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1. Bisacchi D, Noonan DM, Carlone S, Albini A, Pfeffer U: Kaposi's sarcoma and human chorionic gonadotropin: mechanisms, moieties and mysteries. Biol Chem; 2002 Sep;383(9):1315-20
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  • Kaposi's Sarcoma (KS) is a highly angiogenic neoplasm associated with infection by the human gamma-herpesvirus, HHV-8 or Kaposi's sarcoma herpes virus (KSHV).
  • Today, KS is a more common pathology due to its high incidence in AIDS, in immuno-suppressed transplantation patients and, in its endemic form, in Africa.
  • The variable effect in clinical trials using urinary preparations of the hormone (u-hCG) has led to the hypothesis that contaminating moieties present in these preparations may account for the anti-KS effect observed in vitro.
  • [MeSH-major] Chorionic Gonadotropin / therapeutic use. Sarcoma, Kaposi / drug therapy
  • [MeSH-minor] AIDS-Related Opportunistic Infections / drug therapy. Animals. Female. Herpesviridae Infections / drug therapy. Herpesvirus 8, Human / growth & development. Humans. Male. Pregnancy

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  • (PMID = 12437123.001).
  • [ISSN] 1431-6730
  • [Journal-full-title] Biological chemistry
  • [ISO-abbreviation] Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin
  • [Number-of-references] 52
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2. Kenney JL, Guinness ME, Reiss M, Lacy J: Antisense to the Epstein-Barr virus (EBV)-encoded latent membrane protein 1 (LMP-1) sensitizes EBV-immortalized B cells to transforming growth factor-beta and chemotherapeutic agents. Int J Cancer; 2001 Jan 1;91(1):89-98
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  • [Title] Antisense to the Epstein-Barr virus (EBV)-encoded latent membrane protein 1 (LMP-1) sensitizes EBV-immortalized B cells to transforming growth factor-beta and chemotherapeutic agents.
  • In previous studies, we have shown that short-term treatment of EBV-positive lymphoblastoid cell lines (LCLs) with LMP-1 antisense oligodeoxynucleotides can dramatically reduce levels of LMP-1 protein in association with inhibition of proliferation, stimulation of apoptosis, down-regulation of Bcl-2 and Mcl-1 and enhanced sensitivity to the chemotherapeutic agent, etoposide.
  • In addition, LMP-1 antisense sensitizes LCLs to chemotherapeutic drugs from diverse classes, including etoposide, vincristine and dexamethasone, by enhancing apoptotic cell death.
  • Finally, the anti-proliferative and apoptotic effects of LMP-1 antisense treatment were observed not only in laboratory-derived LCLs, but also in an EBV-positive cell line derived from an AIDS-related lymphoma.
  • [MeSH-major] B-Lymphocytes / metabolism. DNA, Antisense / metabolism. Transforming Growth Factor beta / metabolism. Viral Matrix Proteins / genetics
  • [MeSH-minor] Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Cell Division / drug effects. Cell Line, Transformed. Cell Separation. Cyclin D2. Cyclins / metabolism. Dexamethasone / pharmacology. Down-Regulation. Etoposide / pharmacology. Flow Cytometry. Humans. Immunoblotting. Lymphoma / metabolism. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Tumor Cells, Cultured. Vincristine / pharmacology

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  • (PMID = 11149426.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 67396
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Antineoplastic Agents, Phytogenic; 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / DNA, Antisense; 0 / EBV-associated membrane antigen, Epstein-Barr virus; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Transforming Growth Factor beta; 0 / Viral Matrix Proteins; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone
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3. Grigorian A, Hurford R, Chao Y, Patrick C, Langford TD: Alterations in the Notch4 pathway in cerebral endothelial cells by the HIV aspartyl protease inhibitor, nelfinavir. BMC Neurosci; 2008 Feb 26;9:27
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  • BACKGROUND: Aspartyl protease inhibitors (PIs) used to treat HIV belong to an important group of drugs that influence significantly endothelial cell functioning and angiogenic capacity, although specific mechanisms are poorly understood.
  • Recently, PIs, particularly Nelfinavir, were reported to disrupt Notch signaling in the HIV-related endothelial cell neoplasm, Kaposi's sarcoma.

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  • (PMID = 18302767.001).
  • [ISSN] 1471-2202
  • [Journal-full-title] BMC neuroscience
  • [ISO-abbreviation] BMC Neurosci
  • [Language] ENG
  • [Grant] United States / NIMH NIH HHS / MH / K01 MH071206; United States / NINDS NIH HHS / NS / R21 NS055639; United States / NHLBI NIH HHS / HL / T35HL007491-25; United States / NIMH NIH HHS / MH / R24 MH059745; United States / NIA NIH HHS / AG / T35AG026757; United States / NINDS NIH HHS / NS / NS055639; United States / NIMH NIH HHS / MH / R01 MH062962; United States / NIMH NIH HHS / MH / MH071206; United States / NIA NIH HHS / AG / T35 AG026757; United States / NHLBI NIH HHS / HL / T35 HL007491; United States / NIMH NIH HHS / MH / MH59745; United States / NIMH NIH HHS / MH / MH62962
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / C14orf129 protein, human; 0 / HIV Protease Inhibitors; 0 / NOTCH4 protein, human; 0 / Proto-Oncogene Proteins; 0 / Reactive Oxygen Species; 0 / Receptor, Notch1; 0 / Receptors, Notch; 0 / Repressor Proteins; 1406-18-4 / Vitamin E; 5W6YA9PKKH / Indinavir; EC 3.4.23.- / Aspartic Acid Endopeptidases; HO3OGH5D7I / Nelfinavir; L3JE09KZ2F / Saquinavir; O3J8G9O825 / Ritonavir
  • [Other-IDs] NLM/ PMC2268698
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4. Ruff KR, Puetter A, Levy LS: Growth regulation of simian and human AIDS-related non-Hodgkin's lymphoma cell lines by TGF-beta1 and IL-6. BMC Cancer; 2007 Feb 26;7:35
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  • [Title] Growth regulation of simian and human AIDS-related non-Hodgkin's lymphoma cell lines by TGF-beta1 and IL-6.
  • BACKGROUND: AIDS-related non-Hodgkin's lymphoma (AIDS-NHL) is the second most frequent cancer associated with AIDS, and is a frequent cause of death in HIV-infected individuals.
  • Experimental analysis of AIDS-NHL has been facilitated by the availability of an excellent animal model, i.e., simian Acquired Immunodeficiency Syndrome (SAIDS) in the rhesus macaque consequent to infection with simian immunodeficiency virus.
  • The authors concluded that TGF-beta acts as a negative growth regulator of the lymphoma-derived cell line and, potentially, as an inhibitory factor in the regulatory network of AIDS-related lymphomagenesis.
  • The present study was conducted to assess whether other SAIDS-NHL and AIDS-NHL cell lines are similarly sensitive to the growth inhibitory effects of TGF-beta, and to test the hypothesis that interleukin-6 (IL-6) may represent a counteracting positive influence in their growth regulation.
  • Intracellular flow cytometry was used to analyze the activation of signaling pathways and to examine the expression of anti-apoptotic proteins and distinguishing hallmarks of AIDS-NHL subclass.
  • By comparison, human AIDS-NHL cell lines differed in their responsiveness to TGF-beta1 and IL-6.
  • Analysis of a recently derived AIDS-NHL cell line, UMCL01-101, indicated that it represents immunoblastic AIDS-DLCBL.
  • CONCLUSION: These studies indicate that the sensitivity of immunoblastic AIDS- or SAIDS-DLBCL to TGF-beta1-mediated growth inhibition may be overcome through the stimulation of proliferative and anti-apoptotic signals by IL-6, particularly through the rapid activation of STAT3.

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  • (PMID = 17324269.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA074731; United States / NCI NIH HHS / CA / R01 CA74731
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Interleukin-6; 0 / Transforming Growth Factor beta1
  • [Other-IDs] NLM/ PMC1810304
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5. Samantas E, Kalofonos H, Linardou H, Nicolaides C, Mylonakis N, Fountzilas G, Kosmidis P, Skarlos D: Phase II study of pegylated liposomal doxorubicin: inactive in recurrent small-cell lung cancer. A Hellenic Cooperative Oncology Group Study. Ann Oncol; 2000 Nov;11(11):1395-7
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  • [Title] Phase II study of pegylated liposomal doxorubicin: inactive in recurrent small-cell lung cancer. A Hellenic Cooperative Oncology Group Study.
  • PURPOSE: Although clinical experience with liposomal doxorubicin is still limited in solid tumours, single agent Caelyx (pegylated liposomal doxorubicin) treatment has shown promising results in AIDS-related Kaposi's sarcoma, metastatic breast and ovarian cancer and anecdotally in other solid tumours.
  • This is the first report of its use in small-cell lung cancer (SCLC).
  • CONCLUSIONS: These results demonstrate limited activity of Caelyx in this patient population, which may be related to the poor prognostic features of such patients.

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  • (PMID = 11142478.001).
  • [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; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
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6. Mallery SR, Morse MA, Wilson RF, Pei P, Ness GM, Bradburn JE, Renner RJ, Schuller DE, Robertson FM: AIDS-related Kaposi's sarcoma cells rapidly internalize endostatin, which co-localizes to tropomysin microfilaments and inhibits cytokine-mediated migration and invasion. J Cell Biochem; 2003 May 1;89(1):133-43
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  • [Title] AIDS-related Kaposi's sarcoma cells rapidly internalize endostatin, which co-localizes to tropomysin microfilaments and inhibits cytokine-mediated migration and invasion.
  • AIDS-related Kaposi's sarcoma (KS) is the most common HIV-related malignancy.
  • Therefore, the angiogenic phenotype, which is crucial for cancer progression, is inherent to KS tumor cells.
  • Due to the recognized importance of angiogenesis in cancer progression, numerous angiostatic agents are being investigated as potential therapeutic agents.
  • One such agent is endostatin, which is a 20-kDa carboxyl-terminal fragment of collagen XVIII that has demonstrated potent angiostatic activities at both the in vivo and in vitro levels.
  • Since endostatin is recognized as a potent angiostatic agent, the majority of in vitro endostatin studies have evaluated its effects on endothelial cells.
  • [MeSH-minor] Actin Cytoskeleton / metabolism. Angiogenesis Inhibitors / metabolism. Angiogenesis Inhibitors / pharmacology. Cell Movement / drug effects. Collagen Type XVIII. Cytokines / metabolism. Endostatins. Endothelial Growth Factors / pharmacology. Fibroblast Growth Factor 2 / pharmacology. Humans. In Vitro Techniques. Intercellular Signaling Peptides and Proteins / pharmacology. Lymphokines / pharmacology. NF-kappa B / metabolism. Neoplasm Invasiveness. Neovascularization, Pathologic. Recombinant Proteins / metabolism. Recombinant Proteins / pharmacology. Transcription Factor AP-1 / metabolism. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • [Copyright] Published 2003 Wiley-Liss, Inc.
  • (PMID = 12682914.001).
  • [ISSN] 0730-2312
  • [Journal-full-title] Journal of cellular biochemistry
  • [ISO-abbreviation] J. Cell. Biochem.
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / P01 DE 12704; United States / NCI NIH HHS / CA / P30 CA 16058; United States / NCI NIH HHS / CA / U01 CA 66531
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Collagen Type XVIII; 0 / Cytokines; 0 / Endostatins; 0 / Endothelial Growth Factors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / NF-kappa B; 0 / Peptide Fragments; 0 / Recombinant Proteins; 0 / Transcription Factor AP-1; 0 / Tropomyosin; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 103107-01-3 / Fibroblast Growth Factor 2; 9007-34-5 / Collagen
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7. Hernández-Morales DE, Hernández-Zaccaro AE: Gastrointestinal and cutaneous AIDS-related Kaposi's sarcoma: different activity of liposomal doxorubicin according to location of lesions. Eur J Cancer Care (Engl); 2005 Jul;14(3):264-6
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  • [Title] Gastrointestinal and cutaneous AIDS-related Kaposi's sarcoma: different activity of liposomal doxorubicin according to location of lesions.
  • Kaposi's sarcoma (KS) continues to be a frequent neoplasm in third world AIDS patients.
  • The study included 15 male AIDS patients aged between 25 and 35 years (mean: 27 years) with more than 25 cutaneous lesions and extensive gastrointestinal KS.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Doxorubicin / administration & dosage. Gastrointestinal Neoplasms / drug therapy. Sarcoma, Kaposi / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adult. Drug Administration Schedule. Humans. Liposomes. Male. Prospective Studies. Treatment Outcome

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  • (PMID = 15952971.001).
  • [ISSN] 0961-5423
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Liposomes; 80168379AG / Doxorubicin
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8. Lan K, Murakami M, Bajaj B, Kaul R, He Z, Gan R, Feldman M, Robertson ES: Inhibition of KSHV-infected primary effusion lymphomas in NOD/SCID mice by gamma-secretase inhibitor. Cancer Biol Ther; 2009 Nov;8(22):2136-43
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  • Primary effusion lymphoma (PEL) is a common cancer in AIDS patients closely associated with Kaposi's sarcoma-associated herpesvirus (KSHV).
  • Our study provides further evidence to suggest that targeted downregulation of abnormal Notch signaling has therapeutic potential for KSHV related primary effusion lymphomas.
  • [MeSH-major] Amyloid Precursor Protein Secretases / antagonists & inhibitors. Dipeptides / therapeutic use. Herpesviridae Infections. Herpesvirus 8, Human / pathogenicity. Lymphoma, Primary Effusion / drug therapy. Neoplasm Proteins / antagonists & inhibitors. Receptor, Notch1 / antagonists & inhibitors. Tumor Virus Infections
  • [MeSH-minor] Animals. Antigens, Viral / physiology. Apoptosis. Burkitt Lymphoma / pathology. Cell Line, Tumor / transplantation. Herpesvirus 4, Human / isolation & purification. Herpesvirus 4, Human / pathogenicity. Mice. Mice, Inbred NOD. Mice, SCID. Necrosis. Nuclear Proteins / physiology. Random Allocation. Signal Transduction / drug effects. Specific Pathogen-Free Organisms. Xenograft Model Antitumor Assays

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  • [CommentIn] Cancer Biol Ther. 2009 Nov;8(22):2144-6 [20068386.001]
  • (PMID = 19783901.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / PHS HHS / / A1067037; United States / NCI NIH HHS / CA / CA091792; United States / NCI NIH HHS / CA / CA108461; United States / NIDCR NIH HHS / DE / DE017338
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral; 0 / Dipeptides; 0 / N-(N-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester; 0 / Neoplasm Proteins; 0 / Notch1 protein, mouse; 0 / Nuclear Proteins; 0 / Receptor, Notch1; 0 / latency-associated nuclear antigen; EC 3.4.- / Amyloid Precursor Protein Secretases
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9. Attia S, Dezube BJ, Torrealba JR, Sosman JM, McHaffie DR, Pfau PR, Bailey HH, Kozak KR: AIDS-related Kaposi's sarcoma of the gastrointestinal tract. J Clin Oncol; 2010 Jun 01;28(16):e250-1
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  • [Title] AIDS-related Kaposi's sarcoma of the gastrointestinal tract.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / diagnosis. Sarcoma, Kaposi / drug therapy. Sarcoma, Kaposi / pathology. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology
  • [MeSH-minor] Adult. Antiretroviral Therapy, Highly Active / methods. Biopsy, Needle. Doxorubicin / therapeutic use. Drug Therapy, Combination. Follow-Up Studies. Gastrointestinal Neoplasms / drug therapy. Gastrointestinal Neoplasms / etiology. Gastrointestinal Neoplasms / pathology. HIV Infections / complications. HIV Infections / diagnosis. HIV Infections / drug therapy. Humans. Immunohistochemistry. Male. Neoplasm Staging. Risk Assessment. Severity of Illness Index. Treatment Outcome


10. Hatse S: Mechanistic study on the cytostatic and tumor cell differentiation-inducing properties of 9-(2-phosphonylmethoxyethyl)adenine (PMEA, adefovir)-collected publications. Verh K Acad Geneeskd Belg; 2000;62(5):373-84
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  • The therapeutic potential of the antiretroviral drug 9-(2-phosphonylmethoxyethyl)adenine (PMEA, adefovir) for the treatment of human immunodeficiency virus (HIV)- and human hepatitis B virus (HBV) infections is currently being explored in advanced clinical trials.
  • In the present study, we investigated the impact of PMEA on cellular functioning (cell cycle, nucleotide metabolism, nucleic acid synthesis, ...).
  • Moreover, we have unraveled the molecular/biochemical basis underlying the marked differentiation-inducing activity of PMEA (and related analogues) in tumor cells.
  • These findings open new perspectives for the possible application of this type of compounds in cancer chemotherapy.
  • The fact that AIDS patients frequently develop certain types of differentiation-susceptible malignancies (e.g.
  • [MeSH-major] Adenine / analogs & derivatives. Adenine / pharmacology. Antineoplastic Agents / pharmacology. Cell Differentiation / drug effects. HIV Infections / drug therapy. Hepatitis B / drug therapy. Neoplasms / drug therapy. Organophosphonates
  • [MeSH-minor] Animals. Antiviral Agents / pharmacology. Antiviral Agents / therapeutic use. Cell Division / drug effects. Cell Transformation, Neoplastic / drug effects. Drug Resistance, Neoplasm. Humans. Rats. Tumor Cells, Cultured / drug effects

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  • (PMID = 11144686.001).
  • [ISSN] 0302-6469
  • [Journal-full-title] Verhandelingen - Koninklijke Academie voor Geneeskunde van België
  • [ISO-abbreviation] Verh. K. Acad. Geneeskd. Belg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Belgium
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antiviral Agents; 0 / Organophosphonates; 6GQP90I798 / adefovir; JAC85A2161 / Adenine
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11. Lavolé A, Epaud C, Rosencher L, Gounant V, Wislez M, Cadranel J: [Lung cancer in HIV-positive patients]. Rev Pneumol Clin; 2007 Jun;63(3):167-75
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  • [Title] [Lung cancer in HIV-positive patients].
  • [Transliterated title] Le cancer broncho-pulmonaire chez les patients séropositifs pour le virus de l'immunodéficience humaine.
  • Since 1996, AIDS-related mortality has declined considerably with the introduction of tritherapy (HAART).
  • This decline in mortality has been associated with an increase in the proportion of deaths caused by cancers unrelated to AIDS, particularly lung cancer.
  • The risk of developing lung cancer is higher in the HIV-seropositive population than in the aged-matched general population, undoubtedly because of the high rate of smoking, particularly among drug abusers, but also because of other reasons which remain to be determined.
  • Mean age at the discovery of lung cancer in HIV+ patients is 45 years, and most are symptomatic.
  • The diagnosis is established at a locally advanced or metastatic stage in 75-90% of patients, as in the general population.
  • Adenocarcinoma is the most common histological type.
  • Prospective clinical studies are needed to define a better management strategy for lung cancer in HIV-positive patients.
  • [MeSH-minor] Adenocarcinoma / complications. Age Factors. Antineoplastic Agents / therapeutic use. Antiretroviral Therapy, Highly Active. Humans. Neoplasm Staging. Pneumonectomy. Prognosis. Risk Factors

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  • (PMID = 17675940.001).
  • [ISSN] 0761-8417
  • [Journal-full-title] Revue de pneumologie clinique
  • [ISO-abbreviation] Rev Pneumol Clin
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 66
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12. Dzierzbicka K, Kołodziejczyk AM: Synthesis and antitumor activity of conjugates of muramyldipeptide or normuramyldipeptide with hydroxyacridine/acridone derivatives. J Med Chem; 2003 Jan 2;46(1):183-9
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  • A series of MDP (muramyldipeptide) or nor-MDP (normuramyldipeptide) analogues modified at the C-terminus post of the molecule by a formation of an ester bond between the carboxylic group of isoglutamine and the hydroxyl function of the respective derivatives of 4-carboxamide-acridine/9-acridone or 1-nitro-9-hydroxyalkylaminoacridines were synthesized as potential anticancer agents.
  • The compounds O-(1-O-benzyl-N-acetyl-muramyl-l-alanyl-d-gamma-isoglutaminyl)-9-(ethylamino)-1-nitroacridine ester 3j and O-(1-O-benzyl-N-acetyl-muramyl-l-alanyl-d-gamma-isoglutaminyl)-9-propylamino-1-nitroacridine ester 3k exhibited high in vitro cytotoxic activity against a panel of human cell lines, prostate cancer and AIDS-related lymphoma (ARL).
  • [MeSH-major] Acetylmuramyl-Alanyl-Isoglutamine / chemical synthesis. Acridines / chemical synthesis. Antineoplastic Agents / chemical synthesis
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor. Humans. Lymphoma, AIDS-Related / drug therapy. Male. Mice. Mice, Nude. Neoplasm Transplantation. Prostatic Neoplasms / drug therapy. Structure-Activity Relationship. Tumor Cells, Cultured

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  • (PMID = 12502372.001).
  • [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 / Acridines; 0 / Antineoplastic Agents; 53678-77-6 / Acetylmuramyl-Alanyl-Isoglutamine; 578-95-0 / acridone
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13. Martellotta F, Berretta M, Vaccher E, Schioppa O, Zanet E, Tirelli U: AIDS-related Kaposi's sarcoma: state of the art and therapeutic strategies. Curr HIV Res; 2009 Nov;7(6):634-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AIDS-related Kaposi's sarcoma: state of the art and therapeutic strategies.
  • In the HAART era Kaposi's sarcoma (KS) remains the second most frequent tumor in HIV-infected patients worldwide, and it has become the most common cancer in Sub-Saharan Africa.
  • KS lesions are comprised of both distinctive spindle cells of endothelial origin and a variable inflammatory infiltrate, which suggests that KS may result from reactive hyperproliferation induced by chronic inflammation, and therefore it is not a true neoplasm.
  • Treatment decisions must take into consideration the extent and the rate of tumor growth, patient's symptoms, immune system conditions and concurrent HIV-related complications.
  • The angiogenic nature of KS makes it particularly suitable for therapies based on targeted agents such as metalloproteinase inhibitors, angiogenesis inhibitors and tyrosine kinase inhibitors.
  • The aim of this article is to provide an up-to-date review of the current status and perspectives of AIDS-related KS in the HAART era.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / complications. Sarcoma, Kaposi / drug therapy. Sarcoma, Kaposi / pathology


14. Tejada-Berges T, Granai CO, Gordinier M, Gajewski W: Caelyx/Doxil for the treatment of metastatic ovarian and breast cancer. Expert Rev Anticancer Ther; 2002 Apr;2(2):143-50
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  • [Title] Caelyx/Doxil for the treatment of metastatic ovarian and breast cancer.
  • The FDA and EMEA have approved its use for the treatment of AIDS-related Kaposi's sarcoma and, more recently, for recurrent epithelial ovarian cancer (EOC).
  • Numerous investigations have focused on its use in the treatment of metastatic breast cancer, as well as recurrent squamous cell cervical carcinoma, soft tissue sarcoma, squamous head and neck cancers, prostate cancers and malignant gliomas.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Breast Neoplasms / drug therapy. Doxorubicin / administration & dosage. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Animals. Clinical Trials as Topic / methods. Clinical Trials as Topic / statistics & numerical data. Female. Humans. Neoplasm Recurrence, Local / drug therapy


15. Volkow P, Zinser JW, Correa-Rotter R: Molecularly targeted therapy for Kaposi's sarcoma in a kidney transplant patient: case report, "what worked and what did not". BMC Nephrol; 2007;8:6
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  • BACKGROUND: Imatinib is a tyrosine-kinase inhibitor; for which there is limited information regarding its effects on AIDS Kaposi's sarcoma and none in patients with transplant-associated Kaposi's sarcoma.
  • Sirolimus, an immunosuppressive drug used for kidney transplant, exhibits antiangiogenic activity related to impaired production of VEGF (vascular endothelial growth factor), clinical benefit has been reported in Kaposi's sarcoma associated with renal graft.
  • CASE PRESENTATION: Here we report a case of an 80 year old male, who developed Kaposi's Sarcoma nine months after receiving a living non-related donor kidney transplant at age 74.
  • Three years after treatment with different chemotherapeutic agents for progressive cutaneous Kaposi's Sarcoma with no visceral involvement, he was prescribed Imatinib (200 mg/day for two weeks followed by 400 mg/day) after four weeks of treatment he developed anasarca, further progression of KS and agranulocytosis.
  • [MeSH-major] Kidney Transplantation / adverse effects. Piperazines / adverse effects. Pyrimidines / adverse effects. Sarcoma, Kaposi / drug therapy. Sirolimus / therapeutic use. Skin Neoplasms / drug therapy
  • [MeSH-minor] Aged, 80 and over. Benzamides. Biopsy, Needle. Dose-Response Relationship, Drug. Drug Administration Schedule. Follow-Up Studies. Humans. Imatinib Mesylate. Immunohistochemistry. Kidney Failure, Chronic / diagnosis. Kidney Failure, Chronic / surgery. Male. Neoplasm Staging. Retreatment. Risk Assessment. Treatment Outcome

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  • (PMID = 17386117.001).
  • [ISSN] 1471-2369
  • [Journal-full-title] BMC nephrology
  • [ISO-abbreviation] BMC Nephrol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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16. Levine AM, Sadeghi S, Espina B, Tulpule A, Nathwani B: Characteristics of indolent non-Hodgkin lymphoma in patients with type 1 human immunodeficiency virus infection. Cancer; 2002 Mar 1;94(5):1500-6
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  • [Title] Characteristics of indolent non-Hodgkin lymphoma in patients with type 1 human immunodeficiency virus infection.
  • BACKGROUND: There is recent evidence that the incidence of indolent non-Hodgkin lymphoma (NHL) appears to be increased in persons with the acquired immunodeficiency syndrome (AIDS).
  • METHODS: The current report was a retrospective study of 10 cases of indolent NHL identified from the AIDS-Lymphoma Registry at the University of Southern California School of Medicine.
  • These patients were compared with 336 consecutive patients with systemic intermediate/high-grade AIDS-related NHL who were diagnosed and treated at a single institution.
  • When comparing the indolent lymphomas with the intermediate/high-grade AIDS-NHL cases, no differences were observed with regard to demographic characteristics or history of prior opportunistic infection.
  • [MeSH-minor] Adult. Aged. Female. Humans. Male. Middle Aged. Neoplasm Staging. Prognosis. Survival Analysis


17. van der Kuyl AC, van den Burg R, Zorgdrager F, Dekker JT, Maas J, van Noesel CJ, Goudsmit J, Cornelissen M: Primary effect of chemotherapy on the transcription profile of AIDS-related Kaposi's sarcoma. BMC Cancer; 2002 Sep 2;2:21
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  • [Title] Primary effect of chemotherapy on the transcription profile of AIDS-related Kaposi's sarcoma.
  • BACKGROUND: Drugs & used in anticancer chemotherapy have severe effects upon the cellular transcription and replication machinery.
  • From in vitro studies it has become clear that these drugs can affect specific genes, as well as have an effect upon the total transcriptome.
  • METHODS: Total mRNA from two skin lesions from a single AIDS-KS patient was analyzed with the SAGE (Serial Analysis of Gene Expression) technique to assess changes in the transcriptome induced by chemotherapy.
  • KS-24 and KS-48 were compared to SAGE libraries of untreated AIDS-KS, and to libraries generated from normal skin and from isolated CD4+ T-cells, using the programs USAGE and HTM.
  • RESULTS: In order to assess the primary response of AIDS-related Kaposi's sarcoma (AIDS-KS) to chemotherapy in vivo, we analyzed the transcriptome of AIDS-KS skin lesions from a HIV-1 seropositive patient at two time points after therapy.
  • The mRNA profile was found to have changed dramatically within 24 hours after drug treatment.
  • There was an almost complete absence of transcripts highly expressed in AIDS-KS, probably due to a transcription block.
  • IGCs are known to fuse after transcription inhibition, probably affecting poly(A)+RNA distribution.Forty-eight hours after chemotherapy, mRNA isolated from the lesion was largely derived from infiltrating lymphocytes, confirming the transcriptional block in the AIDS-KS tissue.
  • CONCLUSIONS: These in vivo findings indicate that the effect of anti-cancer drugs is likely to be more global than up- or downregulation of specific genes, at least in this single patient with AIDS-KS.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / drug therapy. Acquired Immunodeficiency Syndrome / genetics. Gene Expression Regulation, Neoplastic / drug effects. Sarcoma, Kaposi / drug therapy. Sarcoma, Kaposi / genetics. Skin Neoplasms / drug therapy. Skin Neoplasms / genetics. Transcription, Genetic / drug effects
  • [MeSH-minor] Gene Expression Profiling / methods. Gene Library. Genes / drug effects. Genes, Neoplasm / drug effects. Humans. Poly A / analysis. RNA / analysis. RNA, Messenger / analysis. RNA, Neoplasm / analysis. Time Factors

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  • (PMID = 12204098.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, mitochondrial; 24937-83-5 / Poly A; 63231-63-0 / RNA
  • [Other-IDs] NLM/ PMC126247
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18. Rivera E: Current status of liposomal anthracycline therapy in metastatic breast cancer. Clin Breast Cancer; 2003 Nov;4 Suppl 2:S76-83
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  • [Title] Current status of liposomal anthracycline therapy in metastatic breast cancer.
  • Doxorubicin is a mainstay for the treatment of metastatic breast cancer (MBC); however, its use is limited by toxicity, particularly cardiotoxicity.
  • Novel drug delivery systems using liposomes have been developed to maintain the clinical utility of conventional doxorubicin while minimizing cardiotoxicity.
  • Liposomal daunorubicin, currently approved in the United States for the treatment of AIDS-related Kaposi sarcoma, has shown preliminary activity in MBC in a phase I trial; further investigation is ongoing.
  • Nonpegylated liposomal doxorubicin, which is not available in the United States, has demonstrated activity similar to that of conventional doxorubicin (both as a single agent and in combinations).
  • Pegylated liposomal doxorubicin has demonstrated activity in phase II and III trials when used alone or in combination with other chemotherapeutic agents in patients with MBC.
  • It is currently approved in the United States and Europe for AIDS-related Kaposi sarcoma and platinum/paclitaxel-refractory ovarian carcinoma; in Europe and Canada, it is also approved as monotherapy for MBC.
  • Based on these encouraging experiences, randomized clinical trials are ongoing or planned to further assess the therapeutic potential of pegylated liposomal doxorubicin as a single agent and in combination with other chemotherapeutic agents and targeted agents, such as trastuzumab, for MBC.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Breast Neoplasms / drug therapy. Doxorubicin / administration & dosage
  • [MeSH-minor] Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Drug Delivery Systems. Female. Humans. Neoplasm Metastasis. Randomized Controlled Trials as Topic

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  • (PMID = 14667278.001).
  • [ISSN] 1526-8209
  • [Journal-full-title] Clinical breast cancer
  • [ISO-abbreviation] Clin. Breast Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
  • [Number-of-references] 47
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19. Olivero OA, Vazquez IL, Cooch CC, Ming J, Keller E, Yu M, Borojerdi JP, Braun HM, McKee E, Poirier MC: Long-term AZT exposure alters the metabolic capacity of cultured human lymphoblastoid cells. Toxicol Sci; 2010 May;115(1):109-17
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  • An exposure-related increase in the frequency of micronuclei (MN) was observed in cells exposed to either 10 or 800 microM AZT during P(1)-P(14).

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  • (PMID = 20106944.001).
  • [ISSN] 1096-0929
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / DNA Adducts; 4B9XT59T7S / Zidovudine; 9007-49-2 / DNA; EC 2.7.1.21 / Thymidine Kinase; EC 2.7.1.21 / thymidine kinase 1; VC2W18DGKR / Thymidine
  • [Other-IDs] NLM/ PMC2855349
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20. Catrina SB, Lewitt M, Massambu C, Dricu A, Grünler J, Axelson M, Biberfeld P, Brismar K: Insulin-like growth factor-I receptor activity is essential for Kaposi's sarcoma growth and survival. Br J Cancer; 2005 Apr 25;92(8):1467-74
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  • Kaposi's sarcoma (KS) is a highly vascular tumour and is the most common neoplasm associated with human immunodeficiency virus (HIV-1) infection.
  • The IGF-I receptors (IGF-IR) were identified by immunohistochemistry in biopsies taken from patients with different AIDS/HIV-related KS stages and on KSIMM cells (an established KS-derived cell line).
  • [MeSH-major] Podophyllotoxin / analogs & derivatives. Receptor, IGF Type 1 / metabolism. Sarcoma, Kaposi / metabolism. Sarcoma, Kaposi / pathology
  • [MeSH-minor] Acquired Immunodeficiency Syndrome / complications. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Somatomedins / pharmacology. Vascular Endothelial Growth Factor A / pharmacology

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  • (PMID = 15812560.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Somatomedins; 0 / Vascular Endothelial Growth Factor A; 0F35AOI227 / picropodophyllin; EC 2.7.10.1 / Receptor, IGF Type 1; L36H50F353 / Podophyllotoxin
  • [Other-IDs] NLM/ PMC2362008
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21. Lim ST, Tupule A, Espina BM, Levine AM: Weekly docetaxel is safe and effective in the treatment of advanced-stage acquired immunodeficiency syndrome-related Kaposi sarcoma. Cancer; 2005 Jan 15;103(2):417-21
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  • [Title] Weekly docetaxel is safe and effective in the treatment of advanced-stage acquired immunodeficiency syndrome-related Kaposi sarcoma.
  • BACKGROUND: Intravenous paclitaxel, 100 mg/m(2), given over 3 hours every 2 weeks is associated with a response rate of 59% in patients with recurrent or refractory acquired immunodeficiency syndrome (AIDS)-related Kaposi sarcoma (KS).
  • Moreover, no effective therapies have been defined for use after treatment failure with this agent.
  • Treatment was well tolerated, with no Grade 4 toxicity of any type.
  • CONCLUSIONS: Weekly docetaxel is safe, with reasonable antitumor activity in patients with advanced-stage, recurrent, or refractory AIDS-related KS.
  • [MeSH-major] Acquired Immunodeficiency Syndrome / complications. Sarcoma, Kaposi / drug therapy. Sarcoma, Kaposi / pathology. Skin Neoplasms / pathology. Taxoids / administration & dosage
  • [MeSH-minor] Adult. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Staging. Risk Assessment. Survival Analysis. Treatment Outcome


22. Mantovani A, Allavena P, Sica A, Balkwill F: Cancer-related inflammation. Nature; 2008 Jul 24;454(7203):436-44
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  • [Title] Cancer-related inflammation.
  • In some types of cancer, inflammatory conditions are present before a malignant change occurs.
  • Conversely, in other types of cancer, an oncogenic change induces an inflammatory microenvironment that promotes the development of tumours.
  • It aids in the proliferation and survival of malignant cells, promotes angiogenesis and metastasis, subverts adaptive immune responses, and alters responses to hormones and chemotherapeutic agents.
  • The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.
  • [MeSH-minor] Gonadal Steroid Hormones / metabolism. Humans. Leukocytes / immunology. Leukocytes / metabolism. Neoplasm Invasiveness. Oncogenes / genetics. Oncogenes / physiology

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  • (PMID = 18650914.001).
  • [ISSN] 1476-4687
  • [Journal-full-title] Nature
  • [ISO-abbreviation] Nature
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0501974; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones
  • [Number-of-references] 98
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23. Bray J, Sludden J, Griffin MJ, Cole M, Verrill M, Jamieson D, Boddy AV: Influence of pharmacogenetics on response and toxicity in breast cancer patients treated with doxorubicin and cyclophosphamide. Br J Cancer; 2010 Mar 16;102(6):1003-9
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  • [Title] Influence of pharmacogenetics on response and toxicity in breast cancer patients treated with doxorubicin and cyclophosphamide.
  • BACKGROUND: Doxorubicin and cyclophosphamide (AC) therapy is an effective treatment for early-stage breast cancer.
  • Cyclophosphamide is a prodrug that requires oxidation to 4-hydroxycyclophosphamide, which yields a cytotoxic alkylating agent.
  • Polymorphic variants of the genes coding for these enzymes and transporters have been identified, which may influence the systemic pharmacology of the two drugs.
  • METHODS: Germ line DNA samples from 230 patients with breast cancer on AC therapy were genotyped for the following SNPs: ABCB1 C1236T, G2677T/A and C3435T, SLC22A16 A146G, T312C, T755C and T1226C, CYP2B6*2, *8, *9, *3, *4 and *5, CYP2C9*2 and *3, CYP3A5*3 and CYP2C19*2.
  • RESULTS: A lower incidence of dose delay, indicative of less toxicity, was seen in carriers of the SLC22A16 A146G, T312C, T755C variants.
  • In contrast, a higher incidence of dose delay was seen in carriers of the SLC22A16 1226C, CYP2B6*2 and CYP2B6*5 alleles.
  • CONCLUSION: Variant alleles in the ABCB1, SLC22A16 and CYP2B6 genes are associated with response to AC therapy in the treatment of breast cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Carcinoma, Ductal, Breast / drug therapy. Cyclophosphamide / administration & dosage. Doxorubicin / administration & dosage. Pharmacogenetics
  • [MeSH-minor] Aryl Hydrocarbon Hydroxylases / genetics. Biomarkers, Pharmacological / analysis. Biomarkers, Tumor / genetics. Cytochrome P-450 CYP2B6. Drug Resistance, Neoplasm / genetics. Drug-Related Side Effects and Adverse Reactions / genetics. Female. Gene Frequency. Genotype. Humans. Middle Aged. Organic Cation Transport Proteins / genetics. Oxidoreductases, N-Demethylating / genetics. P-Glycoprotein / genetics. P-Glycoproteins. Polymorphism, Single Nucleotide. Retrospective Studies. Survival Analysis

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  • (PMID = 20179710.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Biomarkers, Pharmacological; 0 / Biomarkers, Tumor; 0 / Organic Cation Transport Proteins; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / SLC22A16 protein, human; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP2B6 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP2B6; EC 1.5.- / Oxidoreductases, N-Demethylating
  • [Other-IDs] NLM/ PMC2844036
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24. Tan B, Piwnica-Worms D, Ratner L: Multidrug resistance transporters and modulation. Curr Opin Oncol; 2000 Sep;12(5):450-8
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  • Multidrug resistance (MDR), whereby tumor cells simultaneously possess intrinsic or acquired cross-resistance to diverse chemotherapeutic agents, hampers the effective treatment of cancer.
  • Molecular investigations in MDR resulted in the isolation and characterization of genes coding for several proteins associated with MDR, including P-glycoprotein (P-gp), the multidrug resistance associated protein (MRP1), the lung resistance protein (LRP), and, more recently, the breast cancer resistance protein (BCRP).
  • These transmembrane proteins cause MDR either by decreasing the total intracellular retention of drugs or redistributing intracellular accumulation of drugs away from target organelles.
  • These proteins are expressed at varying degrees in different neoplasms, including the AIDS-associated non-Hodgkin lymphoma and Kaposi sarcoma and are generally associated with poor prognosis.
  • Several MDR-reversing agents are in various stages of clinical development.
  • First-generation modulators such as verapamil, quinidine, and cyclosporin required high doses of drugs to reverse MDR and were associated with unacceptable toxicities.
  • Limitations to the use of these modulators include multiple and redundant cellular mechanisms of resistance, alterations in pharmacokinetics of cytotoxic agents, and clinical toxicities.
  • A potential use of these agents may be to enhance intestinal drug absorption and increase drug penetration to biologically important protective barriers, such as the blood-brain, blood-cerebrospinal fluid, and the maternal-fetal barriers.
  • The use of MDR modulators with drugs such as the antiviral protease inhibitors and cytotoxics may enhance drug accumulation in sanctuary sites that are traditionally impenetrable to these agents.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Antineoplastic Agents / therapeutic use. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Multidrug Resistance-Associated Proteins
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Biological Transport. Cyclosporins / therapeutic use. DNA-Binding Proteins / metabolism. Humans. Lymphoma, AIDS-Related / drug therapy. Lymphoma, AIDS-Related / metabolism. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / metabolism. MutS Homolog 3 Protein. Neoplasm Proteins / metabolism. Prognosis. Vault Ribonucleoprotein Particles / metabolism

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  • (PMID = 10975553.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P20 CA86251
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Antineoplastic Agents; 0 / Cyclosporins; 0 / DNA-Binding Proteins; 0 / MSH3 protein, human; 0 / Multidrug Resistance-Associated Proteins; 0 / MutS Homolog 3 Protein; 0 / Neoplasm Proteins; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; Y49M64GZ4Q / multidrug resistance-associated protein 1
  • [Number-of-references] 96
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25. Krown SE: Therapy of AIDS-associated Kaposi's sarcoma: targeting pathogenetic mechanisms. Hematol Oncol Clin North Am; 2003 Jun;17(3):763-83
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  • [Title] Therapy of AIDS-associated Kaposi's sarcoma: targeting pathogenetic mechanisms.
  • Only a small number of the many agents with the potential to inhibit factors known to stimulate KS growth have been tested clinically, and many were investigated at a time when treatment options for HIV infection were relatively ineffective.
  • The failure of some of these agents to induce KS regression may not signify failure to achieve a relevant biologic effect in all cases, but may simply mean that in a neoplasm that expresses a broad array of growth factors, inhibition of a single factor may be insufficient to achieve tumor regression.
  • Moreover, agents that inhibit angiogenesis may be expected to stabilize tumors rather then eradicate them, but tumor stabilization is a difficult endpoint to quantify.
  • In fact, given the redundancy of growth factors believed to be involved in KS development, it is perhaps remarkable that members of several classes of agents (eg, a synthetic retinoid, an MMPI, thalidomide, IL-12) have induced KS regression in a substantial minority of patients.
  • It is likely, however, that drug combinations that target several pathogenetic mechanisms will be more effective than will single drugs in suppressing KS growth.
  • A particular need. especially in the early evaluation of therapies aimed at specific pathogenic targets, is the development of assays to measure specific biologic effects (eg, changes in the activity of signal transduction pathways within tumor biopsy specimens) related to the agent's putative mechanism of action.
  • Greater availability and clinical application of these types of markers of biologic efficacy may speed the identification of potentially active agents that could then be "fast tracked" into larger efficacy trials and combination studies.
  • [MeSH-major] AIDS-Related Opportunistic Infections / therapy. Sarcoma, Kaposi / therapy

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  • (PMID = 12852655.001).
  • [ISSN] 0889-8588
  • [Journal-full-title] Hematology/oncology clinics of North America
  • [ISO-abbreviation] Hematol. Oncol. Clin. North Am.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / UO1 CA70054
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cytokines
  • [Number-of-references] 141
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26. Alas S, Ng CP, Bonavida B: Rituximab modifies the cisplatin-mitochondrial signaling pathway, resulting in apoptosis in cisplatin-resistant non-Hodgkin's lymphoma. Clin Cancer Res; 2002 Mar;8(3):836-45
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  • PURPOSE: Rituximab (chimeric anti-CD20) can reverse the cisplatin-resistant phenotype of AIDS-related non-Hodgkin's lymphoma cell lines and results in cisplatin-mediated apoptosis.
  • EXPERIMENTAL DESIGN: The AIDS-related lymphoma (ARL) cell line 2F7 was treated with rituximab, cisplatin, and a combination of the two and analyzed by Western blot analyses for signaling proteins involved in the death receptor-mediated and mitochondrial pathways.
  • However, other proteins analyzed [namely, Apaf-1, Bax, Bid, caspase-3, caspase-8, caspase-9, X-linked inhibitor of apoptosis protein (XIAP), cellular inhibitor of apoptosis protein (cIAP)-1, cIAP-2, cytochrome c, Fas, Fas ligand, FLIP, p53, and poly(ADP-ribose) polymerase] were not affected by either rituximab or cisplatin.
  • Decreased expression of additional proteins (Apaf-1, cIAP-1, cIAP-2, and XIAP) paralleled apoptosis detected at 24 h.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Apoptosis / drug effects. Cisplatin / pharmacology. Drug Resistance, Neoplasm. Intracellular Signaling Peptides and Proteins. Lymphoma, AIDS-Related / metabolism. Mitochondria / drug effects. Signal Transduction / drug effects
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antigens, CD95 / metabolism. Antineoplastic Combined Chemotherapy Protocols. Apoptotic Protease-Activating Factor 1. Blotting, Western. CASP8 and FADD-Like Apoptosis Regulating Protein. Carrier Proteins. Caspase Inhibitors. Caspases / metabolism. Combined Modality Therapy. Cytochrome c Group / metabolism. Dose-Response Relationship, Drug. Enzyme Activation / drug effects. Enzyme Inhibitors / pharmacology. Fas Ligand Protein. Humans. Membrane Glycoproteins / metabolism. Proteins / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Reactive Oxygen Species / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Rituximab. Tumor Cells, Cultured / drug effects

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  • (PMID = 11895917.001).
  • [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 / NIAID NIH HHS / AI / AI07126-23
  • [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 / APAF1 protein, human; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD95; 0 / Apoptotic Protease-Activating Factor 1; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / Carrier Proteins; 0 / Caspase Inhibitors; 0 / Cytochrome c Group; 0 / Enzyme Inhibitors; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Glycoproteins; 0 / Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Reactive Oxygen Species; 4F4X42SYQ6 / Rituximab; EC 3.4.22.- / Caspases; Q20Q21Q62J / Cisplatin
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27. Siegel RS, Gartenhaus RB, Kuzel TM: Human T-cell lymphotropic-I-associated leukemia/lymphoma. Curr Treat Options Oncol; 2001 Aug;2(4):291-300
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  • Human T-cell lymphotropic virus-I (HTLV-I)-related adult T-cell leukemia/lymphoma (ATL) is a model disease for proof of viral oncogenesis.
  • Combination chemotherapy with cytotoxic agents has yielded complete response rates of 20% to 45%, but responses usually last only a few months [3].
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antiviral Agents / therapeutic use. Blood Transfusion / adverse effects. Child. Child, Preschool. Deltaretrovirus Infections / epidemiology. Deltaretrovirus Infections / transmission. Drug Resistance, Neoplasm. Epidemiologic Methods. Female. Human T-lymphotropic virus 1 / drug effects. Human T-lymphotropic virus 1 / genetics. Human T-lymphotropic virus 1 / physiology. Humans. Infant. Infant, Newborn. Male. Middle Aged. Pregnancy. Pregnancy Complications, Infectious. Prevalence. Prognosis. Radiotherapy, Adjuvant

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  • (PMID = 12057109.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents
  • [Number-of-references] 87
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28. Holmlund JT: Applying antisense technology: Affinitak and other antisense oligonucleotides in clinical development. Ann N Y Acad Sci; 2003 Dec;1002:244-51
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  • Progress in the development of antisense drugs over the last decade has led to the approval of the first such drug--Vitravene for AIDS-related CMV retinitis--and the development of a large number of antisense drugs in clinical trials.
  • Antisense drugs are now being studied in Phase 3 trials for patients with cancer and inflammatory bowel disease.
  • Other antisense drugs are in development for rheumatoid arthritis, other inflammatory conditions, and hepatitis C.
  • Still other antisense drugs are entering clinical trials for treatment of metabolic conditions such as diabetes and hyperlipidemia.
  • Improved antisense chemistry, which will enhance the feasibility of subcutaneous and oral administration of antisense drugs and offer the potential of less frequent dosing, is expected to further expand the opportunities for antisense drug development.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms. Oligonucleotides, Antisense / pharmacology
  • [MeSH-minor] Humans. Inhibitor of Apoptosis Proteins. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / genetics. Microtubule-Associated Proteins / biosynthesis. Microtubule-Associated Proteins / genetics. Neoplasm Proteins. Oligodeoxyribonucleotides, Antisense / pharmacology. Phosphorothioate Oligonucleotides. Protein Kinase C / antagonists & inhibitors. Protein Kinase C / genetics. Protein Kinase C-alpha. RNA, Messenger / drug effects. Thionucleotides / pharmacology

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  • (PMID = 14751839.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BIRC5 protein, human; 0 / ISIS 2503; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Oligodeoxyribonucleotides, Antisense; 0 / Oligonucleotides, Antisense; 0 / Phosphorothioate Oligonucleotides; 0 / RNA, Messenger; 0 / Thionucleotides; 0 / alicaforsen; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 2.7.11.13 / PRKCA protein, human; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C-alpha
  • [Number-of-references] 20
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29. Partridge AH, Archer L, Kornblith AB, Gralow J, Grenier D, Perez E, Wolff AC, Wang X, Kastrissios H, Berry D, Hudis C, Winer E, Muss H: Adherence and persistence with oral adjuvant chemotherapy in older women with early-stage breast cancer in CALGB 49907: adherence companion study 60104. J Clin Oncol; 2010 May 10;28(14):2418-22
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  • [Title] Adherence and persistence with oral adjuvant chemotherapy in older women with early-stage breast cancer in CALGB 49907: adherence companion study 60104.
  • PATIENTS AND METHODS: Cancer and Leukemia Group B study CALGB 49907 was a randomly assigned trial comparing standard chemotherapy versus oral chemotherapy with capecitabine in patients age 65 years or older with early-stage breast cancer.
  • Adherence was calculated as the number of doses taken divided by doses expected, taking into account toxicity-related dosing changes.
  • Adherence was not related to age, tumor stage, or hormone receptor status.
  • CONCLUSION: Most older women with early-stage breast cancer were adherent to short-term oral chemotherapy in a randomized clinical trial.

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  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U10 CA032291; United States / NCI NIH HHS / CA / CA33601; United States / NCI NIH HHS / CA / CA77406; United States / NCI NIH HHS / CA / CA32291; United States / NCI NIH HHS / CA / N01 CA032102; United States / NCI NIH HHS / CA / U10 CA077202; United States / NCI NIH HHS / CA / U10 CA021115; United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / CA77651; United States / NCI NIH HHS / CA / U10 CA033601; United States / NCI NIH HHS / CA / U10 CA105409; United States / NCI NIH HHS / CA / U10 CA032102; United States / NCI NIH HHS / CA / U10 CA077651; United States / NCI NIH HHS / CA / CA105409; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA77202; United States / NCI NIH HHS / CA / CA25224; United States / NCI NIH HHS / CA / .CA31946; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / U10 CA025224
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; U3P01618RT / Fluorouracil
  • [Other-IDs] NLM/ PMC2881723
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30. Fracasso PM, Blum KA, Ma MK, Tan BR, Wright LP, Goodner SA, Fears CL, Hou W, Arquette MA, Picus J, Denes A, Mortimer JE, Ratner L, Ivy SP, McLeod HL: Phase I study of pegylated liposomal doxorubicin and the multidrug-resistance modulator, valspodar. Br J Cancer; 2005 Jul 11;93(1):46-53
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  • Treatment with PEG-LD 25 mg m(-2) in combination with valspodar results in a moderate prolongation of total doxorubicin clearance and half-life but did not increase the toxicity of this agent.
  • [MeSH-major] AIDS-Related Opportunistic Infections / drug therapy. Antibiotics, Antineoplastic / therapeutic use. Cyclosporins / therapeutic use. Doxorubicin / therapeutic use. Sarcoma, Kaposi / drug therapy
  • [MeSH-minor] Drug Resistance, Multiple. Drug Resistance, Neoplasm. Humans. Liposomes

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  • (PMID = 15942626.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA091842
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; 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] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Cyclosporins; 0 / Liposomes; 121584-18-7 / valspodar; 80168379AG / Doxorubicin
  • [Other-IDs] NLM/ PMC2361488
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31. Tanaka PY, Calore EE: P-glycoprotein expression in non-Hodgkin's lymphomas of human immunodeficiency virus infected patients. Pathol Res Pract; 2007;203(1):1-7
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  • Multidrug resistance (MDR) is a challenge in cancer treatment.
  • One of the most studied mechanisms is P-glycoprotein (P-gp), which acts as a drug efflux pump, with decreased intracellular accumulation of drugs.
  • AIDS-related lymphomas have aggressive behavior, and although a complete response could be achieved, relapse is not uncommon.
  • Our results show that P-gp is expressed before treatment of non-Hodgkin's lymphoma of HIV patients, and is related to poor response to treatment and overall survival.
  • [MeSH-major] Acquired Immunodeficiency Syndrome. Lymphoma, AIDS-Related / metabolism. P-Glycoprotein / biosynthesis
  • [MeSH-minor] Adolescent. Adult. Anti-HIV Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Antiretroviral Therapy, Highly Active / mortality. Biomarkers, Tumor / metabolism. Cell Count. Cyclophosphamide / therapeutic use. Disease-Free Survival. Doxorubicin / therapeutic use. Drug Resistance, Multiple / genetics. Drug Resistance, Neoplasm / genetics. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prednisone / therapeutic use. Retrospective Studies. Survival Rate. Vincristine / therapeutic use

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  • [ErratumIn] Pathol Res Pract. 2007;203(10):763
  • (PMID = 17157997.001).
  • [ISSN] 0344-0338
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Biomarkers, Tumor; 0 / P-Glycoprotein; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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32. Puoti M, Bruno R, Soriano V, Donato F, Gaeta GB, Quinzan GP, Precone D, Gelatti U, Asensi V, Vaccher E, HIV HCC Cooperative Italian-Spanish Group: Hepatocellular carcinoma in HIV-infected patients: epidemiological features, clinical presentation and outcome. AIDS; 2004 Nov 19;18(17):2285-93
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  • PATIENTS AND METHODS: All HIV-infected subjects with a diagnosis of HCC included in three cancer registry databases were enrolled in the study as cases.
  • HCC cases that occurred in the province of Brescia, North Italy, in the period 1995-1998 and all cases reported at the Italian Liver Cancer Project were enrolled as controls.
  • [MeSH-minor] AIDS-Related Opportunistic Infections / complications. AIDS-Related Opportunistic Infections / epidemiology. Adult. Alcohol Drinking / epidemiology. Female. HIV Seropositivity / complications. HIV Seropositivity / drug therapy. HIV Seropositivity / epidemiology. Hepatitis C / complications. Hepatitis C / epidemiology. Humans. Italy / epidemiology. Male. Middle Aged. Neoplasm Metastasis. Prevalence. Risk Factors. Survival Analysis


33. Kino N, Sata T, Sato Y, Sugase M, Matsukura T: Molecular cloning and nucleotide sequence analysis of a novel human papillomavirus (Type 82) associated with vaginal intraepithelial neoplasia. Clin Diagn Lab Immunol; 2000 Jan;7(1):91-5
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  • [Title] Molecular cloning and nucleotide sequence analysis of a novel human papillomavirus (Type 82) associated with vaginal intraepithelial neoplasia.
  • The results indicated that HPV-82 is an etiologic agent for vaginal and cervical intraepithelial neoplasia.
  • By nucleotide sequence similarity of L1 open reading frame (ORF), HPV-82 was closely related to HPV-26, -51, and -69.
  • [MeSH-minor] Base Sequence. Biopsy. Cloning, Molecular. Codon, Initiator. DNA, Viral. Female. Humans. Neoplasm Staging

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  • (PMID = 10618284.001).
  • [ISSN] 1071-412X
  • [Journal-full-title] Clinical and diagnostic laboratory immunology
  • [ISO-abbreviation] Clin. Diagn. Lab. Immunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
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  • [Other-IDs] NLM/ PMC95829
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34. Cantarella G, Risuglia N, Dell'eva R, Lempereur L, Albini A, Pennisi G, Scoto GM, Noonan DN, Bernardini R: TRAIL inhibits angiogenesis stimulated by VEGF expression in human glioblastoma cells. Br J Cancer; 2006 May 22;94(10):1428-35
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  • Tumour growth is tightly related to new blood vessel formation, tissue remodelling and invasiveness capacity.
  • A number of tissular factors fuel the growth of glioblastoma multiforme, the most aggressive brain neoplasm.
  • In fact, gene array analyses demonstrated that the proapoptotic cytokine tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) inhibited mRNA expression of VEGF, along with those of matrix metalloproteinase-2 (MMP-2), its inhibitor tissue inhibitor of matrix metalloproteinases-2 (TIMP-2), as well as the tumour invasiveness-related gene secreted protein acid rich in cysteine (SPARC) in different human glioblastoma cell lines.
  • Moreover, the expression of MMP-2, its inhibitor TIMP-2 and the tumour invasiveness-related protein SPARC were effectively inhibited by TRAIL in glioblastoma cell lines.
  • In conclusion, our data indicate that TRAIL inhibits the orchestra of factors contributing to glioblastoma biological aggressiveness.
  • Thus, the TRAIL system could be regarded as a molecular target to exploit for innovative therapy of this type of tumour.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis Regulatory Proteins / therapeutic use. Brain Neoplasms / blood supply. Glioblastoma / blood supply. Membrane Glycoproteins / therapeutic use. Neovascularization, Pathologic / drug therapy. Tumor Necrosis Factor-alpha / therapeutic use. Vascular Endothelial Growth Factor A / genetics
  • [MeSH-minor] Animals. Blotting, Western. Cell Survival. Endothelium, Vascular / drug effects. Enzyme-Linked Immunosorbent Assay. Gene Expression Profiling. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 2 / metabolism. Mice. Mice, Inbred C57BL. Oligonucleotide Array Sequence Analysis. Osteonectin / genetics. Osteonectin / metabolism. RNA, Messenger / metabolism. TNF-Related Apoptosis-Inducing Ligand. Tissue Inhibitor of Metalloproteinase-2 / genetics. Tissue Inhibitor of Metalloproteinase-2 / metabolism. Tumor Cells, Cultured

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  • (PMID = 16622457.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Osteonectin; 0 / RNA, Messenger; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tnfsf10 protein, mouse; 0 / Tumor Necrosis Factor-alpha; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; EC 3.4.24.24 / Matrix Metalloproteinase 2
  • [Other-IDs] NLM/ PMC2361261
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35. Rajput S, Wilber A: Roles of inflammation in cancer initiation, progression, and metastasis. Front Biosci (Schol Ed); 2010;2:176-83
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  • [Title] Roles of inflammation in cancer initiation, progression, and metastasis.
  • Inflammatory cells and signals contribute to the initiation and development of cancer.
  • In fact, persistent inflammatory conditions resulting from infection or injury can exist before a normal cell is transformed into a cancer cell.
  • Alternatively, cancer development unrelated to inflammation can stimulate the development of an inflammatory microenvironment that promotes tumor cell proliferation.
  • Whether chronic or tumor-derived, inflammation and inflammation-related stimuli within the tumor microenvironment permits proliferation and survival of cancer cells, promotes blood and lymphatic vessel formation, and aids in invasion and metastasis.
  • The inflammatory status of the tumor microenvironment can act to quell the body's natural immune response and effectively ameliorate a positive response to many commonly used anti-cancer antibodies and chemotherapeutic agents.
  • New evidence suggests that the molecular pathways and consequences of inflammation specifically related to the tumor microenvironment are starting to be understood.
  • [MeSH-major] Cytokines / metabolism. Inflammation / complications. Neoplasm Metastasis / physiopathology. Neoplasms / etiology. Signal Transduction / physiology
  • [MeSH-minor] Disease Progression. Drug Delivery Systems. Humans. Hypoxia-Inducible Factor 1 / metabolism. NF-kappa B / metabolism. Nitric Oxide Synthase Type II / metabolism. Prostaglandin-Endoperoxide Synthases / metabolism

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  • (PMID = 20036938.001).
  • [ISSN] 1945-0524
  • [Journal-full-title] Frontiers in bioscience (Scholar edition)
  • [ISO-abbreviation] Front Biosci (Schol Ed)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / Hypoxia-Inducible Factor 1; 0 / NF-kappa B; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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