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3. Yang AD, Fan F, Camp ER, van Buren G, Liu W, Somcio R, Gray MJ, Cheng H, Hoff PM, Ellis LM: Chronic oxaliplatin resistance induces epithelial-to-mesenchymal transition in colorectal cancer cell lines. Clin Cancer Res; 2006 Jul 15;12(14 Pt 1):4147-53
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  • [Title] Chronic oxaliplatin resistance induces epithelial-to-mesenchymal transition in colorectal cancer cell lines.
  • PURPOSE: Epithelial-to-mesenchymal transition (EMT) is a process whereby cells acquire molecular alterations that facilitate cell motility and invasion.
  • In preliminary studies, we observed that oxaliplatin-resistant (OxR) colorectal cancer (CRC) cells underwent morphologic changes suggestive of a migratory phenotype, leading us to hypothesize that OxR CRC cells undergo EMT.
  • Morphologic and molecular changes characteristic of EMT were determined by immunofluorescence staining and Western blot analyses.
  • Immunofluorescence staining of OxR cells revealed translocation of E-cadherin and beta-catenin from their usual membrane-bound complex to the cytoplasm and nucleus, respectively.
  • The OxR cells also had decreased expression of the epithelial adhesion molecules E-cadherin and plakoglobin and an increase in the mesenchymal marker vimentin.
  • CONCLUSION: We hypothesize that induction of EMT may contribute to the decreased efficacy of therapy in chemoresistant CRC, as the tumor cells switch from a proliferative to invasive phenotype.
  • Further understanding of the mechanisms of chemoresistance in CRC will enable improvements in chemotherapy for metastatic disease.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / pathology. Drug Resistance, Neoplasm. Epithelium / metabolism. Mesoderm / metabolism. Organoplatinum Compounds / pharmacology
  • [MeSH-minor] Cadherins / metabolism. Cell Line, Tumor. Cell Movement. Cell Proliferation. Humans. Immunohistochemistry. Neoplasm Invasiveness. Neoplasm Metastasis. Spindle Apparatus


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4. Zhoul J, Hernandez G, Tu SW, Huang CL, Tseng CP, Hsieh JT: The role of DOC-2/DAB2 in modulating androgen receptor-mediated cell growth via the nongenomic c-Src-mediated pathway in normal prostatic epithelium and cancer. Cancer Res; 2005 Nov 1;65(21):9906-13
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  • [Title] The role of DOC-2/DAB2 in modulating androgen receptor-mediated cell growth via the nongenomic c-Src-mediated pathway in normal prostatic epithelium and cancer.
  • The onset of the androgen-independent prostate cancer is often associated with up-regulation of the androgen receptor that can cause antagonists to exhibit agonistic activity, which could lead to the failure of androgen ablation therapy.
  • However, DOC-2/DAB2 does not change the capacity of androgen receptor to regulate the transcription of androgen-responsive reporter genes, indicating that DOC-2/DAB2 selectively inhibits androgen receptor-mediated cell growth in androgen-independent prostate cancer by disrupting the androgen receptor/c-Src complex.
  • We conclude that DOC-2/DAB2 can modulate androgen receptor-mediated cell growth in both normal and malignant prostatic epithelial cells and the outcome of this study could evolve into a new therapeutic strategy of prostate cancer.
  • [MeSH-major] Adaptor Proteins, Vesicular Transport / physiology. Genes, Tumor Suppressor / physiology. Phosphotransferases / metabolism. Prostatic Neoplasms / pathology. Proto-Oncogene Proteins / metabolism. Receptors, Androgen / physiology
  • [MeSH-minor] Adaptor Proteins, Signal Transducing. Androgen Receptor Antagonists. Binding, Competitive. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Dihydrotestosterone / pharmacology. Epithelium / enzymology. Epithelium / metabolism. Humans. Male. Prostate / cytology. Prostate / enzymology. Prostate / metabolism. Protein-Tyrosine Kinases. RNA Interference. Signal Transduction. Transfection. Tumor Suppressor Proteins. src-Family Kinases

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  • (PMID = 16267015.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK63661
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Adaptor Proteins, Vesicular Transport; 0 / Androgen Receptor Antagonists; 0 / DAB2 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Androgen; 0 / Tumor Suppressor Proteins; 08J2K08A3Y / Dihydrotestosterone; EC 2.7.- / Phosphotransferases; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases
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5. Shieh YA, Yang SJ, Wei MF, Shieh MJ: Aptamer-based tumor-targeted drug delivery for photodynamic therapy. ACS Nano; 2010 Mar 23;4(3):1433-42
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  • [Title] Aptamer-based tumor-targeted drug delivery for photodynamic therapy.
  • Herein we report a novel strategy of using G-quadruplex as a drug carrier to target cancer cells for photodynamic therapy (PDT).
  • A G-quadruplex forming AS1411 aptamer could be physically conjugated with six molecules of porphyrin derivative, 5,10,15,20-tetrakis(1-methylpyridinium-4-yl)porphyrin (TMPyP4), to fabricate the apt-TMP complex.
  • The TMPyP4 molecules in the complex were identified to bind tightly to the aptamer by intercalation and outside binding.
  • The results showed that the apt-TMP complex exhibited a higher TMPyP4 accumulation in MCF7 breast cancer cells than in M10 normal epithelium cells.
  • These results indicated that the TMPyP4 delivery and uptake were mediated by the specific interaction of the apt-TMP complex with nucleolin on the cellular surface and that the use of the AS1411 aptamer as a drug carrier may be a potential tactic in cancer therapy.
  • [MeSH-major] Aptamers, Nucleotide / chemistry. Drug Carriers / chemistry. Neoplasms / drug therapy. Neoplasms / metabolism. Photochemotherapy / methods
  • [MeSH-minor] Base Sequence. Biological Transport. Cell Line, Tumor. Cell Nucleus / metabolism. Circular Dichroism. Flow Cytometry. G-Quadruplexes. Gene Expression Regulation, Neoplastic. Humans. Ligands. Microscopy, Electron, Transmission. Organ Specificity. Phosphoproteins / metabolism. Porphyrins / chemistry. Porphyrins / metabolism. Porphyrins / pharmacology. RNA-Binding Proteins / metabolism. Spectrophotometry, Ultraviolet

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  • (PMID = 20166743.001).
  • [ISSN] 1936-086X
  • [Journal-full-title] ACS nano
  • [ISO-abbreviation] ACS Nano
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aptamers, Nucleotide; 0 / Drug Carriers; 0 / Ligands; 0 / Phosphoproteins; 0 / Porphyrins; 0 / RNA-Binding Proteins; 0 / nucleolin; 38673-65-3 / tetra(4-N-methylpyridyl)porphine
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6. Wei S, Carroll W, Lazenby A, Bell W, Lopez R, Said-Al-Naief N: Sinonasal teratocarcinosarcoma: report of a case with review of literature and treatment outcome. Ann Diagn Pathol; 2008 Dec;12(6):415-25
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  • [Title] Sinonasal teratocarcinosarcoma: report of a case with review of literature and treatment outcome.
  • Sinonasal teratocarcinosarcoma is a highly malignant, polymorphous neoplasm that combines features of carcinosarcoma and teratoma.
  • The patient presented with a history of multiple episodes of epistaxis, nasal obstruction and frontal headaches.
  • Computerized tomography scans and magnetic resonance imaging revealed a large mass filling the left nasal cavity and extending to the cribriform plate with involvement of the ethmoid sinuses, lamina papyracea, and orbit.
  • The patient underwent a complex procedure for a T3N0 tumor.
  • Histologic examination revealed a heterogeneous admixture of epithelial, mesenchymal, and neuroepithelial elements.
  • The epithelial components vary from clear cells, nonkeratinizing epithelium to glandular pattern, and keratin containing cysts.
  • Immature neuroepithelium and olfactory neuroblastomalike tissue are highlighted with neuroendocrine markers.
  • Postoperatively, the patient had a rapid local recurrence of the tumor and underwent reexcision, and was treated with radiotherapy and chemotherapy.
  • Twelve months after his primary resection, computerized tomography scans revealed an intrathoracic tumor with dominant mass in the left hilum and metastases to the mediastinum, left pleural space, and both lungs.
  • Among 54 cases of reported sinonasal teratocarcinosarcoma, 67% of patients with initial single surgical resection and 80% of patients primarily treated with radiotherapy had recurrence, or metastatsis, or unresponsiveness to treatment.
  • Almost half of the patients died of tumor within 3 years of diagnosis, despite aggressive therapy.
  • Seventy percent of the patients who survived more than 1 year had the initial therapeutic regiments of combined surgery and adjuvant therapies, suggesting that aggressive therapeutic approaches may improve the treatment outcome.
  • [MeSH-major] Carcinosarcoma / diagnosis. Carcinosarcoma / therapy. Nose Neoplasms / diagnosis. Nose Neoplasms / therapy. Teratoma / diagnosis. Teratoma / therapy
  • [MeSH-minor] Adult. Combined Modality Therapy. Humans. Magnetic Resonance Imaging. Male. Paranasal Sinuses / pathology. Paranasal Sinuses / surgery. Prognosis. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 18995206.001).
  • [ISSN] 1532-8198
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 33
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7. McGruder BM, Atha DH, Wang W, Huppi K, Wei WQ, Abnet CC, Qiao YL, Dawsey SM, Taylor PR, Jakupciak JP: Real-time telomerase assay of less-invasively collected esophageal cell samples. Cancer Lett; 2006 Nov 28;244(1):91-100
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  • [Title] Real-time telomerase assay of less-invasively collected esophageal cell samples.
  • Genomic and proteomic efforts have discovered a complex list of biomarkers that identify human disease, stratify risk of disease within populations, and monitor drug or therapy responses for treatment.
  • Telomerase activity is correlated with tumor progression, indicating cells that express telomerase possess aggressive clinical behavior and that telomerase activity could be a clinically important cancer biomarker.
  • Traditionally, the detection of cancer has involved invasive procedures to procure samples.
  • There is a need for less invasive approaches suitable for population- and clinic-based assays for cancer early detection.
  • Esophageal balloon cytology (EBC) is a low-invasive screening technique, which samples superficial epithelial cells from the esophagus.
  • Since telomerase activity is absent in superficial cells of normal esophageal squamous epithelium but is often present in superficial cells from dysplastic lesions and ESCCs, measuring telomerase activity in EBC samples may be a good way to screen for these lesions.
  • The development of rapid real-time telomerase activity assays raises the possibility of extending such screening to high-risk populations.
  • In this study, we evaluate the feasibility of using rapid Real-Time Telomerase Repeat Amplification Protocol (RTTRAP) for the analysis of NIST telomerase candidate reference material and esophageal clinical samples.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Squamous Cell / genetics. Esophageal Neoplasms / genetics. Precancerous Conditions / genetics. Telomerase / genetics
  • [MeSH-minor] Clinical Enzyme Tests. Cytodiagnosis. Electrophoresis, Capillary. Esophagus / metabolism. Esophagus / pathology. Humans. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16569479.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / CCR NIH HHS / RC / N01-RC-91019; United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase
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8. Wu DL, Yi HX, Sui FY, Jiang XH, Jiang XM, Zhao YY: Expression of ATP7B in human gastric cardiac carcinomas in comparison with distal gastric carcinomas. World J Gastroenterol; 2006 Dec 21;12(47):7695-8
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  • [Title] Expression of ATP7B in human gastric cardiac carcinomas in comparison with distal gastric carcinomas.
  • AIM: To analyze expression of ATP7B in gastric cardiac adenocarcinomas, its clinicopathologic significance, in comparison with distal gastric adenocarcinomas.
  • METHODS: Immunohistochemical avidin-biotin peroxidase complex method was applied to detect the expression of ATP7B in 49 cases of cardiac carcinomas, the corresponding adjacent non-neoplastic epithelium and 55 cases of distal gastric carcinomas.
  • RESULTS: The proportion of ATP7B positive samples in gastric cardiac carcinomas (51.0%, 25 of 49) was significantly higher than that in the corresponding adjacent non-neoplastic epithelium (22.4%, 11 of 49) (P = 0.003).
  • ATP7B expression in gastric cardiac carcinomas was independent of age, tumor size, nodal stage and metastasis status.
  • ATP7B protein was detected in 30.9% (17/55 cases) of distal gastric carcinomas, markedly lower than that in gastric cardiac carcinomas (P = 0.037).
  • ATP7B expression in gastric cardiac carcinomas is significantly higher than that in distal gastric carcinomas, which might partially explain the difference of chemotherapy response and prognosis between these two gastric carcinomas.
  • [MeSH-major] Adenocarcinoma / metabolism. Adenosine Triphosphatases / metabolism. Cation Transport Proteins / metabolism. Esophageal Sphincter, Lower / metabolism. Stomach / metabolism. Stomach Neoplasms / metabolism

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  • (PMID = 17171802.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cation Transport Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.3.4 / Wilson disease protein
  • [Other-IDs] NLM/ PMC4088055
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9. Schuster A, Apfelstedt-Sylla E, Pusch CM, Zrenner E, Thirkill CE: Autoimmune retinopathy with RPE hypersensitivity and 'negative ERG' in X-linked hyper-IgM syndrome. Ocul Immunol Inflamm; 2005 Apr-Jun;13(2-3):235-43
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  • PURPOSE: To report the clinical, electrophysiological, and immunological features of a patient with X-linked hyper-IgM immunodeficiency syndrome type 1 (HIGM1) accompanied by a novel type of autoimmune retinopathy, including retinal pigment epithelium (RPE) hypersensitivity.
  • METHODS: Comprehensive ophthalmological examinations, electrophysiological function testing, and inquiries into the immunological status of a 13-year-old presenting with subacute loss of vision in association with a molecularly confirmed diagnosis of HIGM1 were performed.
  • The patient later developed indications of RPE hypersensitivity.
  • A massively reduced light-peak to dark-trough ratio of the EOG slow oscillations (L/D ratio) corresponded to impaired RPE-photoreceptor complex function. (3) Molecular genetic analyses revealed the patient to be nullizygous for the tumor necrosis factor ligand member 5 gene (TNFSF5; CD40LG).
  • In this case, peripheral stem-cell transfusion with its associated chemotherapy failed to benefit the patient's vision; indications of autoimmunity appeared to increase following this treatment.
  • [MeSH-major] Autoimmune Diseases / immunology. Genetic Diseases, X-Linked / immunology. Hypergammaglobulinemia / immunology. Immunologic Deficiency Syndromes / immunology. Pigment Epithelium of Eye / immunology. Retinal Diseases / immunology

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  • (PMID = 16019685.001).
  • [ISSN] 0927-3948
  • [Journal-full-title] Ocular immunology and inflammation
  • [ISO-abbreviation] Ocul. Immunol. Inflamm.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / 1 P30 EY 12576-01
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / PSMG2 protein, human; 0 / Proteins; EC 3.6.1.- / Chaperonins
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10. Lee KR, Nucci MR: Ovarian mucinous and mixed epithelial carcinomas of mullerian (endocervical-like) type: a clinicopathologic analysis of four cases of an uncommon variant associated with endometriosis. Int J Gynecol Pathol; 2003 Jan;22(1):42-51
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  • [Title] Ovarian mucinous and mixed epithelial carcinomas of mullerian (endocervical-like) type: a clinicopathologic analysis of four cases of an uncommon variant associated with endometriosis.
  • The epithelial cells of ovarian mucinous carcinomas may sometimes appear similar to those of gastrointestinal or endocervical mucinous carcinomas, but most are composed of cells that do not suggest any particular derivation.
  • Two patients had bilateral tumors confined to the ovaries at initial staging; both also had synchronous endometrial carcinomas of the mucinous type.
  • In one of the latter cases a mullerian (endocervical-like) mucinous borderline tumor (MMBT) of the opposite ovary had been removed 5 years earlier, and in this case and two other cases the ovarian carcinomas had foci resembling MMBT, suggesting that they may be an invasive counterpart to these tumors.
  • They were composed of closely packed glands, cysts, and cysts containing complex papillae.
  • The epithelial cells were well differentiated with infrequent mitoses and most were tall with mucinous cytoplasm resembling normal endocervical glandular cells.
  • One tumor had a focally infiltrative growth pattern with a desmoplastic stromal reaction; the remaining five tumors had an exclusively confluent (expansile) pattern of invasion.
  • Endometriosis was present in residual ovarian tissue adjacent to four tumors in three patients and had marked epithelial proliferation in three.
  • All patients were treated postoperatively with chemotherapy and were without clinical recurrence with follow-up intervals of 8 months, 1.2 years, 2.9 years, and 3.8 years.
  • By immunohistochemical analysis the neoplastic epithelium was positive for estrogen and progesterone receptor proteins, vimentin, and cytokeratin 7, and negative or only focally positive for carcinoembryonic antigen and cytokeratin 20, a profile that differs from that of the usual mucinous ovarian carcinoma and is supportive of a mullerian derivation.
  • To better understand their clinicopathologic features and pathogenesis, this uncommon variant should be separated from the usual type in future studies of mucinous carcinomas of the ovary.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Carcinoma, Endometrioid / pathology. Endometriosis / pathology. Neoplasms, Multiple Primary / pathology. Ovarian Neoplasms / pathology

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  • (PMID = 12496697.001).
  • [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
  • [Chemical-registry-number] 0 / Biomarkers
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11. Zhou HY, Pon YL, Wong AS: HGF/MET signaling in ovarian cancer. Curr Mol Med; 2008 Sep;8(6):469-80
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  • While deregulated HGF/MET signaling is observed in many tumors, the consequences of MET activation are complex and context dependent.
  • We will begin with a brief discussion on the role of HGF and MET in the physiology of normal ovarian surface epithelium (OSE) and ovarian cancer development.
  • The involvement of HGF in other aspects of tumor progression, such as invasion and metastasis, and novel downstream target genes activated by HGF is summarized next.
  • The therapeutic potential of HGF to treat ovarian cancer and to improve response to conventional chemotherapy is also described.
  • Finally, the most recent progress in drug development and future areas of research in terms of their potential clinical implications are discussed.
  • [MeSH-major] Hepatocyte Growth Factor / metabolism. Ovarian Neoplasms / metabolism. Proto-Oncogene Proteins c-met / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Cell Transformation, Neoplastic. Disease Progression. Drug Therapy. Epithelium / physiology. Female. Humans. Neovascularization, Pathologic. Ovary / anatomy & histology. Ovary / pathology

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  • (PMID = 18781954.001).
  • [ISSN] 1566-5240
  • [Journal-full-title] Current molecular medicine
  • [ISO-abbreviation] Curr. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / HGF protein, human; 67256-21-7 / Hepatocyte Growth Factor; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
  • [Number-of-references] 172
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12. Algeciras-Schimnich A, Pietras EM, Barnhart BC, Legembre P, Vijayan S, Holbeck SL, Peter ME: Two CD95 tumor classes with different sensitivities to antitumor drugs. Proc Natl Acad Sci U S A; 2003 Sep 30;100(20):11445-50
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  • [Title] Two CD95 tumor classes with different sensitivities to antitumor drugs.
  • CD95 type I and II cells differ in their dependence on mitochondria to execute apoptosis, because antiapoptotic members of the Bcl-2 family render only type II cells resistant to death receptor-induced apoptosis.
  • They can also be distinguished by a more efficient formation of the death-inducing signaling complex in type I cells.
  • We have identified a soluble form of CD95 ligand (S2) that is cytotoxic to type II cells but does not kill type I cells.
  • By testing 58 tumor cell lines of the National Cancer Institute's anticancer drug-screening panel for apoptosis sensitivity to S2 and performing death-inducing signaling complex analyses, we determined that half of the CD95-sensitive cells are type I and half are type II.
  • Most of the type I cell lines fall into a distinct class of tumor cells expressing mesenchymal-like genes, whereas the type II cell lines preferentially express epithelium-like markers.
  • This suggests that type I and II tumor cells represent different stages of carcinogenesis that resemble the epithelial-mesenchymal transition.
  • We then screened the National Cancer Institute database of >42,000 compounds for reagents with patterns of growth inhibition that correlated with either type I or type II cell lines and found that actin-binding compounds selectively inhibited growth of type I cells, whereas tubulin-interacting compounds inhibited growth of type II cells.
  • Our analysis reveals fundamental differences in programs of gene expression between type I and type II cells and could impact the way actin- and microtubule-disrupting antitumor agents are used in tumor therapy.

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  • (PMID = 14504390.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM061712; United States / NCI NIH HHS / CA / T32 CA009594; United States / NCI NIH HHS / CA / 5T32CA09594; United States / NIGMS NIH HHS / GM / GM61712
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC208777
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13. Zimecki M, Artym J: [Therapeutic properties of proteins and peptides from colostrum and milk]. Postepy Hig Med Dosw (Online); 2005;59:309-23
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  • [Title] [Therapeutic properties of proteins and peptides from colostrum and milk].
  • The immunotropic properties of these proteins prompted investigators research their potential application in prevention and therapy.
  • It is protective with regard to intestinal epithelium, promotes bone growth, and accelerates the recovery of immune system function in immunocompromised animals.
  • LF was tried in the treatment of hepatitis C infection and the intestinal form of graft-versus-host disease (GvHD).
  • The protein hydrolyzates were also protective in diabetic animals, reduced tumor growth, had antihypertensive activity and diminished colicky symptoms in infants.
  • HAMLET, a complex of LA and oleic acid, was effective in patients with cutaneous papillomas.
  • Lysozyme found application in infant formulas, the treatment of periodentitis, and the prevention of tooth decay.
  • In conclusion, preparations derived from milk and colostrum are effective, easily bioaccessible, and safe, finding wide application in prevention and therapy for newborns and adults.

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  • (PMID = 15995598.001).
  • [ISSN] 1732-2693
  • [Journal-full-title] Postepy higieny i medycyny doswiadczalnej (Online)
  • [ISO-abbreviation] Postepy Hig Med Dosw (Online)
  • [Language] POL
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Antineoplastic Agents; 0 / Caseins; 0 / Milk Proteins; 0 / Peptides; 0 / colostrinine; EC 1.11.1.- / Lactoperoxidase; EC 3.4.21.- / Lactoferrin
  • [Number-of-references] 164
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14. Yamaguchi J, Sasaki M, Sato Y, Itatsu K, Harada K, Zen Y, Ikeda H, Nimura Y, Nagino M, Nakanuma Y: Histone deacetylase inhibitor (SAHA) and repression of EZH2 synergistically inhibit proliferation of gallbladder carcinoma. Cancer Sci; 2010 Feb;101(2):355-62
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  • Polycomb group protein EZH2, frequently overexpressed in malignant tumors, is the catalytic subunit of polycomb repressive complex 2 (PRC2).
  • PRC2 interacts with HDACs in transcriptional silencing and relates to tumor suppressor loss.
  • We used 48 surgically resected gallbladders and cultures of human gallbladder epithelial cells (HGECs), gallbladder carcinoma (TGBC2TKB), and cholangiocarcinoma (HuCCT-1 and TFK-1) cell lines for examination.
  • Immunohistochemically, EZH2 was overexpressed in gallbladder carcinoma, especially poorly differentiated carcinoma, but not in normal epithelium.
  • In contrast, HDAC1/2 were expressed in both carcinoma and normal epithelium in vivo.
  • Interestingly, SAHA treatment caused significant cell number decline in three carcinoma cells, and this effect was synergized with EZH2 siRNA treatment; however, HGECs were resistant to SAHA.
  • In TGBC2TKB cells, the expression of EZH2 and HDAC1/2 were decreased by SAHA treatment, and p16(INK4a), E-cadherin, and p21were simultaneously activated; however, no such findings were obtained in HGECs, suggesting that the effect of SAHA depends on the EZH2-mediated tumor suppressor loss.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DNA-Binding Proteins / antagonists & inhibitors. Gallbladder Neoplasms / drug therapy. Histone Deacetylase Inhibitors / pharmacology. Transcription Factors / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p16 / analysis. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Female. Histone Deacetylases / analysis. Humans. Immunohistochemistry. Male. Middle Aged. Polycomb Repressive Complex 2. RNA, Small Interfering / pharmacology

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  • (PMID = 19860841.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA-Binding Proteins; 0 / Histone Deacetylase Inhibitors; 0 / RNA, Small Interfering; 0 / Transcription Factors; EC 2.1.1.43 / EZH2 protein, human; EC 2.1.1.43 / Polycomb Repressive Complex 2; EC 3.5.1.98 / Histone Deacetylases
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15. Henry MD, Wen S, Silva MD, Chandra S, Milton M, Worland PJ: A prostate-specific membrane antigen-targeted monoclonal antibody-chemotherapeutic conjugate designed for the treatment of prostate cancer. Cancer Res; 2004 Nov 1;64(21):7995-8001
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  • [Title] A prostate-specific membrane antigen-targeted monoclonal antibody-chemotherapeutic conjugate designed for the treatment of prostate cancer.
  • PSMA is a transmembrane receptor whose expression is largely restricted to prostatic epithelium and prostate cancer cells with its expression level increasing during the progression of malignancy.
  • MLN2704 consists of a de-immunized, monoclonal antibody that is specific for PSMA conjugated to drug maytansinoid 1 (DM1), a microtubule-depolymerizing compound.
  • After antibody binding to PSMA and the subsequent cellular internalization of this complex, DM1 is released leading to cell death.
  • MLN2704 has an approximate half-life of 39 hours in scid mice bearing CWR22 tumor tissue, and the antibody effectively penetrates xenograft tumor tissue.
  • Tumor growth delays of approximately 100 days could be achieved on the optimized schedule of one dose of 60 mg/kg MLN2704 every 14 days for five doses (q14dx5).
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Glutamate Carboxypeptidase II / antagonists & inhibitors. Immunotoxins / therapeutic use. Maytansine / analogs & derivatives. Prostatic Neoplasms / therapy
  • [MeSH-minor] Animals. Antigens, Surface. Bone Neoplasms / secondary. Humans. Male. Mice. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 15520207.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Surface; 0 / Antineoplastic Agents; 0 / Immunotoxins; 14083FR882 / Maytansine; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
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16. Sonis ST: The biologic role for nuclear factor-kappaB in disease and its potential involvement in mucosal injury associated with anti-neoplastic therapy. Crit Rev Oral Biol Med; 2002;13(5):380-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The biologic role for nuclear factor-kappaB in disease and its potential involvement in mucosal injury associated with anti-neoplastic therapy.
  • Oral mucosal barrier injury (mucositis) is a frequent, painful, serious, dose-limiting toxicity associated with many anti-neoplastic drugs and radiation to the head and neck.
  • Results of recent studies suggest that mucositis is the result of a complex series of interactive biological events that take place in the submucosa and epithelium.
  • The nuclear transcription factor NF-kappaB has been implicated in the control of a broad range of biological responses, the activation of a large number of specific cellular genes, and the determination of the fate of cells exposed to ionizing radiation and anti-neoplastic drugs.
  • Of particular importance to mucositis is the fact that NF-kappaB regulates key elements in the apparent sequence that leads to normal tissue toxicity.
  • In particular, a paradox exists between the potential pro-apoptotic effect NF-kappaB exerts on normal cells, and the anti-apoptotic and cytoprotective effect it causes in tumor cells.
  • This paper provides a review of the structure and function of NF-kappaB and speculates how its apparent enigmatic effect on normal and tumor cells may occur.
  • [MeSH-minor] Animals. Antineoplastic Agents / adverse effects. Apoptosis / drug effects. Apoptosis / genetics. Cranial Irradiation / adverse effects. Gene Expression Regulation, Developmental. Gene Expression Regulation, Neoplastic. Humans. Mouth Mucosa / drug effects. Mouth Mucosa / radiation effects. Transcriptional Activation

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  • (PMID = 12393757.001).
  • [ISSN] 1045-4411
  • [Journal-full-title] Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists
  • [ISO-abbreviation] Crit. Rev. Oral Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / NF-kappa B
  • [Number-of-references] 87
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17. Faro A, Boj SF, Clevers H: Fishing for intestinal cancer models: unraveling gastrointestinal homeostasis and tumorigenesis in zebrafish. Zebrafish; 2009 Dec;6(4):361-76
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  • Given that the molecular pathways involved in epithelial carcinogenesis appear to be conserved across vertebrates, zebrafish is now considered as a valid model to study tumor biology.
  • Development and homeostasis in multicellular organisms are dependent on a complex interplay between cell proliferation, migration, differentiation, and cell death.
  • The Wnt signaling pathway is a major signaling pathway during embryonic development and is the key regulator of self-renewal homeostasis in several adult tissues.
  • A large body of knowledge on adult stem-cell biology has arisen from the study of the intestinal epithelium over the past 20 years.
  • Recently, zebrafish models have been developed to study Wnt pathway-induced cancer.
  • [MeSH-major] Cell Transformation, Neoplastic / metabolism. Homeostasis. Intestinal Neoplasms / drug therapy. Intestinal Neoplasms / metabolism. Zebrafish / metabolism

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  • (PMID = 19929219.001).
  • [ISSN] 1557-8542
  • [Journal-full-title] Zebrafish
  • [ISO-abbreviation] Zebrafish
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Wnt Proteins
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18. Steinmetzer T, Schweinitz A, Stürzebecher A, Dönnecke D, Uhland K, Schuster O, Steinmetzer P, Müller F, Friedrich R, Than ME, Bode W, Stürzebecher J: Secondary amides of sulfonylated 3-amidinophenylalanine. New potent and selective inhibitors of matriptase. J Med Chem; 2006 Jul 13;49(14):4116-26
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  • Matriptase is an epithelium-derived type II transmembrane serine protease and has been implicated in the activation of substrates such as pro-HGF/SF and pro-uPA, which are likely involved in tumor progression and metastasis.
  • X-ray analyses of analogues 8 and 31 in complex with matriptase revealed that these inhibitors occupy, in addition to part of the previously described S4-binding site, the cleft formed by the molecular surface and the unique 60 loop of matriptase.
  • Compared to control, both inhibitors reduced tumor growth, as well as tumor dissemination.
  • [MeSH-minor] Animals. Catalytic Domain. Crystallography, X-Ray. Humans. Kinetics. Male. Mice. Mice, Nude. Models, Molecular. Neoplasm Metastasis. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Structure-Activity Relationship. Xenograft Model Antitumor Assays

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  • (PMID = 16821772.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amides; 0 / Amidines; 0 / Serine Proteinase Inhibitors; 0 / Sulfones; 47E5O17Y3R / Phenylalanine; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / matriptase
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19. Deng L, Broaddus RR, McCampbell A, Shipley GL, Loose DS, Stancel GM, Pickar JH, Davies PJ: Identification of a novel estrogen-regulated gene, EIG121, induced by hormone replacement therapy and differentially expressed in type I and type II endometrial cancer. Clin Cancer Res; 2005 Dec 1;11(23):8258-64
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  • [Title] Identification of a novel estrogen-regulated gene, EIG121, induced by hormone replacement therapy and differentially expressed in type I and type II endometrial cancer.
  • Here, we describe the expression pattern of a novel estrogen-induced gene, EIG121, in distinct types of endometrial cancer.
  • EXPERIMENTAL DESIGN: EIG121 was identified by cDNA microarray analysis of endometrial RNA from women receiving either placebo or estrogen replacement therapy.
  • The expression level of EIG121 was then measured by real-time quantitative reverse transcription-PCR in benign, hyperplastic, and malignant endometrial samples.
  • RESULTS: In postmenopausal endometrium, estrogen replacement therapy with Premarin and synthetic estrogen sulfate conjugates induced the expression of EIG121 2- and 3-fold, respectively.
  • In endometrial complex, hyperplasia, and endometrioid adenocarcinoma, neoplastic proliferations associated with estrogen excess, the expression of EIG121 was significantly elevated (on average 3.8-fold in hyperplasias and 21-fold in grade 1 tumors).
  • Although the level of EIG121 mRNA in grade 3 endometrioid carcinoma was still 3.5-fold of that in benign endometrium, EIG121 expression tended to decline with increasing tumor grade and disease stage.
  • Immunohistochemistry showed faint staining of normal endometrial epithelium, but intense staining of endometrioid tumors.
  • In sharp contrast, EIG121 expression was significantly suppressed in both uterine papillary serous carcinoma and uterine malignant mixed mullerian tumor, two tumors not associated with estrogen exposure, to <5% of the level in benign endometrium.
  • CONCLUSIONS: Our results suggest that EIG121 is a good endometrial biomarker associated with a hyperestrogenic state and estrogen-related type I endometrial adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / genetics. Endometrial Neoplasms / genetics. Estrogen Replacement Therapy. Estrogens / therapeutic use. Gene Expression Regulation, Neoplastic / drug effects. Neoplasm Proteins / genetics
  • [MeSH-minor] Case-Control Studies. Endometrial Hyperplasia / genetics. Endometrial Hyperplasia / pathology. Estrogens, Conjugated (USP) / therapeutic use. Estrone / analogs & derivatives. Estrone / therapeutic use. Expressed Sequence Tags. Female. Gene Expression Profiling. Humans. Immunohistochemistry. Oligonucleotide Array Sequence Analysis. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16322283.001).
  • [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 / 1P50CA098258-01; United States / NICHD NIH HHS / HD / 5T32 HD007324-18
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogens; 0 / Estrogens, Conjugated (USP); 0 / KIAA1324 protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 2DI9HA706A / Estrone; QTL48N278K / estrone sulfate
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20. Goedegebuure PS, Watson MA, Viehl CT, Fleming TP: Mammaglobin-based strategies for treatment of breast cancer. Curr Cancer Drug Targets; 2004 Sep;4(6):531-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mammaglobin-based strategies for treatment of breast cancer.
  • Mammaglobin is a gene that is expressed almost exclusively in the normal breast epithelium and human breast cancer.
  • We have focused on the tissue-specificity of mammaglobin as a potential mechanism for the specific killing of breast cancer cells.
  • This would include > 80% of all breast cancers and some normal breast epithelium.
  • This type of targeted killing could be conceptualized as a biochemical mastectomy, that is, genetic ablation of breast tumor cells and perhaps non-malignant breast epithelium while preserving the adipose and stromal components of the breast.
  • If this finding is validated, this creates the possibility that mammaglobin can be tagged with radioisotope or toxin, so that binding of the tagged-mammaglobin complex results in the specific killing of that breast cancer cell.
  • In vitro studies have demonstrated that T cell-mediated immune responses can be induced against mammaglobin-derived peptides expressed by MHC molecules on tumor cells and antigen-presenting cells.
  • [MeSH-major] Biomarkers, Tumor / physiology. Breast Neoplasms / metabolism. Breast Neoplasms / therapy. Neoplasm Proteins / physiology. Uteroglobin / physiology

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  • [Copyright] Copyright 2004 Bentham Science Publishers Ltd.
  • (PMID = 15462037.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mammaglobin A; 0 / Neoplasm Proteins; 0 / SCGB2A2 protein, human; 9060-09-7 / Uteroglobin
  • [Number-of-references] 71
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21. Baldwin RL, Tran H, Karlan BY: Loss of c-myc repression coincides with ovarian cancer resistance to transforming growth factor beta growth arrest independent of transforming growth factor beta/Smad signaling. Cancer Res; 2003 Mar 15;63(6):1413-9
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  • Many epithelial carcinomas, including ovarian, are refractory to the antiproliferative effects of transforming growth factor (TGF) beta.
  • Primary ovarian epithelial cell cultures were used as a model system to determine the mechanisms of TGF-beta resistance.
  • To simulate in vivo responses to TGF-beta, primary cultures derived from normal human ovarian surface epithelium (HOSE) and from ovarian carcinomas (CSOC) were grown on collagen I gel, the predominant matrix molecule in the ovarian tumor milieu.
  • To assess functional differences of the TGF-beta pathway in TGF-beta-sensitive HOSE and TGF-beta-resistant CSOC, we measured Smad2/4 and 3/4 complex induction after TGF-beta treatment.
  • HOSE and CSOC showed equivalent Smad2/4 and 3/4 complex induction after TGF-beta exposure for 0, 0.5, 2, and 4 h.
  • However, our data show equivalent SnoN degradation in HOSE and CSOC, and equivalent SnoN mRNA induction after TGF-beta treatment.
  • Surprising, TGF-beta-induced Ski degradation was not observed in HOSE or CSOC, suggesting that Ski may not function as a TGF-beta/Smad corepressor in ovarian epithelial cells.
  • These data suggest that TGF-beta/Smad signaling is blocked downstream of Smad complex formation or that an alternate signaling pathway other than TGF-beta/Smad may transmit TGF-beta-induced cell cycle arrest in the ovarian epithelium.
  • [MeSH-major] DNA-Binding Proteins / physiology. Genes, myc / physiology. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / genetics. Trans-Activators / physiology. Transforming Growth Factor beta / pharmacology. Transforming Growth Factor beta / physiology
  • [MeSH-minor] Cell Division / drug effects. Cell Division / genetics. Down-Regulation. Drug Resistance, Neoplasm. Extracellular Matrix / physiology. Female. Humans. Intracellular Signaling Peptides and Proteins. Proto-Oncogene Proteins / physiology. Signal Transduction / drug effects. Smad Proteins. Transforming Growth Factor beta1

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  • (PMID = 12649207.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA083636; United States / NCI NIH HHS / CA / 5 P50 CA83636
  • [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 / DNA-Binding Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / Proto-Oncogene Proteins; 0 / SKIL protein, human; 0 / Smad Proteins; 0 / TGFB1 protein, human; 0 / Trans-Activators; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 126648-96-2 / SKI protein, human
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22. Weber B, Serafin A, Michie J, Van Rensburg C, Swarts JC, Bohm L: Cytotoxicity and cell death pathways invoked by two new rhodium-ferrocene complexes in benign and malignant prostatic cell lines. Anticancer Res; 2004 Mar-Apr;24(2B):763-70
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  • BACKGROUND: Apoptotic propensity is currently viewed as an important parameter in drug-induced toxicity.
  • This investigation explores the onset of apoptosis and abnormal morphology in response to 3 drugs i.e.
  • Cisplatin, a novel Ferrocene (fctfa) and a novel Rhodium-Ferrocene [Rh(fctfa)(cod)] complex.
  • MATERIALS AND METHODS: A pair of prostate cell lines from normal human prostate epithelium (1542N) and malignant human prostate epithelium (1542T) were exposed to increasing concentrations of the drugs for 24 hours, double-stained with FITC-Annexin V and with Propidium Iodide and analysed by dual parameter flow cytometry to quantitate viable cells in quadrant I, early apoptotic cells in quadrant IV and late apoptotic/necrotic cells in quadrant III.
  • CONCLUSION: The 3 drugs Cisplatin, the novel Ferrocene and the novel Rhodium-Ferrocene complexes show similar toxicities in the 1-10 micro-molar range in prostate cell lines.
  • However the drugs differ significantly in the activation of death pathways.
  • Unlike Cisplatin-treated cells which enter apoptosis and necrosis sequentially, the 2 Ferrocene drugs invoke direct entry of cells into late necrosis without first entering the early apoptotic compartment.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Ferrous Compounds / pharmacology. Prostatic Neoplasms / drug therapy. Rhodium / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cisplatin / pharmacology. Humans. Inhibitory Concentration 50. Male. Organometallic Compounds / chemistry. Organometallic Compounds / pharmacology

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  • (PMID = 15161024.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / (1-ferrocenyl-4,4,4-trifluoro-1,3-butanedionat-k2O,O')rhodium(I); 0 / Antineoplastic Agents; 0 / Ferrous Compounds; 0 / Organometallic Compounds; 0 / ferrocenoyltrifluoroacetone; DMK383DSAC / Rhodium; Q20Q21Q62J / Cisplatin; U96PKG90JQ / ferrocene
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23. Tan X, Wen X, Liu Y: Paricalcitol inhibits renal inflammation by promoting vitamin D receptor-mediated sequestration of NF-kappaB signaling. J Am Soc Nephrol; 2008 Sep;19(9):1741-52
Hazardous Substances Data Bank. PARICALCITOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Induction of RANTES was localized primarily to the tubular epithelium, underscoring a role for tubular cells in renal inflammation.
  • The vitamin D receptor (VDR) and p65 formed a complex in tubular cells after paricalcitol treatment, which inhibited the ability of p65 to trans-activate gene transcription.

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  • (PMID = 18525004.001).
  • [ISSN] 1533-3450
  • [Journal-full-title] Journal of the American Society of Nephrology : JASN
  • [ISO-abbreviation] J. Am. Soc. Nephrol.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK064005; United States / NIDDK NIH HHS / DK / R01 DK071040; United States / NIDDK NIH HHS / DK / DK061408; United States / NIDDK NIH HHS / DK / R01 DK061408; United States / NIDDK NIH HHS / DK / DK071040; United States / NIDDK NIH HHS / DK / DK064005
  • [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 / Chemokine CCL5; 0 / Ergocalciferols; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / Receptors, Calcitriol; 0 / Rela protein, mouse; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha; 6702D36OG5 / paricalcitol
  • [Other-IDs] NLM/ PMC2518439
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24. Comuzzi B, Lambrinidis L, Rogatsch H, Godoy-Tundidor S, Knezevic N, Krhen I, Marekovic Z, Bartsch G, Klocker H, Hobisch A, Culig Z: The transcriptional co-activator cAMP response element-binding protein-binding protein is expressed in prostate cancer and enhances androgen- and anti-androgen-induced androgen receptor function. Am J Pathol; 2003 Jan;162(1):233-41
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Progression of human prostate cancer toward therapy resistance occurs in the presence of wild-type or mutated androgen receptors (ARs) that, in some cases, exhibit aberrant activation by various steroid hormones and anti-androgens.
  • The AR associates with a number of co-activators that possess histone acetylase activity and act as bridging molecules to components of the transcription initiation complex.
  • In prostate cancer DU-145 cells, which were transiently transfected with CBP cDNA, hydroxyflutamide enhanced AR activity to a greater extent than bicalutamide in the presence of either wild-type or the mutated AR 730 val-->met.
  • In two sublines of LNCaP cells that contain the mutated AR 877 thr-->ala and overexpressed CBP, increase in AR activity was observed after treatment with hydroxyflutamide but not with bicalutamide.
  • Endogenous CBP protein was detected by Western blot in nuclear extracts from the three prostate cancer cell lines, LNCaP, PC-3, and DU-145, all derived from therapy-resistant prostate cancer.
  • In addition, CBP was expressed in both basal and secretory cells of benign prostate epithelium, high-grade prostate intraepithelial neoplasia, and prostate cancer clinical specimens, as evidenced by immunohistochemical staining.
  • Taken together, our findings demonstrate the selective enhancement of agonistic action of the anti-androgen hydroxyflutamide by the transcriptional co-activator CBP, which is a new, potentially relevant mechanism contributing to the acquisition of therapy resistance in prostate cancer.
  • [MeSH-major] Androgen Antagonists / pharmacology. Androgens / pharmacology. Carcinoma / metabolism. Nuclear Proteins / biosynthesis. Prostatic Neoplasms / metabolism. Receptors, Androgen / metabolism. Trans-Activators / biosynthesis
  • [MeSH-minor] CREB-Binding Protein. Humans. Lymphatic Metastasis. Male. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. Transcriptional Activation / drug effects. Tumor Cells, Cultured / drug effects

  • Genetic Alliance. consumer health - Prostate cancer.
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  • (PMID = 12507906.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / CREBBP protein, human; 0 / Nuclear Proteins; 0 / Receptors, Androgen; 0 / Trans-Activators; EC 2.3.1.48 / CREB-Binding Protein
  • [Other-IDs] NLM/ PMC1851122
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25. Männistö M, Vanderkerken S, Toncheva V, Elomaa M, Ruponen M, Schacht E, Urtti A: Structure-activity relationships of poly(L-lysines): effects of pegylation and molecular shape on physicochemical and biological properties in gene delivery. J Control Release; 2002 Sep 18;83(1):169-82
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • DNA binding, condensation, complex size and morphology, cell uptake and transfection efficiency were determined.
  • [MeSH-major] Drug Delivery Systems / methods. Genetic Therapy / methods. Polylysine / administration & dosage. Polylysine / analogs & derivatives. Structure-Activity Relationship
  • [MeSH-minor] Chemistry, Physical. Humans. Molecular Structure. Physicochemical Phenomena. Pigment Epithelium of Eye / cytology. Pigment Epithelium of Eye / drug effects. Pigment Epithelium of Eye / metabolism. Polyethylene Glycols / administration & dosage. Polyethylene Glycols / chemistry. Polyethylene Glycols / pharmacokinetics. Tumor Cells, Cultured

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  • [Copyright] Copyright 2002 Elsevier Science B.V.
  • (PMID = 12220848.001).
  • [ISSN] 0168-3659
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 25104-18-1 / Polylysine; 30IQX730WE / Polyethylene Glycols
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26. Brantley-Sieders DM, Zhuang G, Hicks D, Fang WB, Hwang Y, Cates JM, Coffman K, Jackson D, Bruckheimer E, Muraoka-Cook RS, Chen J: The receptor tyrosine kinase EphA2 promotes mammary adenocarcinoma tumorigenesis and metastatic progression in mice by amplifying ErbB2 signaling. J Clin Invest; 2008 Jan;118(1):64-78
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Overexpression of the receptor tyrosine kinase EPH receptor A2 (EphA2) is commonly observed in aggressive breast cancer and correlates with a poor prognosis.
  • EphA2 deficiency impaired tumor initiation and metastatic progression in mice overexpressing ErbB2 (also known as Neu) in the mammary epithelium (MMTV-Neu mice), but not in mice overexpressing the polyomavirus middle T antigen in mammary epithelium (MMTV-PyV-mT mice).
  • Histologic and ex vivo analyses of MMTV-Neu mouse mammary epithelium indicated that EphA2 enhanced tumor proliferation and motility.
  • Biochemical analyses revealed that EphA2 formed a complex with ErbB2 in human and murine breast carcinoma cells, resulting in enhanced activation of Ras-MAPK signaling and RhoA GTPase.
  • Additionally, MMTV-Neu, but not MMTV-PyV-mT, tumors were sensitive to therapeutic inhibition of EphA2.
  • These data suggest that EphA2 cooperates with ErbB2 to promote tumor progression in mice and may provide a novel therapeutic target for ErbB2-dependent tumors in humans.
  • Moreover, EphA2 function in tumor progression appeared to depend on oncogene context, an important consideration for the application of therapies targeting EphA2.

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  • (PMID = 18079969.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA95004; United States / NCI NIH HHS / CA / R01 CA095004; United States / NCI NIH HHS / CA / R01 CA114301; United States / NCI NIH HHS / CA / CA1179151-02; United States / NCI NIH HHS / CA / CA114301
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; EC 2.7.10.1 / ERBB2 protein, human; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, EphA2; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.6.5.2 / RhoA protein, mouse; EC 3.6.5.2 / rho GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2129239
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27. Dass CR, Contreras KG, Dunstan DE, Choong PF: Chitosan microparticles encapsulating PEDF plasmid demonstrate efficacy in an orthotopic metastatic model of osteosarcoma. Biomaterials; 2007 Jul;28(19):3026-33
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  • The major stumbling block for most therapies against deep-seated disease, including tumours, is inefficient drug delivery.
  • Such a concern is particularly important for osteosarcoma, the predominant form of bone cancer, and the largest cancer of its type in the paediatric age group.
  • Pigment epithelium-derived factor (PEDF) is the most potent anti-angiogenic factor found endogenously in the body, with an increasing number of reports pointing to its direct antitumour activity.
  • In this report, when a plasmid expressing PEDF (pPEDF) was encapsulated within two types of chitosan microparticles, anti-invasion and increased adhesion of the osteosarcoma cell line SaOS-2 was noted.
  • Microparticles were formulated using two methods of complex coacervation and were approximately 400-600 nm in diameter.
  • In vivo, the better pPEDF microparticle resulted in a decrease in primary tumour growth, reduced bone lysis and reduced establishment of lung metastases in a clinically relevant orthotopic model of osteosarcoma.
  • Thus, this new mode of localised gene delivery may hold promise for molecular therapy of osteosarcoma.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Bone Neoplasms. Chitosan / metabolism. Drug Compounding. Eye Proteins / therapeutic use. Nerve Growth Factors / therapeutic use. Osteosarcoma. Plasmids / metabolism. Serpins / therapeutic use
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Genes, Reporter. Green Fluorescent Proteins / genetics. Green Fluorescent Proteins / metabolism. Humans. Lung Neoplasms / secondary. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Metastasis. Particle Size. Transfection

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  • (PMID = 17408737.001).
  • [ISSN] 0142-9612
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Eye Proteins; 0 / Nerve Growth Factors; 0 / Serpins; 0 / pigment epithelium-derived factor; 147336-22-9 / Green Fluorescent Proteins; 9012-76-4 / Chitosan
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28. Bazzaro M, Lee MK, Zoso A, Stirling WL, Santillan A, Shih IeM, Roden RB: Ubiquitin-proteasome system stress sensitizes ovarian cancer to proteasome inhibitor-induced apoptosis. Cancer Res; 2006 Apr 1;66(7):3754-63
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Herein, we show that ovarian carcinoma manifests an overstressed UPS by comparison with normal tissues by accumulation of ubiquitinated proteins despite elevated proteasome levels.
  • Elevated levels of total ubiquitinated proteins and 19S and 20S proteasome subunits are evident in both low-grade and high-grade ovarian carcinoma tissues relative to benign ovarian tumors and in ovarian carcinoma cell lines relative to immortalized surface epithelium.
  • We find that ovarian carcinoma cell lines exhibit greater sensitivity to apoptosis in response to proteasome inhibitors than immortalized ovarian surface epithelial cells.
  • Furthermore, treatment with the licensed proteasome inhibitor PS-341 slows the growth of ES-2 ovarian carcinoma xenograft in immunodeficient mice.
  • In sum, elevated proliferation and metabolic rate resulting from malignant transformation of the epithelium stresses the UPS and renders ovarian carcinoma more sensitive to apoptosis in response to proteasomal inhibition.
  • [MeSH-major] Apoptosis / drug effects. Ovarian Neoplasms / drug therapy. Ovarian Neoplasms / metabolism. Protease Inhibitors / pharmacology. Proteasome Endopeptidase Complex / metabolism. Proteasome Inhibitors. Ubiquitin / metabolism
  • [MeSH-minor] Animals. Boronic Acids / pharmacology. Bortezomib. Caspases / metabolism. Cell Division / drug effects. Cell Line, Tumor. Female. G2 Phase / drug effects. Humans. Leupeptins / pharmacology. Mice. Mice, Nude. Oligopeptides / pharmacology. Pyrazines / pharmacology. Xenograft Model Antitumor Assays


29. Silvestri A, Colombatti A, Calvert VS, Deng J, Mammano E, Belluco C, De Marchi F, Nitti D, Liotta LA, Petricoin EF, Pierobon M: Protein pathway biomarker analysis of human cancer reveals requirement for upfront cellular-enrichment processing. Lab Invest; 2010 May;90(5):787-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tissues are complex structures composed of different cell types, each of which present specific functions and characteristics.
  • To better understand and measure the effect of tumor cell enrichment on protein pathway profiling and drug target activation measurements, the signaling activation portraits of laser capture microdissected (LCM) cancer epithelium and tumor stroma were compared with patient-matched whole-tissue specimens from 53 primary colorectal cancer samples.
  • Microdissected material and whole-tissue lysate from contiguous cryostat sections were subjected to reverse-phase protein microarray analysis to determine the level of phopshorylation and expression of 75 different proteins known to be involved in cancer progression.
  • The results revealed distinct differences in the protein activation portraits of cancer epithelium and stroma.
  • Moreover, we found that the signaling activation profiles of the undissected whole-tissue specimens are profoundly different from the matched LCM material.
  • Attempts to rescale the undissected pathway information based on percent endogenous tumor epithelium content were unsuccessful in recapitulating the LCM tumor epithelial signatures.
  • On the basis of these data, we conclude that accurate protein pathway activation status, which is under evaluation as a basis for patient selection and stratification for personalized therapy, must include upfront cellular-enrichment techniques such as LCM to generate accurate drug target activation status.
  • [MeSH-major] Biomarkers, Tumor / analysis. Neoplasms / metabolism. Proteins / analysis. Signal Transduction
  • [MeSH-minor] Blotting, Western. Cluster Analysis. Cyclooxygenase 2 / metabolism. Epithelium / metabolism. Epithelium / pathology. Humans. Lasers. Microarray Analysis / methods. Microdissection / methods. Phosphorylation. Proteomics / methods. Receptor, Epidermal Growth Factor / metabolism

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  • (PMID = 20195244.001).
  • [ISSN] 1530-0307
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [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 / Biomarkers, Tumor; 0 / Proteins; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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