate the course of the cancer disease and its response to antineoplastic drugs.
  • METHODS: The expression profiles of MAGE-A2, -A3, -A4, -A6 and -A10 in five own oral squamous cell carcinoma cell lines were characterised by rt-PCR, qrt-PCR and immunocytochemistry with a global MAGE-A antibody (57B) and compared with those of an adult keratinocyte cell line (NHEK).
  • RESULTS: All tumour cell lines expressed MAGE-A antigens.
  • MAGE-A10 was not expressed in the cell lines tested.
  • The MAGE-A gene products detected in the adult keratinocyte cell line NHEK were used as a reference.
  • CONCLUSION: MAGE-A antigens are expressed in oral squamous cell carcinomas.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Carcinoma, Squamous Cell / immunology. Mouth Neoplasms / immunology
  • [MeSH-minor] Adult. Cell Line, Tumor. Female. Gene Expression. Gene Expression Regulation, Neoplastic. Humans. Male. Neoplasm Proteins / metabolism

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  • (PMID = 19358718.001).
  • [ISSN] 1746-160X
  • [Journal-full-title] Head & face medicine
  • [ISO-abbreviation] Head Face Med
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / MAGE-A10 antigen; 0 / MAGEA3 protein, human; 0 / MAGEA4 protein, human; 0 / MAGEA6 protein, human; 0 / Mage-a2 antigen; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2690579
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72. Veraldi GF, Tasselli S, De Manzoni G, Cordiano C: Surgical treatment of abdominal aortic aneurysm with concomitant renal cell carcinoma: a single-centre experience with review of the literature. J Cardiovasc Surg (Torino); 2006 Dec;47(6):643-9
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  • [Title] Surgical treatment of abdominal aortic aneurysm with concomitant renal cell carcinoma: a single-centre experience with review of the literature.
  • In 61 cases (6.7%) an association with a solid neoplasm was found; in 12 cases (1.3%) the neoplasm was a renal cell carcinoma.
  • Performing a two-stage approach, the procedure for the disease regarded as life-threatening is performed first.
  • Priority should be given to renal cell neoplasm in selected cases.
  • [MeSH-major] Aortic Aneurysm, Abdominal / surgery. Aortic Rupture / surgery. Carcinoma, Renal Cell / surgery. Kidney Neoplasms / surgery. Nephrectomy. Vascular Surgical Procedures


73. Oehlrich N, Devitt G, Linnebacher M, Schwitalle Y, Grosskinski S, Stevanovic S, Zöller M: Generation of RAGE-1 and MAGE-9 peptide-specific cytotoxic T-lymphocyte lines for transfer in patients with renal cell carcinoma. Int J Cancer; 2005 Nov 01;117(2):256-64
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  • [Title] Generation of RAGE-1 and MAGE-9 peptide-specific cytotoxic T-lymphocyte lines for transfer in patients with renal cell carcinoma.
  • Renal cell carcinomas (RCCs) are supposed to be immunogenic, and several clinical trials of immunotherapy using tumor lysate-pulsed dendritic cells (DCs) have been performed.
  • CTLs were generated by coculture with peptide-pulsed, activated B cells, which were easily generated in great quantities and displayed functional activity for a prolonged period of time.
  • MAGE-9 and RAGE-1 peptide-specific CTL lines were strictly peptide-specific and displayed high cytotoxic activity not only against peptide-loaded T2 cells but also against HLA-A*0201-positive RCC lines, which naturally express MAGE-9, RAGE-1 or both.
  • Thus, B cells are well suited as APCs for the generation of large numbers of tumor peptide-specific CTLs for adoptive transfer.
  • [MeSH-major] Antigens, Neoplasm / genetics. Carcinoma, Renal Cell / immunology. Mitogen-Activated Protein Kinases / genetics. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 15900605.001).
  • [ISSN] 0020-7136
  • [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 / Antigens, Neoplasm; 0 / HLA-A Antigens; 0 / HLA-A*02:01 antigen; 0 / HLA-A2 Antigen; 0 / MAGE-9 antigen, human; 0 / Peptide Fragments; EC 2.7.11.22 / MOK protein, human; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
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74. Chaiswing L, Zhong W, Cullen JJ, Oberley LW, Oberley TD: Extracellular redox state regulates features associated with prostate cancer cell invasion. Cancer Res; 2008 Jul 15;68(14):5820-6
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  • [Title] Extracellular redox state regulates features associated with prostate cancer cell invasion.
  • We have examined the possible role of extracellular reduction-oxidation (redox) state in regulation of biological/biochemical features associated with prostate cancer cell invasion.
  • DU145, PC-3, and RWPE1-derived human prostate cancer (WPE1-NB26) cell lines were used for the present in vitro analysis.
  • Increasing levels of nitric oxide using S-nitroso-N-acetylpenicillamine resulted in a decrease in cell invasion ability, whereas increasing levels of extracellular superoxide radical (O(2)(*-)) using xanthine/xanthine oxidase resulted in an increase in cell invasion ability in these three cell lines.
  • WPE1-NB26 cells exhibited an increased glutathione/glutathione disulfide ratio in the medium in comparison with RWPE1 cells (immortalized but nonmalignant prostate epithelial cells), suggesting an alteration of extracellular redox state of WPE1-NB26 cells.
  • We hypothesized that O(2)(*-) production at or near the plasma membrane or in the adjacent extracellular matrix at least partially regulated prostate cancer cell invasion.
  • Using adenovirus-mediated extracellular superoxide dismutase (EC-SOD) gene transduction to enzymatically decrease O(2)(*-) levels, we showed that in the presence of heparin, adenovirus EC-SOD gene transduction resulted in an increase in the expression of EC-SOD outside the cells with resultant inhibition of cell invasion ability.
  • This inhibition correlated with reduced metalloproteinase [matrix metalloproteinase (MMP) 2/membrane type 1-MMP] activities and increased levels of extracellular nitrite.
  • Our results suggest a prominent role of extracellular redox status in regulation of cell invasion, which may provide opportunities for therapeutic interventions.
  • [MeSH-minor] Cell Line, Tumor. Glutathione / metabolism. Humans. Male. Matrix Metalloproteinases / metabolism. Models, Biological. Models, Chemical. NADPH Oxidase / metabolism. Neoplasm Invasiveness. Nitrites / metabolism. Oxygen / metabolism. Superoxide Dismutase / metabolism

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  • (PMID = 18632636.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nitrites; EC 1.15.1.1 / Superoxide Dismutase; EC 1.6.3.1 / NADPH Oxidase; EC 3.4.24.- / Matrix Metalloproteinases; GAN16C9B8O / Glutathione; S88TT14065 / Oxygen
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75. Ding HY, Gao LX: [Spindle cell carcinoma of breast with neuroendocrine differentiation]. Zhonghua Bing Li Xue Za Zhi; 2006 Jan;35(1):13-7
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  • [Title] [Spindle cell carcinoma of breast with neuroendocrine differentiation].
  • OBJECTIVE: To describe the morphologic features and immunohistochemistry of spindle cell carcinoma of breast with neuroendocrine differentiation.
  • METHODS: Retrospective review of 2500 cases of breast carcinoma showed 5 cases (0.2%) with a predominance (> 80%) of spindle cell component.
  • Amongst the 5 cases studied, 2 represented intraductal spindle cell carcinoma and 3 represented invasive spindle cell carcinoma.
  • Histologically, all tumors were predominantly composed of elongated spindle cells.
  • Three of these cases also contained tumor cells with vacuolated cytoplasm, alcian blue-positive tumor cells were observed in 4 cases.
  • Immunohistochemically, the spindle tumor cells in all cases expressed AE1/AE3, CEA, EMA, E-cadherin and synaptophysin.
  • Two cases of intraductal spindle cell carcinoma and 1 of the 3 cases of invasive spindle cell carcinoma were classified as neuroendocrine carcinoma of spindle cell type, while the remaining 2 cases of invasive spindle cell carcinoma were considered as metaplastic carcinoma with neuroendocrine differentiation.
  • Amongst the 4 patients with follow-up information available, 3 were still alive 24 to 58 months after the initial diagnosis.
  • One patient died within 27 months of diagnosis.
  • CONCLUSIONS: The presence of spindle tumor cells and sometimes intracytoplasmic mucin are useful morphologic clues in diagnosing spindle cell carcinoma of the breast with neuroendocrine differentiation.
  • Intraductal neuroendocrine spindle cell carcinoma needs to be distinguished from usual ductal hyperplasia and intraductal papilloma.
  • On the other hand, invasive spindle cell carcinoma with neuroendocrine differentiation needs to be distinguished from spindle cell myoepithelioma, malignant melanoma and sometimes soft tissue neoplasm.
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Chromogranin A. Chromogranins / analysis. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Middle Aged. Phosphopyruvate Hydratase / analysis. Retrospective Studies. Synaptophysin / analysis


76. Laurenti L, Tarnani M, Efremov DG, Chiusolo P, De Padua L, Sica S, Leone G: Efficacy and safety of low-dose alemtuzumab as treatment of autoimmune hemolytic anemia in pretreated B-cell chronic lymphocytic leukemia. Leukemia; 2007 Aug;21(8):1819-21; author reply 1821
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  • [Title] Efficacy and safety of low-dose alemtuzumab as treatment of autoimmune hemolytic anemia in pretreated B-cell chronic lymphocytic leukemia.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal / administration & dosage. Antibodies, Neoplasm / administration & dosage. Antineoplastic Agents / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / complications


77. Munday JS, Howe L, French A, Squires RA, Sugiarto H: Detection of papillomaviral DNA sequences in a feline oral squamous cell carcinoma. Res Vet Sci; 2009 Apr;86(2):359-61
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  • [Title] Detection of papillomaviral DNA sequences in a feline oral squamous cell carcinoma.
  • Oral squamous cell carcinomas (OSCCs) are common and often fatal feline neoplasms.
  • Factors that predispose to neoplasm development in cats are poorly defined.
  • To determine if PVs are associated with OSCCs in cats, three sets of consensus primers were used to evaluate 20 feline OSCCs and 20 non-neoplastic feline oral lesions for the presence of PV DNA.
  • Papillomaviral sequences were detected within one OSCC, but no non-neoplastic lesion.
  • Sequencing of the amplified DNA revealed a previously unreported PV that was most similar to human PV type 76.
  • However, while these results suggest that feline gingival epithelial cells can be infected by PVs, they do not support a causal association between viral infection and the development of feline OSCCs.
  • [MeSH-major] Cat Diseases / virology. Mouth Neoplasms / veterinary. Neoplasms, Squamous Cell / veterinary. Papillomaviridae / isolation & purification. Papillomavirus Infections / veterinary

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  • (PMID = 18715602.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ EF535004
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Viral
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78. Ban JO, Yuk DY, Woo KS, Kim TM, Lee US, Jeong HS, Kim DJ, Chung YB, Hwang BY, Oh KW, Hong JT: Inhibition of cell growth and induction of apoptosis via inactivation of NF-kappaB by a sulfurcompound isolated from garlic in human colon cancer cells. J Pharmacol Sci; 2007 Aug;104(4):374-83
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  • [Title] Inhibition of cell growth and induction of apoptosis via inactivation of NF-kappaB by a sulfurcompound isolated from garlic in human colon cancer cells.
  • Nuclear transcription factor-kappaB (NF-kappaB) has been known to be an implicated factor in apoptotic cell death of several cancer cells.
  • In this study, we investigated whether a sulfurcompound (named thiacremonone) isolated from garlic could modulate NF-kappaB activity and thereby induce apoptotic cell death of colon cancer cells.
  • Treatment with different concentrations (30 - 150 microg/ml) of thiacremonone for various periods (0 - 48 h) inhibited colon cancer cell (SW620 and HCT116) growth followed by induction of apoptosis in a dose-dependent manner.
  • Moreover, thiacremonone suppressed NF-kappaB target anti-apoptotic genes (Bcl-2, cIAP1/2, and XIAP) and inflammatory genes (iNOS and COX-2), whereas it induced apoptotic genes (Bax, cleaved caspse-3, and cleaved PARP) expression.
  • These results suggest that a novel sulfurocompound from garlic inhibited colon cancer cell growth through induction of apoptotic cell death by modulating of NF-kappaB.
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Colonic Neoplasms / genetics. Colonic Neoplasms / metabolism. DNA, Neoplasm / drug effects. DNA, Neoplasm / metabolism. Dose-Response Relationship, Drug. Electrophoretic Mobility Shift Assay. Humans. Tetradecanoylphorbol Acetate. Transcription, Genetic / drug effects. Tumor Necrosis Factor-alpha / drug effects. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 17721042.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / NF-kappa B; 0 / Thiophenes; 0 / Tumor Necrosis Factor-alpha; 0 / thiacremonone; NI40JAQ945 / Tetradecanoylphorbol Acetate
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79. Sirianni N, Wang J, Ferris RL: Antiviral activity of Cidofovir on a naturally human papillomavirus-16 infected squamous cell carcinoma of the head and neck (SCCHN) cell line improves radiation sensitivity. Oral Oncol; 2005 Apr;41(4):423-8
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  • [Title] Antiviral activity of Cidofovir on a naturally human papillomavirus-16 infected squamous cell carcinoma of the head and neck (SCCHN) cell line improves radiation sensitivity.
  • High risk HPV types 16 and 18 are associated with cervical cancer and squamous cell carcinoma of the head and neck (SCCHN).
  • Cidofovir is an antiviral drug used to treat HPV-induced laryngeal papillomatosis and other viral infections, with initial reports suggesting activity in cervical carcinoma cells.
  • We investigated the effects of Cidofovir on a naturally HPV-16-transformed SCCHN cell line (UPCI:SCC090), in comparison with a cervical carcinoma cell line (CasKi) of similar viral characteristics, to evaluate its therapeutic potential.
  • HPV-16 gene transcription was only marginally reduced, and the antiviral and p53 restorative effects were modest in SCC90 cells.
  • However, combination with irradiation enhanced the effects of Cidofovir treatment on these cells.
  • Several days of treatment were required for this effect, which may limit its clinical applicability.
  • Future therapies for HPV-associated tumors may include intralesional antiviral therapy in combination with radiation therapy, but optimization for clinical utility is needed.
  • [MeSH-major] Antiviral Agents / pharmacology. Carcinoma, Squamous Cell / virology. Cytosine / analogs & derivatives. Cytosine / pharmacology. Head and Neck Neoplasms / virology. Organophosphonates / pharmacology. Papillomaviridae / drug effects
  • [MeSH-minor] Adult. Blotting, Western. Cell Survival / drug effects. Cell Survival / radiation effects. Humans. Male. Neoplasm Proteins / metabolism. Oncogene Proteins, Viral / metabolism. Papillomavirus Infections / complications. Papillomavirus Infections / metabolism. Radiation Tolerance / drug effects. Repressor Proteins / metabolism. Reverse Transcriptase Polymerase Chain Reaction / methods. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15792615.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / E6 protein, Human papillomavirus type 16; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Viral; 0 / Organophosphonates; 0 / Repressor Proteins; 0 / Tumor Suppressor Protein p53; 8J337D1HZY / Cytosine; JIL713Q00N / cidofovir
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80. Yokoyama H, Ikehara Y, Kodera Y, Ikehara S, Yatabe Y, Mochizuki Y, Koike M, Fujiwara M, Nakao A, Tatematsu M, Nakanishi H: Molecular basis for sensitivity and acquired resistance to gefitinib in HER2-overexpressing human gastric cancer cell lines derived from liver metastasis. Br J Cancer; 2006 Dec 4;95(11):1504-13
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  • [Title] Molecular basis for sensitivity and acquired resistance to gefitinib in HER2-overexpressing human gastric cancer cell lines derived from liver metastasis.
  • We developed three new HER2-overexpressing gastric cancer cell lines (GLM-1, GLM-2, GLM-4) without epidermal growth factor receptor (EGFR) mutations derived from such liver metastasis, two of which had HER2 gene amplifications.
  • All these GLM series of cell lines were highly sensitive to gefitinib in vitro, a specific inhibitor of EGFR tyrosine kinase (Iressa) rather than anti-HER2 antibody trastuzumab (Herceptin), whereas most of the HER2 low-expressing counterparts were not.
  • On the other hand, gefitinib-resistant cells (GLM-1R) exhibited increased EGFR expression, followed by constitutive activation of mitogen-activated protein kinase (MAPK) pathway.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Resistance, Neoplasm / physiology. Liver Neoplasms / metabolism. Quinazolines / pharmacology. Receptor, ErbB-2 / metabolism. Stomach Neoplasms / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Humans. Immunohistochemistry. Male. Mice. Mice, Nude. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / metabolism


81. Lewis KG, Weinstock MA, Weaver AL, Otley CC: Adjuvant local irradiation for Merkel cell carcinoma. Arch Dermatol; 2006 Jun;142(6):693-700
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  • [Title] Adjuvant local irradiation for Merkel cell carcinoma.
  • OBJECTIVES: To determine the effect of adjuvant local irradiation on (1) disease recurrence and (2) survival rates in Merkel cell carcinoma (MCC).
  • DATA SOURCES: An Ovid MEDLINE search (January 1966-May 26, 2004) was performed using the following criteria: group 1, "Merkel cell OR trabecular OR neuroendocrine skin OR APUDoma skin OR primary small cell skin OR primary undifferentiated skin OR endocrine skin OR neuroepithelial" AND group 2, "carcinoma OR tumor OR cancer" with mapping modifiers "-title, -abstract, -keyword, -subject heading."
  • (1) a histopathologic diagnosis of MCC;.
  • (5) during the postoperative follow-up period, disease recurrence, progression, and survival and/or duration of event-free interval was documented with (6) a minimum follow-up of 1 month.
  • [MeSH-major] Carcinoma, Merkel Cell / radiotherapy. Neoplasm Recurrence, Local / radiotherapy. Skin Neoplasms / radiotherapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Staging. Radiotherapy, Adjuvant. Survival Analysis


82. Suzigan S, Drut R, Faria P, Argani P, De Marzo AM, Barbosa RN, Mello Denadai ER, Martins-Filho J, Martucci RC, Bauab T Jr: Xp11 translocation carcinoma of the kidney presenting with multilocular cystic renal cell carcinoma-like features. Int J Surg Pathol; 2007 Apr;15(2):199-203
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  • [Title] Xp11 translocation carcinoma of the kidney presenting with multilocular cystic renal cell carcinoma-like features.
  • Partial nephrectomy revealed an epithelial neoplasm with multilocular cystic renal cell carcinoma pattern.
  • The cells exhibited strong nuclear reactivity for TFE3 protein and supported the diagnosis of Xp11 translocation carcinoma of the kidney.
  • The example emphasizes the high index of suspicion needed for an accurate diagnosis of renal carcinomas.
  • [MeSH-major] Carcinoma, Renal Cell / genetics. Chromosomes, Human, Pair 1. Chromosomes, Human, X. Kidney Neoplasms / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Basic Helix-Loop-Helix Leucine Zipper Transcription Factors / metabolism. Cell Nucleus / metabolism. Cell Nucleus / pathology. Female. Humans. Nephrectomy

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  • (PMID = 17478783.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Basic Helix-Loop-Helix Leucine Zipper Transcription Factors; 0 / TFE3 protein, human
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83. Hu Y, Lin DM, Cheng SJ, Liu YN, Feng FY: [Influences of PC cell-derived growth factor and breast cancer resistance protein on the curative effects of platinum-based chemotherapeutic regimens for advanced non-small cell lung cancer]. Zhonghua Yi Xue Za Zhi; 2006 Oct 10;86(37):2611-4
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  • [Title] [Influences of PC cell-derived growth factor and breast cancer resistance protein on the curative effects of platinum-based chemotherapeutic regimens for advanced non-small cell lung cancer].
  • OBJECTIVE: To investigate the influences of PC cell-derived growth factor (PCDGF) and breast cancer resistance protein (BCRP) on the curative effects of platinum-based chemotherapeutic regimens for advanced non-small cell lung cancer (NSCLC).
  • [MeSH-major] ATP-Binding Cassette Transporters / biosynthesis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Intercellular Signaling Peptides and Proteins / biosynthesis. Lung Neoplasms / drug therapy. Neoplasm Proteins / biosynthesis
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Adult. Aged. Cisplatin / administration & dosage. Drug Resistance, Neoplasm. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging

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  • (PMID = 17198586.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / GRN protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; Q20Q21Q62J / Cisplatin
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84. Günther S, Ruhe C, Derikito MG, Böse G, Sauer H, Wartenberg M: Polyphenols prevent cell shedding from mouse mammary cancer spheroids and inhibit cancer cell invasion in confrontation cultures derived from embryonic stem cells. Cancer Lett; 2007 May 18;250(1):25-35
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  • [Title] Polyphenols prevent cell shedding from mouse mammary cancer spheroids and inhibit cancer cell invasion in confrontation cultures derived from embryonic stem cells.
  • The prognosis of cancer disease is worsened upon shedding of tumor cells from the primary tumor, which escape to the blood stream and form metastases at distant sites within the body.
  • Inhibition of cell shedding from the primary tumor could therefore be exploited to avoid metastasis and delay the progression of the cancer disease.
  • In the present study, we investigated the effects of the polyphenols resveratrol, baicalein, epicatechin, epigallocatechin and polyphenon 60 on cell shedding from multicellular tumor spheroids of the murine mammacarcinoma cell line 4T1, cell invasion into embryonic stem cell-derived tissues, generation of reactive oxygen species (ROS) and expression of matrix metalloproteinase 9 (MMP-9).
  • With increasing tumor spheroid growth MMP-9 expression was upregulated and cells detached from tumor spheroids and formed subspheroids that displayed pronounced ROS generation.
  • Upon incubation with polyphenols tumor growth was arrested and cell shedding was totally abolished.
  • Furthermore, polyphenols significantly inhibited invasion of tumor cells into embryonic stem cell-derived, vascularized tissues.
  • Our data suggest, that polyphenols inhibit cell shedding and invasion by their anti-oxidative capacity and downregulation of MMP-9 expression.
  • [MeSH-major] Embryonic Stem Cells. Flavonoids / pharmacology. Mammary Neoplasms, Experimental / pathology. Neoplasm Invasiveness / prevention & control. Phenols / pharmacology. Spheroids, Cellular / drug effects
  • [MeSH-minor] Animals. Cell Culture Techniques / methods. Cell Line. Immunohistochemistry. Matrix Metalloproteinase 9 / metabolism. Mice. Polyphenols. Reactive Oxygen Species / metabolism

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  • (PMID = 17070989.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Flavonoids; 0 / Phenols; 0 / Polyphenols; 0 / Reactive Oxygen Species; EC 3.4.24.35 / Matrix Metalloproteinase 9
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85. Lissitchkov T, Arnaudov G, Peytchev D, Merkle Kh: Phase-I/II study to evaluate dose limiting toxicity, maximum tolerated dose, and tolerability of bendamustine HCl in pre-treated patients with B-chronic lymphocytic leukaemia (Binet stages B and C) requiring therapy. J Cancer Res Clin Oncol; 2006 Feb;132(2):99-104
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  • [Title] Phase-I/II study to evaluate dose limiting toxicity, maximum tolerated dose, and tolerability of bendamustine HCl in pre-treated patients with B-chronic lymphocytic leukaemia (Binet stages B and C) requiring therapy.
  • PURPOSE: Bendamustine hydrochloride, an anti-neoplastic agent with unique mechanism of action, is known to cause impressive remissions in relapsed non-Hodgkin's lymphoma and chronic lymphocytic leukaemia (CLL).
  • Bendamustine was given at a starting dose of 100 mg/m2 on days 1 and 2 every 3 weeks based on the previous results in lymphoma.
  • A bendamustine dose of 100 mg/m2 is the recommended dose for further clinical investigations.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Nitrogen Mustard Compounds / administration & dosage. Nitrogen Mustard Compounds / adverse effects
  • [MeSH-minor] Aged. Bendamustine Hydrochloride. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Time Factors. Treatment Outcome

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  • [Cites] Semin Oncol. 2002 Aug;29(4 Suppl 13):33-45 [12170431.001]
  • [Cites] Anticancer Drugs. 1996 Jun;7(4):415-21 [8826610.001]
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  • [Cites] Semin Oncol. 2002 Aug;29(4 Suppl 13):19-22 [12170428.001]
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  • (PMID = 16292542.001).
  • [ISSN] 0171-5216
  • [Journal-full-title] Journal of cancer research and clinical oncology
  • [ISO-abbreviation] J. Cancer Res. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitrogen Mustard Compounds; 981Y8SX18M / Bendamustine Hydrochloride
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86. Paoluzzi L, Gonen M, Bhagat G, Furman RR, Gardner JR, Scotto L, Gueorguiev VD, Heaney ML, Manova K, O'Connor OA: The BH3-only mimetic ABT-737 synergizes the antineoplastic activity of proteasome inhibitors in lymphoid malignancies. Blood; 2008 Oct 1;112(7):2906-16
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  • Overexpression of antiapoptotic members of the Bcl-2 family is observed in approximately 80% of B-cell lymphomas, contributing to intrinsic and acquired drug resistance.
  • ABT-737 is a BH3-only mimetic and potent inhibitor of the antiapoptotic Bcl-2 family members Bcl-2, Bcl-X(L), and Bcl-w.
  • In vitro, ABT-737 exhibited concentration-dependent cytotoxicity against a broad panel of lymphoma cell lines including mantle cell lymphoma (MCL) and diffuse large B-cell lymphoma (DLBCL).
  • ABT-737 showed synergism when combined with the proteasome inhibitors bortezomib or carfilzomib in select lymphoma cell lines and induced potent mitochondrial membrane depolarization and apoptosis when combined with either.
  • ABT-737 plus bortezomib also induced significant apoptosis in primary samples of MCL, DLBCL, and chronic lymphocytic leukemia (CLL) but no significant cytotoxic effect was observed in peripheral blood mononuclear cells from healthy donors.
  • Collectively, these data suggest that ABT-737 alone or in combination with a proteasome inhibitor represents a novel and potentially important platform for the treatment of B-cell malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biphenyl Compounds / pharmacology. Enzyme Inhibitors / pharmacology. Lymphoma / enzymology. Lymphoma / pathology. Molecular Mimicry / drug effects. Nitrophenols / pharmacology. Proteasome Inhibitors. Sulfonamides / pharmacology
  • [MeSH-minor] Animals. Boronic Acids / pharmacology. Bortezomib. Cell Death / drug effects. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm / drug effects. Drug Synergism. Health. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukocytes, Mononuclear / drug effects. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / pathology. Membrane Potential, Mitochondrial / drug effects. Mice. Microscopy, Confocal. Piperazines / pharmacology. Proto-Oncogene Proteins c-bcl-2 / metabolism. Pyrazines / pharmacology. Tissue Donors. Xenograft Model Antitumor Assays

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  • (PMID = 18591385.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABT-737; 0 / Antineoplastic Agents; 0 / Biphenyl Compounds; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Nitrophenols; 0 / Piperazines; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Pyrazines; 0 / Sulfonamides; 69G8BD63PP / Bortezomib
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87. Grubstein A, Givon-Madhala O, Morgenstern S, Cohen M: Extranodal primary B-cell non-Hodgkin lymphoma of the breast mimicking acute mastitis. J Clin Ultrasound; 2005 Mar-Apr;33(3):140-2
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  • [Title] Extranodal primary B-cell non-Hodgkin lymphoma of the breast mimicking acute mastitis.
  • We report a case of primary, high-grade non-Hodgkin B-cell lymphoma in the breast of a young woman.
  • The clinical and sonographic presentation was not of a mass but of an infiltrating anechoic process mimicking mastitis.
  • Primary breast lymphoma is a rare entity, especially in young females.
  • In previous imaging reports of breast lymphoma, it has always been considered as a mass, though the presence of markedly hypoechoic regions that look like fluid collections is a well known sonographic characteristic of lymphoma.
  • [MeSH-major] Breast Neoplasms / ultrasonography. Lymphoma, B-Cell / ultrasonography. Mastitis / diagnosis
  • [MeSH-minor] Acute Disease. Adult. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Positron-Emission Tomography. Tomography, X-Ray Computed. Ultrasonography, Mammary


88. Ito N, Eto M, Nakamura E, Takahashi A, Tsukamoto T, Toma H, Nakazawa H, Hirao Y, Uemura H, Kagawa S, Kanayama H, Nose Y, Kinukawa N, Nakamura T, Jinnai N, Seki T, Takamatsu M, Masui Y, Naito S, Ogawa O: STAT3 polymorphism predicts interferon-alfa response in patients with metastatic renal cell carcinoma. J Clin Oncol; 2007 Jul 1;25(19):2785-91
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  • [Title] STAT3 polymorphism predicts interferon-alfa response in patients with metastatic renal cell carcinoma.
  • PURPOSE: To clarify the effect of genetic polymorphisms on the response to interferon alfa (IFN-alpha) for metastatic renal cell carcinoma (MRCC), and to find a reliable molecular marker to select those patients with MRCC who would benefit from IFN-alpha immunotherapy.
  • Genotype-dependent expressions of STAT3 in B lymphocyte cell lines and the enhanced growth inhibitory effects of IFN- by STAT3 suppression in an RCC cell line supported the results of the present association study.
  • [MeSH-major] Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / genetics. Interferon-alpha / therapeutic use. Kidney Neoplasms / drug therapy. Polymorphism, Genetic. STAT3 Transcription Factor / genetics. STAT3 Transcription Factor / physiology
  • [MeSH-minor] Female. Humans. Immunotherapy / methods. Japan. Linkage Disequilibrium. Male. Neoplasm Metastasis. Odds Ratio. Polymorphism, Single Nucleotide. Treatment Outcome


89. Park JK, Jung HY, Park SH, Kang SY, Yi MR, Um HD, Hong SH: Combination of PTEN and gamma-ionizing radiation enhances cell death and G(2)/M arrest through regulation of AKT activity and p21 induction in non-small-cell lung cancer cells. Int J Radiat Oncol Biol Phys; 2008 Apr 1;70(5):1552-60
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  • [Title] Combination of PTEN and gamma-ionizing radiation enhances cell death and G(2)/M arrest through regulation of AKT activity and p21 induction in non-small-cell lung cancer cells.
  • PURPOSE: To identify the role of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) during gamma-ionizing radiation (gamma-IR) treatment for non-small-cell lung cancer cells.
  • METHODS AND MATERIALS: Wild-type PTEN or mutant forms of PTEN plasmids were transfected to construct stable transfectants of the NCI-H1299 non-small-cell lung cancer cell line.
  • Combined effects of PTEN expression and IR treatment were tested using immunoblot, clonogenic, and cell-counting assays.
  • When treated with gamma-IR, wild-type PTEN transfectants showed higher levels of cell death compared with mock vector or mutant transfectants, and showed increased G(2)/M cell-cycle arrest accompanied by p21 induction and CDK1 inactivation.
  • NCI-H1299 cells were treated with phosphosinositide-3 kinase (PI3K)/AKT pathway inhibitor (LY29002), resulting in reduced AKT phosphorylation levels.
  • Treatment of NCI-H1299 cells with LY29002 and gamma-IR resulted in increased cell-cycle arrest and p21 induction.
  • Endogenous wild-type PTEN-containing NCI-H460 cells were treated with PTEN-specific siRNA and then irradiated with gamma-IR: however reduced PTEN levels did not induce cell-cycle arrest or p21 expression.
  • CONCLUSIONS: Taken together, these findings indicate that PTEN may modulate cell death or the cell cycle via AKT inactivation by PTEN and gamma-IR treatment.
  • We also propose that a PTEN-PI3K/AKT-p21-CDK1 pathway could regulate cell death and the cell cycle by gamma-IR treatment.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / radiotherapy. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Lung Neoplasms / radiotherapy. Neoplasm Proteins / metabolism. PTEN Phosphohydrolase / metabolism. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] CDC2 Protein Kinase / antagonists & inhibitors. CDC2 Protein Kinase / metabolism. Cell Cycle / radiation effects. Cell Cycle Proteins / metabolism. Cell Death. Cell Line, Tumor. Cell Survival / radiation effects. Chromones / pharmacology. Enzyme Inhibitors / pharmacology. G2 Phase / physiology. Gamma Rays / therapeutic use. Humans. Morpholines / pharmacology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Phosphatidylinositol 3-Kinases / pharmacology. Phosphorylation. Transfection

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  • (PMID = 18374229.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Chromones; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Neoplasm Proteins; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.22 / CDC2 Protein Kinase; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase
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90. Zhang GY, Chen PP, Li SL, Yin L, Gao DL, Le XP, Chen KS, Zhang YH, Zhang QX: [mRNA expression level of nucleostemin in esophageal squamous cell carcinoma tissue]. Zhonghua Yi Xue Za Zhi; 2008 Mar 4;88(9):602-5
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  • [Title] [mRNA expression level of nucleostemin in esophageal squamous cell carcinoma tissue].
  • OBJECTIVE: To investigate the mRNA expression levels of nucleostemin (NS) in human esophageal squamous cell carcinoma tissue.
  • METHODS: Real-time PCR was used to quantify the mRNA expression of NS in the samples of esophageal squamous cell carcinoma tissue and their matched normal esophageal mucosa tissue from 62 patients, 36 males and 26 females, aged (61 +/- 10) (38-75).
  • The relationship between NS mRNA expression level and clinical pathological features was analyzed.
  • RESULTS: The NS mRNA expression level of the 62 cases of esophageal squamous cell carcinoma tissue was(4.5 +/- 2.1), significantly higher than that of the matched normal esophageal mucosa tissue [(2.1 +/- 1.3), t = -5.045, P = 0.000].
  • The mRNA expression level of NS was associated with tumor grade, depth of infiltration, and lymph node metastasis (all P < 0.05), but not with gender, age, and pathological type (all P > 0.05).
  • Multiple linear regression analysis revealed that clinical and pathological features influenced the NS mRNA expression level (P = 0.
  • CONCLUSION: NS may play an important role in the progression and proliferation of esophageal squamous cell carcinoma.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Carrier Proteins / genetics. Esophageal Neoplasms / pathology. Gene Expression Regulation, Neoplastic. Nuclear Proteins / genetics
  • [MeSH-minor] Adult. Aged. Female. GTP-Binding Proteins. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 18646714.001).
  • [ISSN] 0376-2491
  • [Journal-full-title] Zhonghua yi xue za zhi
  • [ISO-abbreviation] Zhonghua Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / GNL3 protein, human; 0 / Nuclear Proteins; 0 / RNA, Messenger; EC 3.6.1.- / GTP-Binding Proteins
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91. Vega MI, Jazirehi AR, Huerta-Yepez S, Bonavida B: Rituximab-induced inhibition of YY1 and Bcl-xL expression in Ramos non-Hodgkin's lymphoma cell line via inhibition of NF-kappa B activity: role of YY1 and Bcl-xL in Fas resistance and chemoresistance, respectively. J Immunol; 2005 Aug 15;175(4):2174-83
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  • [Title] Rituximab-induced inhibition of YY1 and Bcl-xL expression in Ramos non-Hodgkin's lymphoma cell line via inhibition of NF-kappa B activity: role of YY1 and Bcl-xL in Fas resistance and chemoresistance, respectively.
  • Rituximab treatment of B non-Hodgkin's lymphoma (NHL) cell lines inhibits the constitutive NF-kappaB activity and results in the sensitization of tumor cells to both chemotherapy and Fas-induced apoptosis.
  • Cells expressing dominant active IkappaB or treated with NF-kappaB-specific inhibitors were sensitive to both drugs and Fas agonist mAb (CH-11)-induced apoptosis.
  • Down-regulation of Bcl-xL expression via inhibition of NF-kappaB activity correlated with chemosensitivity.
  • The direct role of Bcl-xL in chemoresistance was demonstrated by the use of Bcl-xL-overexpressing Ramos cells, Ramos hemagglutinin (HA)-Bcl-x, which were not sensitized by rituximab to drug-induced apoptosis.
  • However, inhibition of Bcl-xL in Ramos HA-Bcl-x resulted in sensitization to drug-induced apoptosis.
  • The role of Bcl-xL expression in the regulation of Fas resistance was not apparent; Ramos HA-Bcl-x cells were as sensitive as the wild type to CH-11-induced apoptosis.
  • Several lines of evidence support the direct role of the transcription repressor yin-yang 1 (YY1) in the regulation of resistance to CH-11-induced apoptosis.
  • Inhibition of YY1 activity by either rituximab or the NO donor DETANONOate or after transfection with YY1 small interfering RNA resulted in up-regulation of Fas expression and sensitization to CH-11-induced apoptosis.
  • These findings suggest two mechanisms underlying the chemosensitization and immunosensitization of B-NHL cells by rituximab via inhibition of NF-kappaB.
  • The regulation of chemoresistance by NF-kappaB is mediated via Bcl-xL expression, whereas the regulation of Fas resistance by NF-kappaB is mediated via YY1 expression and activity.
  • The potential clinical significance of these findings is discussed.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antigens, CD95 / physiology. Lymphoma, Non-Hodgkin / immunology. NF-kappa B / antagonists & inhibitors
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Apoptosis / drug effects. Apoptosis / immunology. Cell Line, Tumor. Down-Regulation / drug effects. Down-Regulation / immunology. Drug Resistance, Neoplasm / immunology. Humans. Immunity, Innate. Nitriles / pharmacology. Nitroso Compounds / pharmacology. Rituximab. Sulfones / pharmacology. Up-Regulation / drug effects. Up-Regulation / immunology

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  • (PMID = 16081784.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI28697; United States / FIC NIH HHS / TW / D43TW00013
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD95; 0 / BAY 11-7085; 0 / NF-kappa B; 0 / Nitriles; 0 / Nitroso Compounds; 0 / Sulfones; 146724-94-9 / 2,2'-(hydroxynitrosohydrazono)bis-ethanamine; 4F4X42SYQ6 / Rituximab
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92. Barber A, Sentman CL: Chimeric NKG2D T cells require both T cell- and host-derived cytokine secretion and perforin expression to increase tumor antigen presentation and systemic immunity. J Immunol; 2009 Aug 15;183(4):2365-72
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  • [Title] Chimeric NKG2D T cells require both T cell- and host-derived cytokine secretion and perforin expression to increase tumor antigen presentation and systemic immunity.
  • Treatment of mice bearing established ovarian tumors with T cells expressing chimeric NKG2D receptors (chNKG2D) develop protective host immune responses to tumor Ags.
  • In this study, the mechanisms that chNKG2D T cells require to induce host immunity against ovarian tumors and which of the host immune cells are involved in tumor elimination were determined.
  • Treatment with chNKG2D T cells led to a sustained, increased IFN-gamma production by host NK, CD4(+), and CD8(+) T cells in the spleen and at the tumor site and this continued for many weeks after T cell injection.
  • Tumor Ag presentation was enhanced in chNKG2D T cell-treated mice, and there were greater numbers of tumor-specific T cells at the tumor site and in draining lymph nodes after treatment with chNKG2D T cells.
  • The increase in host cell cytokine secretion and Ag presentation was dependent on chNKG2D T cell-derived perforin, IFN-gamma, and GM-CSF.
  • Host immune mechanisms were involved in tumor elimination because inhibition of tumor growth was limited in mice that lacked perforin, IFN-gamma, NK cells, or T and B cells (Rag1(-/-)).
  • There was no role for host-derived GM-CSF or CD1-dependent NKT cells, because mice deficient in these were able to clear tumors as well as treated wild-type B6 mice.
  • In summary, chNKG2D T cells required both cytotoxicity and cytokine secretion as well as the participation of host immune cells for development of a host antitumor immune response and complete efficacy.

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  • [Cites] Curr Opin Immunol. 2003 Apr;15(2):148-54 [12633663.001]
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  • (PMID = 19625653.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / T32 AI007363-18; United States / NCI NIH HHS / CA / R01 CA130911-02; United States / NCI NIH HHS / CA / CA130911-02; United States / NCI NIH HHS / CA / P30 CA023108; United States / NCI NIH HHS / CA / R01 CA130911; United States / NIAID NIH HHS / AI / T32 AI07363; United States / NIAID NIH HHS / AI / AI007363-18; United States / NIAID NIH HHS / AI / T32 AI007363; United States / NCI NIH HHS / CA / CA130911
  • [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 / Antigens, Neoplasm; 0 / Cytokines; 0 / Epitopes, T-Lymphocyte; 0 / Klrk1 protein, mouse; 0 / Mutant Chimeric Proteins; 0 / NK Cell Lectin-Like Receptor Subfamily K; 126465-35-8 / Perforin
  • [Other-IDs] NLM/ NIHMS176723; NLM/ PMC2825035
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93. Filipovski V, Banev S, Janevska V, Dukova B: Granular cell tumor of the breast: a case report and review of literature. Cases J; 2009;2:8551
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  • [Title] Granular cell tumor of the breast: a case report and review of literature.
  • A 22-year-old female patient presented with a breast mass lesion with a clinical suspicion of a fibroadenoma.
  • Histological evaluation revealed a rare benign neoplasm - granular cell tumor.Granular cell tumor is rare neoplasm that may arise in virtually any body site, and in 5% it occurs in the breast.
  • The histogenesis of this tumor is still rather controversial and currently the most acceptable theory is a Schwann cell origin.
  • The main histological feature is granular cytoplasm of the tumor cells.From a clinical point of view there is a similarity between granular cell tumor and mammary carcinoma on mammography and ultrasound.

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  • (PMID = 19918386.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2769456
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94. Feys T, Poppe B, De Preter K, Van Roy N, Verhasselt B, De Paepe P, De Paepe A, Speleman F: A detailed inventory of DNA copy number alterations in four commonly used Hodgkin's lymphoma cell lines. Haematologica; 2007 Jul;92(7):913-20
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  • [Title] A detailed inventory of DNA copy number alterations in four commonly used Hodgkin's lymphoma cell lines.
  • BACKGROUND AND OBJECTIVES: Classical Hodgkin's lymphoma (cHL) is a common malignant lymphoma characterized by the presence of large, usually multinucleated malignant Hodgkin and Reed Sternberg (HRS) cells which are thought to be derived from germinal center B-cells.
  • In cHL, the HRS cells constitute less than 1% of the tumor volume; consequently the profile of genetic aberrations in cHL is still poorly understood.
  • DESIGN AND METHODS: In this study, we subjected four commonly used cHL cell lines to array comparative genomic hybridization (aCGH) in order to delineate known chromosomal aberrations in more detail and to search for small hitherto undetected genomic imbalances.
  • RESULTS: The aCGH profiles of the four cell lines tested confirmed the complex patterns of rearrangements previously demonstrated with M-FISH and chromosomal CGH (cCGH).
  • Furthermore, we detected 35 hitherto undetected aberrations including a homozygous deletion of chromosomal region 15q26.2 in the cell line HDLM2 encompasing RGMA and CHD2 and an amplification of the STAT6 gene in cell line L1236 leading to STAT6 overexpression.
  • Finally, in cell line KM-H2 we found a 2.35 Mb deletion at 16q12.1 putatively defining a small critical region for the recurrent 16q deletion in cHL.
  • INTERPRETATION AND CONCLUSIONS: aCGH was performed on four cHL cell lines leading to the improved delineation of known chromosomal imbalances and the detection of 35 hitherto undetected aberrations.
  • [MeSH-major] Gene Dosage. Hodgkin Disease / genetics
  • [MeSH-minor] Cell Line, Tumor. Chromosome Aberrations. Cytogenetic Analysis. DNA-Binding Proteins / genetics. Gene Expression Regulation, Neoplastic. Humans. Neoplasm Proteins / genetics. STAT6 Transcription Factor / genetics. Tumor Suppressor Proteins / genetics

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  • (PMID = 17606441.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / CYLD protein, human; 0 / DNA-Binding Proteins; 0 / Neoplasm Proteins; 0 / STAT6 Transcription Factor; 0 / STAT6 protein, human; 0 / Tumor Suppressor Proteins
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95. Aryana A, Esterbrooks DJ, Morris PC: Nonbacterial thrombotic endocarditis with recurrent embolic events as manifestation of ovarian neoplasm. J Gen Intern Med; 2006 Dec;21(12):C12-5
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  • [Title] Nonbacterial thrombotic endocarditis with recurrent embolic events as manifestation of ovarian neoplasm.
  • Transesophageal echocardiography (TEE) established the diagnosis of nonbacterial thrombotic endocarditis (NBTE).
  • In our patient, we diagnosed an ovarian clear cell adenocarcinoma, a malignant disorder that has been rarely reported in association with NBTE.
  • When confronted with findings of NBTE without a clear etiology, an occult neoplasm must be excluded.
  • [MeSH-major] Adenocarcinoma, Clear Cell / complications. Endocarditis / etiology. Ovarian Neoplasms / complications. Pulmonary Embolism / etiology. Venous Thrombosis / etiology
  • [MeSH-minor] Adult. Diagnosis, Differential. Echocardiography, Transesophageal. Endocarditis, Bacterial / diagnosis. Female. Humans. Recurrence. Tomography, X-Ray Computed


96. Bertagnolli MM, Warren RS, Niedzwiecki D, Mueller E, Compton CC, Redston M, Hall M, Hahn HP, Jewell SD, Mayer RJ, Goldberg RM, Saltz LB, Loda M: p27Kip1 in stage III colon cancer: implications for outcome following adjuvant chemotherapy in cancer and leukemia group B protocol 89803. Clin Cancer Res; 2009 Mar 15;15(6):2116-22
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  • The primary endpoint was overall survival (OS); disease-free survival was a secondary endpoint.
  • Combination of p27 status with mismatch repair status, however, identified a small subset of patients that may benefit from IFL (n = 36; 5-year disease-free survival 81%: 95% CI, 0.64-0.98 versus 47%: 95% CI, 0.21-0.72; log-rank P = 0.042; 5-year OS 81%: 95% CI, 0.64-0.98 versus 60%: 95% CI, 0.35-0.85; log-rank P = 0.128).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Cyclin-Dependent Kinase Inhibitor p27. DNA Mismatch Repair. Female. Humans. Male. Microsatellite Instability. Middle Aged. Neoplasm Staging. Prospective Studies. Treatment Outcome

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  • (PMID = 19276255.001).
  • [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 / U10 CA047577; United States / NCI NIH HHS / CA / U10 CA032291; United States / NCI NIH HHS / CA / CA33601; United States / NCI NIH HHS / CA / U10 CA071323; United States / NCI NIH HHS / CA / CA77597; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / CA47577; United States / NCI NIH HHS / CA / CA32291; United States / NCI NIH HHS / CA / CA29165; United States / NCI NIH HHS / CA / U10 CA045564; United States / NCI NIH HHS / CA / U10 CA035279; United States / NCI NIH HHS / CA / U10 CA045808; United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / U10 CA033601; United States / NCI NIH HHS / CA / U10 CA077597; United States / NCI NIH HHS / CA / U10 CA035421; United States / NCI NIH HHS / CA / U10 CA114558; United States / NCI NIH HHS / CA / U10 CA045418; United States / NCI NIH HHS / CA / U10 CA077440; United States / NCI NIH HHS / CA / U10 CA037447; United States / NCI NIH HHS / CA / U10 CA041287; United States / NCI NIH HHS / CA / U10 CA037447-27; United States / NCI NIH HHS / CA / U10 CA047559; United States / NCI NIH HHS / CA / U10 CA077651; United States / NCI NIH HHS / CA / CA04326; United States / NCI NIH HHS / CA / CA71323; United States / NCI NIH HHS / CA / CA45418; United States / NCI NIH HHS / CA / U10 CA074811; United States / NCI NIH HHS / CA / U10 CA047642; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / U10 CA003927
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDKN1B protein, human; 0 / Intracellular Signaling Peptides and Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
  • [Other-IDs] NLM/ NIHMS236431; NLM/ PMC3059545
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97. Geho DH, Bandle RW, Clair T, Liotta LA: Physiological mechanisms of tumor-cell invasion and migration. Physiology (Bethesda); 2005 Jun;20:194-200
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  • [Title] Physiological mechanisms of tumor-cell invasion and migration.
  • Pharmacological blockade of intra- and extracellular signaling events that regulate migration and survival of multiple cell types may disrupt the host-tumor conspiracy that allows escape from normal developmental regulation.
  • [MeSH-major] Cell Movement / physiology. Neoplasm Invasiveness / physiopathology. Neoplasms / pathology. Neoplasms / physiopathology

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  • (PMID = 15888576.001).
  • [ISSN] 1548-9213
  • [Journal-full-title] Physiology (Bethesda, Md.)
  • [ISO-abbreviation] Physiology (Bethesda)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 66
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98. Hishizawa M, Imada K, Sakai T, Nishikori M, Arima N, Tsudo M, Ishikawa T, Uchiyama T: Antibody responses associated with the graft-versus-leukemia effect in adult T-cell leukemia. Int J Hematol; 2006 May;83(4):351-5
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  • [Title] Antibody responses associated with the graft-versus-leukemia effect in adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a peripheral T-cell neoplasm caused by human T-cell leukemia virus type 1 (HTLV-1).
  • The prognosis of ATL, especially the acute and lymphoma subtypes, is poor with conventional and high-dose chemotherapy.
  • The effectiveness of allogeneic hematopoietic stem cell transplantation (allo-HSCT) for ATL has been reported, suggesting the presence of a graft-versus-leukemia (GVL) effect against this malignancy.
  • [MeSH-major] Antibody Formation / immunology. Antigens, Neoplasm / immunology. Graft vs Leukemia Effect / immunology. Leukemia-Lymphoma, Adult T-Cell / immunology. Receptors, Cytokine / immunology
  • [MeSH-minor] Cloning, Molecular. Female. Gene Expression Regulation. Gene Library. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Organ Specificity. Receptors, Autocrine Motility Factor. Transplantation, Homologous. Ubiquitin-Protein Ligases

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  • (PMID = 16757438.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Receptors, Cytokine; EC 2.3.2.27 / AMFR protein, human; EC 2.3.2.27 / Receptors, Autocrine Motility Factor; EC 2.3.2.27 / Ubiquitin-Protein Ligases
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99. Dagvadorj A, Tan SH, Liao Z, Cavalli LR, Haddad BR, Nevalainen MT: Androgen-regulated and highly tumorigenic human prostate cancer cell line established from a transplantable primary CWR22 tumor. Clin Cancer Res; 2008 Oct 01;14(19):6062-72
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  • [Title] Androgen-regulated and highly tumorigenic human prostate cancer cell line established from a transplantable primary CWR22 tumor.
  • PURPOSE: One of the major obstacles in understanding the molecular mechanisms underlying the transition of prostate cancer growth from androgen dependency to a hormone-refractory state is the lack of androgen-regulated and tumorigenic human prostate cancer cell lines.
  • EXPERIMENTAL DESIGN: We have established and characterized a new human prostate cancer cell line, CWR22Pc, derived from the primary CWR22 human prostate xenograft tumors.
  • RESULTS: The growth of CWR22Pc cells is induced markedly by dihydrotestosterone, and CWR22Pc cells express high levels of androgen receptor (AR) and prostate-specific antigen (PSA).
  • Importantly, PSA expression in CWR22Pc cells is regulated by androgens.
  • Stat5a/b, Stat3, Akt, and mitogen-activated protein kinase were constitutively active or cytokine inducible in CWR22Pc cells.
  • The AR in CWR22Pc cells contains the H874Y mutation, but not the exon 3 duplication or other mutations.
  • CONCLUSIONS: This androgen-regulated and tumorigenic human prostate cancer cell line provides a valuable tool for studies on androgen regulation of prostate cancer cells and on the molecular mechanisms taking place in growth promotion of prostate cancer when androgens are withdrawn from the growth environment.
  • CWR22Pc cells also provide a model system for studies on the regulation of transcriptional activity of mutated H874YAR in a prostate cancer cell context.
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Survival. Cytogenetics / methods. Humans. Male. Mice. Mice, Nude. Mutation. Neoplasm Transplantation. Nucleic Acid Hybridization. Prostate-Specific Antigen / biosynthesis. Signal Transduction

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  • (PMID = 18829484.001).
  • [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 / R01 CA113580; United States / NCI NIH HHS / CA / R01 CA113580-01A1; United States / NCI NIH HHS / CA / 1R01 CA 113580-01A1; United States / NCI NIH HHS / CA / P30 CA051008; United States / NCI NIH HHS / CA / R01 CA113580-02; United States / NCI NIH HHS / CA / 1P30 CA 51008; United States / NCI NIH HHS / CA / CA 56036-08; United States / NCI NIH HHS / CA / R01 CA113580-03; United States / NCI NIH HHS / CA / R21 CA178755; United States / NCI NIH HHS / CA / P30 CA056036
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Other-IDs] NLM/ NIHMS73140; NLM/ PMC2570751
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100. Celetti A, Testa D, Staibano S, Merolla F, Guarino V, Castellone MD, Iovine R, Mansueto G, Somma P, De Rosa G, Galli V, Melillo RM, Santoro M: Overexpression of the cytokine osteopontin identifies aggressive laryngeal squamous cell carcinomas and enhances carcinoma cell proliferation and invasiveness. Clin Cancer Res; 2005 Nov 15;11(22):8019-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Overexpression of the cytokine osteopontin identifies aggressive laryngeal squamous cell carcinomas and enhances carcinoma cell proliferation and invasiveness.
  • PURPOSE: Osteopontin is a secreted cytokine that binds to the cell surface CD44v6 receptor.
  • We studied osteopontin and CD44v6 expression in laryngeal squamous cell carcinomas and correlated osteopontin expression levels with clinicopathologic tumor features.
  • EXPERIMENTAL DESIGN: We used immunohistochemistry, immunoblotting, and reverse transcription-PCR to study osteopontin expression in 58 laryngeal squamous cell carcinomas.
  • Cultured squamous carcinoma cells were treated with exogenous osteopontin or with RNA interference to knockdown osteopontin expression.
  • Osteopontin expression was paralleled by intense cell surface reactivity for CD44v6.
  • Treatment of squamous carcinoma cells with recombinant osteopontin sharply increased proliferation and Matrigel invasion in comparison with the untreated cells parallel to activation of the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase/mitogen-activated protein kinase signaling cascade.
  • CONCLUSIONS: These results identify osteopontin as a marker and a potential therapeutic target in cases of aggressive laryngeal squamous cell carcinomas.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Cell Proliferation. Laryngeal Neoplasms / pathology. Sialoglycoproteins / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD44 / analysis. Antigens, CD44 / genetics. Butadienes / pharmacology. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinase Kinases / metabolism. Neoplasm Invasiveness. Nitriles / pharmacology. Osteopontin. RNA Interference. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Survival Analysis. Up-Regulation

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  • (PMID = 16299231.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Butadienes; 0 / Enzyme Inhibitors; 0 / Nitriles; 0 / RNA, Messenger; 0 / SPP1 protein, human; 0 / Sialoglycoproteins; 0 / U 0126; 106441-73-0 / Osteopontin; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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