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1. Mao Q: BCRP/ABCG2 in the placenta: expression, function and regulation. Pharm Res; 2008 Jun;25(6):1244-55
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  • [Title] BCRP/ABCG2 in the placenta: expression, function and regulation.
  • Knowledge concerning transport of maternally administered drugs across the placental barrier is essential for determining potential toxicity of drugs to the fetus and the value of drug therapy during pregnancy.
  • An important determinant for fetal drug exposure is the expression of efflux transporters in the placenta.
  • Among human tissues, the ATP-binding cassette efflux transporter BCRP (gene symbol ABCG2) is most abundantly expressed in the apical membrane of placental syncytiotrophoblasts.
  • Although the precise physiological role of BCRP in the placenta is still unclear, existing data strongly suggest that BCRP plays an important role in protecting the fetus against the potential toxicity of drugs, xenobiotics, and metabolites by expelling them across the placental barrier.
  • In this review, we summarize the current knowledge with respect to the expression, function, and polymorphisms of BCRP, as well as transcriptional and posttranscriptional regulation of the transporter in the placenta.
  • Finally, clinical significance of BCRP in the placenta for drug therapy in pregnant women is discussed.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. Neoplasm Proteins / physiology. Placenta / chemistry

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  • [ErratumIn] Pharm Res. 2008 Jun;25(6):1484
  • (PMID = 18202831.001).
  • [ISSN] 0724-8741
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / P50 HD044404; United States / NICHD NIH HHS / HD / U10 HD047892; United States / NICHD NIH HHS / HD / HD044404; United States / NICHD NIH HHS / HD / HD047892
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; 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 / Neoplasm Proteins
  • [Number-of-references] 105
  • [Other-IDs] NLM/ PMC2346511
  •  go-up   go-down


2. Robey RW, To KK, Polgar O, Dohse M, Fetsch P, Dean M, Bates SE: ABCG2: a perspective. Adv Drug Deliv Rev; 2009 Jan 31;61(1):3-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • With high normal tissue expression in the brain endothelium, gastrointestinal tract, and placenta, ABCG2 is believed to be important in the protection from xenobiotics, regulating oral bioavailability, forming part of the blood-brain barrier, the blood-testis barrier, and the maternal-fetal barrier.
  • While ABCG2 overexpression has been demonstrated in cancer cells after in vitro drug treatment, endogenous ABCG2 expression in certain cancers is likely a reflection of the differentiated phenotype of the cell of origin and likely contributes to intrinsic drug resistance.
  • Notably, research into the transporter's role in cancer drug resistance and its development as a therapeutic target in cancer has lagged.
  • Substrates and inhibitors of the transporter have been described, among them chemotherapy drugs, tyrosine kinase inhibitors, antivirals, HMG-CoA reductase inhibitors, carcinogens, and flavonoids.
  • [MeSH-major] ATP-Binding Cassette Transporters / physiology. Neoplasm Proteins / physiology
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Animals. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Biological Transport. Gene Expression / drug effects. Humans. Neoplasms / drug therapy. Neoplasms / metabolism. Organ Specificity. Substrate Specificity. Tissue Distribution

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  • (PMID = 19135109.001).
  • [ISSN] 1872-8294
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Antineoplastic Agents; 0 / Neoplasm Proteins
  • [Number-of-references] 159
  • [Other-IDs] NLM/ NIHMS291570; NLM/ PMC3105088
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3. Fischer C, Jonckx B, Mazzone M, Zacchigna S, Loges S, Pattarini L, Chorianopoulos E, Liesenborghs L, Koch M, De Mol M, Autiero M, Wyns S, Plaisance S, Moons L, van Rooijen N, Giacca M, Stassen JM, Dewerchin M, Collen D, Carmeliet P: Anti-PlGF inhibits growth of VEGF(R)-inhibitor-resistant tumors without affecting healthy vessels. Cell; 2007 Nov 2;131(3):463-75
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We explored the therapeutic potential and mechanisms of alphaPlGF, an antibody against placental growth factor (PlGF), a VEGF homolog, which regulates the angiogenic switch in disease, but not in health. alphaPlGF inhibited growth and metastasis of various tumors, including those resistant to VEGF(R) inhibitors (VEGF(R)Is), and enhanced the efficacy of chemotherapy and VEGF(R)Is. alphaPlGF inhibited angiogenesis, lymphangiogenesis, and tumor cell motility.
  • Distinct from VEGF(R)Is, alphaPlGF prevented infiltration of angiogenic macrophages and severe tumor hypoxia, and thus, did not switch on the angiogenic rescue program responsible for resistance to VEGF(R)Is.
  • The efficacy and safety of alphaPlGF, its pleiotropic and complementary mechanism to VEGF(R)Is, and the negligible induction of an angiogenic rescue program suggest that alphaPlGF may constitute a novel approach for cancer treatment.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Blood Vessels / drug effects. Blood Vessels / physiology. Drug Resistance, Neoplasm / drug effects. Pregnancy Proteins / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line. Cell Movement / drug effects. Drug Screening Assays, Antitumor. Drug-Related Side Effects and Adverse Reactions. Health. Humans. Lymphangiogenesis / drug effects. Macrophages / cytology. Macrophages / drug effects. Mice. Neoplasm Metastasis. Neoplasms / blood supply. Neoplasms / drug therapy. Neoplasms / pathology. Neovascularization, Pathologic / drug therapy. Treatment Outcome


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4. Shinkaruk S, Bayle M, Laïn G, Déléris G: Vascular endothelial cell growth factor (VEGF), an emerging target for cancer chemotherapy. Curr Med Chem Anticancer Agents; 2003 Mar;3(2):95-117
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular endothelial cell growth factor (VEGF), an emerging target for cancer chemotherapy.
  • When pathological, it contributes to the development of numerous types of tumors, and the formation of metastases.
  • This concept makes the control of tumoral angiogenesis one of the promising therapeutic ways in cancerology.
  • The transition from the latent phase to the invasive and metastatic phase of a cancer is linked to what is called the angiogenic switch.
  • Among them, VEGF, Vascular Endothelial Growth Factor was found in several types of tumors.
  • During the last few years, several members of the VEGF family have been described namely the VEGF-A, B, C, D, E and placenta growth factor (PlGF) among which VEGF-A (121 aminoacids) plays a role of prime importance in angiogenesis.
  • The three-dimensional structure of VEGF has been recently determined, by X-rays diffraction, and NMR spectroscopy.
  • The specific action of the VEGF on the endothelial cells is mainly regulated by two types of RTK of the VEGF family, VEGFR1, or Flt-1, and VEGFR2, or KDR/Flk-1.
  • Therefore angiogenesis mediated by VEGF constitutes a new target for anti-cancer therapy which has explored through different ways of intervention aiming at the blocking of the tumoral angiogenesis.
  • [MeSH-minor] Animals. Endothelium, Vascular. Humans. Intercellular Signaling Peptides and Proteins / physiology. Neoplasm Metastasis / prevention & control. Paracrine Communication. Receptors, Vascular Endothelial Growth Factor / metabolism. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 12678905.001).
  • [ISSN] 1568-0118
  • [Journal-full-title] Current medicinal chemistry. Anti-cancer agents
  • [ISO-abbreviation] Curr Med Chem Anticancer Agents
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Endothelial Growth Factors; 0 / Intercellular Signaling Peptides and Proteins; 0 / Lymphokines; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 195
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5. Brechbuhl HM, Min E, Kariya C, Frederick B, Raben D, Day BJ: Select cyclopentenone prostaglandins trigger glutathione efflux and the role of ABCG2 transport. Free Radic Biol Med; 2009 Sep 15;47(6):722-30
Hazardous Substances Data Bank. TERT-BUTYL HYDROPEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CyPG treatment increased extracellular GSH levels two- to threefold over controls in HN4 and C38 cells and five- to sixfold in SAEC and MDA 1586 cells and was dependent on increased GSH synthesis.
  • Superarray analysis of ABC transporters suggested only ABCG2 expression had a positive relationship in the four cell types compared with extracellular GSH increases after cyPG treatment.
  • The ABCG2 substrate Hoechst 33342 inhibited extracellular GSH increase after 15dPGJ(2) treatment.
  • We report for the first time that ABCG2 may play a role in GSH efflux in response to cyPG treatment and may link inflammatory signaling with antioxidant adaptive responses.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. Glutathione / biosynthesis. Head and Neck Neoplasms / drug therapy. Neoplasm Proteins / metabolism. Prostaglandin D2 / analogs & derivatives. Respiratory Mucosa / drug effects
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Benzimidazoles / pharmacology. Cell Line, Tumor. Chromatography, High Pressure Liquid. Cytoprotection / drug effects. Gene Expression Regulation, Neoplastic. Humans. Oligonucleotide Array Sequence Analysis. Oxidative Stress / drug effects. Substrate Specificity. tert-Butylhydroperoxide / metabolism

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  • (PMID = 19520157.001).
  • [ISSN] 1873-4596
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL084469-02; United States / NHLBI NIH HHS / HL / R01 HL084469; United States / NHLBI NIH HHS / HL / R01 HL075523-04; United States / NHLBI NIH HHS / HL / R01 HL084469-01A2; United States / NHLBI NIH HHS / HL / HL075523; United States / NIEHS NIH HHS / ES / R01 ES017582; United States / NHLBI NIH HHS / HL / R01 HL075523-02; United States / NHLBI NIH HHS / HL / R01 HL075523-01; United States / NHLBI NIH HHS / HL / HL084469; United States / NHLBI NIH HHS / HL / R01 HL075523; United States / NHLBI NIH HHS / HL / R01 HL075523-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 15-deoxy-delta(12,14)-prostaglandin J2; 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Benzimidazoles; 0 / Neoplasm Proteins; 955VYL842B / tert-Butylhydroperoxide; GAN16C9B8O / Glutathione; P976261J69 / bisbenzimide ethoxide trihydrochloride; RXY07S6CZ2 / Prostaglandin D2
  • [Other-IDs] NLM/ NIHMS123320; NLM/ PMC2730198
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6. Dhillo WS, Savage P, Murphy KG, Chaudhri OB, Patterson M, Nijher GM, Foggo VM, Dancey GS, Mitchell H, Seckl MJ, Ghatei MA, Bloom SR: Plasma kisspeptin is raised in patients with gestational trophoblastic neoplasia and falls during treatment. Am J Physiol Endocrinol Metab; 2006 Nov;291(5):E878-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plasma kisspeptin is raised in patients with gestational trophoblastic neoplasia and falls during treatment.
  • Kisspeptin is a 54-amino acid peptide, encoded by the anti-metastasis gene KiSS-1, that activates G protein-coupled receptor 54 (GPR54).
  • KiSS-1 gene expression is increased in the human placenta in normal and molar pregnancies.
  • The present study was designed to determine whether plasma kisspeptin levels are altered in patients with malignant GTN.
  • Thirty-nine blood samples were taken from 11 patients with malignant GTN at presentation during and after chemotherapy.
  • Plasma kisspeptin IR in females was 803 +/- 125 pmol/l in the first trimester of pregnancy (n = 13), 2,483 +/- 302 pmol/l in the third trimester of pregnancy (n = 7), and <2 pmol/l on day 15 postpartum (n = 7).
  • Plasma kisspeptin IR and hCG concentrations in patients with malignant GTN were elevated at presentation and fell during and after treatment with chemotherapy in each patient (mean plasma kisspeptin IR: prechemotherapy 1,363 +/- 1,076 pmol/l vs. post-chemotherapy <2 pmol/l, P < 0.0001; mean plasma hCG: prechemotherapy 227,191 +/- 152,354 U/l vs. postchemotherapy 2 U/l, P < 0.0001).
  • Our results suggest that measurement of plasma kisspeptin IR may be a novel tumor marker in patients with malignant GTN.
  • [MeSH-major] Biomarkers, Tumor / blood. Trophoblastic Neoplasms / blood. Tumor Suppressor Proteins / blood. Uterine Neoplasms / blood
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Chorionic Gonadotropin / blood. Chromatography, Liquid. Female. Humans. Kisspeptins. Pregnancy

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  • (PMID = 16757546.001).
  • [ISSN] 0193-1849
  • [Journal-full-title] American journal of physiology. Endocrinology and metabolism
  • [ISO-abbreviation] Am. J. Physiol. Endocrinol. Metab.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0701679
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Chorionic Gonadotropin; 0 / KISS1 protein, human; 0 / Kisspeptins; 0 / Tumor Suppressor Proteins
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7. Acs G, Zhang PJ, McGrath CM, Acs P, McBroom J, Mohyeldin A, Liu S, Lu H, Verma A: Hypoxia-inducible erythropoietin signaling in squamous dysplasia and squamous cell carcinoma of the uterine cervix and its potential role in cervical carcinogenesis and tumor progression. Am J Pathol; 2003 Jun;162(6):1789-806
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  • [Title] Hypoxia-inducible erythropoietin signaling in squamous dysplasia and squamous cell carcinoma of the uterine cervix and its potential role in cervical carcinogenesis and tumor progression.
  • Tissue hypoxia is a characteristic property of cervical cancers that makes tumors resistant to chemo- and radiation therapy.
  • In addition to human papillomavirus infection, increased bcl-2 expression and decreased apoptosis are thought to play a role in the progression of cervical neoplasia.
  • Our results suggest that increased expression of Epo and EpoR may play a significant role in cervical carcinogenesis and tumor progression.
  • Hypoxia-inducible Epo signaling may play a significant role in the aggressive behavior and treatment resistance of hypoxic cervical cancers.

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  • (PMID = 12759237.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS037814; United States / NINDS NIH HHS / NS / NS37814
  • [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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Receptors, Erythropoietin; 0 / Recombinant Proteins; 0 / Transcription Factors; 11096-26-7 / Erythropoietin
  • [Other-IDs] NLM/ PMC1868129
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8. Feng FZ, Xiang Y, Wan XR, Yin SJ, Yang XY: [Clinical characteristics and management of gestational trophoblastic disease in women aged 50 years or more]. Zhonghua Fu Chan Ke Za Zhi; 2005 Sep;40(9):605-8
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  • The lesions included 5 hydatidiform moles (13%), 19 invasive moles (50%), 12 choriocarcinomas (32%) and 2 placenta site trophoblastic tumors (5%).
  • Twenty-three cases of hydatidiform moles were diagnosed at their first visit to the hospital, and 15 of them received prophylactic chemotherapy, of whom 10 progressed to invasive mole, 3 developed lung metastasis.
  • All of the other 8 cases without prophylactic chemotherapy progressed to malignant changes with metastasis of lung.
  • The use of prophylactic chemotherapy reduced the incidence of subsequent metastasis.
  • All of 38 cases received chemotherapy.
  • CONCLUSIONS: The diagnosis of pregnancy and pregnancy-related disease should be considered in the elderly women presenting with abnormal vaginal bleeding.
  • Once gestational trophoblastic disease in women aged 50 years or more is diagnosed, chemotherapy should be given as soon as possible.
  • [MeSH-major] Gestational Trophoblastic Disease / diagnosis. Gestational Trophoblastic Disease / drug therapy
  • [MeSH-minor] Choriocarcinoma / diagnosis. Choriocarcinoma / drug therapy. Choriocarcinoma / surgery. Female. Humans. Hydatidiform Mole / diagnosis. Hydatidiform Mole / drug therapy. Hydatidiform Mole / surgery. Middle Aged. Pregnancy. Prognosis. Retrospective Studies. Time Factors. Treatment Outcome. Uterine Hemorrhage / diagnosis

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  • (PMID = 16202316.001).
  • [ISSN] 0529-567X
  • [Journal-full-title] Zhonghua fu chan ke za zhi
  • [ISO-abbreviation] Zhonghua Fu Chan Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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9. Aoki Y, Kase H, Kashima K, Yahata T, Tanaka K: Placental site trophoblastic tumor presenting as subaponeurotic metastasis. Int J Gynecol Cancer; 2005 Mar-Apr;15(2):385-8
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  • [Title] Placental site trophoblastic tumor presenting as subaponeurotic metastasis.
  • Cases of metastatic placental site trophoblastic tumor (PSTT) have a very poor prognosis because these tumors tend to be less sensitive to chemotherapy than other types of gestational trophoblastic disease.
  • We describe the case of a 25-year-old woman who presented with occipital tumor and abnormal vaginal bleeding.
  • Hysterectomy, bilateral salpingo-oophorectomy, and occipital tumor removal revealed a primary PSTT in the uterus, with ovarian and occipital subaponeurotic metastases.
  • She received etoposide, methotrexate, actinomycin-D/cyclophosphamide, vincristine chemotherapy and had a complete clinical remission.
  • Fifteen months later, she had a recurrent subaponeurotic occipital tumor invading the cranium and underwent tumor removal along with cranial bone followed by local irradiation.
  • She was then treated with etoposide, cis-platinum/etoposide, methotrexate, actinomycin-D chemotherapy and again had a remission for 5 months.
  • The patient, however, had a left parietal subaponeurotic tumor, invading the dura mater, and received local irradiation.
  • Soon after, she developed left orbital bone metastasis, treated by local irradiation.
  • These bone metastases responded to the radiation completely.
  • However, multiple organ metastases were found, and she died of the disease.
  • This represents the first case of PSTT with initial subaponeurotic metastasis in a living patient.
  • New modalities of treatment for high-risk or metastatic PSTT need to be developed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / secondary. Occipital Bone / pathology. Placenta Diseases / pathology. Skin Neoplasms / secondary. Trophoblastic Neoplasms / secondary. Uterine Neoplasms / pathology

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  • (PMID = 15823131.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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10. Pagès C, Robert C, Thomas L, Maubec E, Sassolas B, Granel-Brocard F, Chevreau C, De Raucourt S, Leccia MT, Fichet D, Khammari A, Boitier F, Stoebner PE, Dalac S, Celerier P, Aubin F, Viguier M: Management and outcome of metastatic melanoma during pregnancy. Br J Dermatol; 2010 Feb 1;162(2):274-81
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  • [Title] Management and outcome of metastatic melanoma during pregnancy.
  • BACKGROUND: Although metastatic melanoma occurrence during pregnancy challenges the physician in several ways, only a few studies have been published.
  • OBJECTIVES: Our aim was to investigate therapeutic management together with maternal and fetal outcomes in pregnant women with advanced melanoma.
  • Data regarding melanoma history, pregnancy, treatment, delivery, maternal and infant outcomes were collected.
  • Therapeutic abstention during pregnancy was observed in three cases, 14 patients underwent surgery, four patients received chemotherapy and one patient was treated with brain radiotherapy alone.
  • Neither neonatal metastases nor deformities were observed.
  • Placenta metastases were found in one case.
  • CONCLUSIONS: Faced with metastatic melanoma, a majority of women chose to continue with pregnancy, giving birth, based on our samples, to healthy, frequently premature infants.
  • Except during the first trimester of pregnancy, conventional melanoma treatment was applied.
  • [MeSH-major] Melanoma / therapy. Pregnancy Complications, Neoplastic / therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Adult. Female. France. Humans. Placenta / pathology. Pregnancy. Pregnancy Outcome. Prognosis. Retrospective Studies. Risk Assessment. Survival Rate. Treatment Outcome. Young Adult

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  • (PMID = 19804595.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
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11. Thelmo MC, Shen EP, Shertukde S: Metastatic pulmonary adenocarcinoma to placenta and pleural fluid: clinicopathologic findings. Fetal Pediatr Pathol; 2010;29(1):45-56
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  • [Title] Metastatic pulmonary adenocarcinoma to placenta and pleural fluid: clinicopathologic findings.
  • OBJECTIVES: To report the clinicopathologic findings of a pregnant woman with Stage IV adenocarcinoma of the lung with placental metastasis.
  • RESULTS: A 31-year-old G(2)P(1001) woman was diagnosed with Stage IV metastatic adenocarcinoma of the lung.
  • Placental pathology was significant for adenocarcinoma with a solid and acinar pattern, consistent with that from the lung.
  • She did not receive chemotherapy and expired one month postpartum.
  • Placental metastasis is extremely uncommon in these cases and can lead to fetal involvement by lung tumor.
  • [MeSH-major] Adenocarcinoma / secondary. Lung Neoplasms / pathology. Placenta Diseases / pathology. Pleural Effusion, Malignant / pathology
  • [MeSH-minor] Adult. Female. Humans. Infant, Newborn. Male. Neoplasm Staging. Pregnancy

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  • (PMID = 20055563.001).
  • [ISSN] 1551-3823
  • [Journal-full-title] Fetal and pediatric pathology
  • [ISO-abbreviation] Fetal Pediatr Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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12. Bonazzi C, Urso M, Dell'Anna T, Sacco S, Buda A, Cantú MG: Placental site trophoblastic tumor: an overview. J Reprod Med; 2004 Aug;49(8):585-8
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  • [Title] Placental site trophoblastic tumor: an overview.
  • OBJECTIVE: To analyze 15 consecutive cases of placental site trophoblastic tumor seen in a single reference institution for gestational trophoblastic disease, San Gerardo Hospital, Monza, Italy.
  • STUDY DESIGN: Consecutive patients affected by placental site trophoblastic tumors were selected from our computerized database.
  • RESULTS: There were 15 patients with placental site trophoblastic tumor, with a median age of 35 years.
  • The median interval from the last pregnancy was 12 months, and the presenting symptom in 11 cases was vaginal bleeding, in 2 cases amenorrhea, in 1case a nephrotic syndrome and in 1 case, presenting with metastatic disease, hemoptysis.
  • Six patients were treated using neoadjuvant chemotherapy with etoposide/methotrexate/actinomycin-etoposide/ vincristine (EMA-CO) followed in 5 of 6 (83%) cases by hysterectomy.
  • One patient had only medical treatment with EMA-CO because of a strong desire for or childbearing and had a complete response; after 15 months she was free from disease.
  • The last 9 patients underwent surgery as the first therapy.
  • Among these patients 1 had presented with metastatic pulmonary disease and underwent chemotherapy, with complete disappearance of the pulmonary lesions.
  • Two of these 9 patients had a relapse; the mirst patient had a pelvic and bladder relapse, and 14 months after multiple chemotherapy and surgery, she died.
  • The second had a suburethral relapse 2 months after initial surgery; after chemotherapy and surgery she was well and free of disease.
  • CONCLUSION: Our experience suggests that the role of chemotherapy may be reconsidered not only for metastatic disease but als of or uterine disease when choosing conservative management in young, fertile patients who desire childbearing.
  • Chemotherapy may play an important role in avoiding relapse or early metastases even in patients who underwent hysterectomy as primary treatment.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasm Recurrence, Local. Placenta Diseases / drug therapy. Placenta Diseases / pathology. Trophoblastic Neoplasms / drug therapy. Trophoblastic Neoplasms / pathology. Uterine Neoplasms / drug therapy. Uterine Neoplasms / pathology
  • [MeSH-minor] Adult. Age Factors. Cyclophosphamide / administration & dosage. Dactinomycin / administration & dosage. Etoposide / administration & dosage. Female. Fertility. Humans. Methotrexate / administration & dosage. Neoplasm Metastasis. Pregnancy. Retrospective Studies. Treatment Outcome. Vincristine / administration & dosage

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  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. DACTINOMYCIN .
  • Hazardous Substances Data Bank. VINCRISTINE .
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  • (PMID = 15457847.001).
  • [ISSN] 0024-7758
  • [Journal-full-title] The Journal of reproductive medicine
  • [ISO-abbreviation] J Reprod Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 1CC1JFE158 / Dactinomycin; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8N3DW7272P / Cyclophosphamide; YL5FZ2Y5U1 / Methotrexate; EMA-CO protocol
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13. Jung SP, Siegrist B, Hornick CA, Wang YZ, Wade MR, Anthony CT, Woltering EA: Effect of human recombinant Endostatin protein on human angiogenesis. Angiogenesis; 2002;5(1-2):111-8
Hazardous Substances Data Bank. HEPARIN .

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  • Tumor growth and metastasis are dependent on the development of new blood vessels.
  • Inhibitors of new vessel growth have been widely investigated as anti-tumor agents.
  • Endostatin, a 20 kDa C-terminal fragment of collagen XVIII inhibits endothelial cell proliferation, induces endothelial cell apoptosis, and can both inhibit and reverse tumor growth in mice.
  • However, human recombinant endostatin has had limited testing against human tissue targets.
  • To investigate the effect of human endostatin on a human vessel target over a broad range of concentrations (10(-l2)-10(-4) M), human placental vein disks were grown for a period of 2 weeks in a 0.3% fibrin clot overlayed with growth medium.
  • For each placenta utilized, a control (medium and 20% fetal bovine serum [FBS]) group and a group treated with heparin (300 microg/ml) and hydrocortisone 21-phosphate (350 microg/ml) (heparin-steroid) at a dose known to inhibit angiogenesis were included.
  • Endostatin was tested at concentrations of 10(-12)-10(-4) M in medium containing 20% FBS.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Collagen / pharmacology. Hydrocortisone / analogs & derivatives. Neovascularization, Pathologic / drug therapy. Neovascularization, Physiologic / drug effects. Peptide Fragments / pharmacology
  • [MeSH-minor] Biological Assay. Collagen Type XVIII. Endostatins. Heparin / pharmacology. Humans. In Vitro Techniques. Placenta / blood supply. Placenta / drug effects. Veins / drug effects

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  • (PMID = 12549868.001).
  • [ISSN] 0969-6970
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Collagen Type XVIII; 0 / Endostatins; 0 / Peptide Fragments; 0388G963HY / hydrocortisone sodium phosphate; 9005-49-6 / Heparin; 9007-34-5 / Collagen; WI4X0X7BPJ / Hydrocortisone
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14. Topuz S, Iyibozkurt C, Mete O, Akhan S, Salihoğlu Y, Bengisu E, Berkman S: Life-saving hysterectomy in choriocarcinoma: presentation of two cases. Eur J Gynaecol Oncol; 2008;29(6):664-5
MedlinePlus Health Information. consumer health - Vaginal Bleeding.

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  • BACKGROUND: Choriocarcinoma is a malignant tumor of the placenta.
  • CASE 1: A 25-year-old, gravida 3, para 1, woman was referred to our emergency clinic with the diagnosis of choriocarcinoma and massive vaginal bleeding.
  • CASE 2: A 54-year-old, gravida 3, para 3, woman was referred to our clinic with heavy bleeding with the diagnosis of choriocarcinoma.
  • She was scanned to look for possible metastases and pulmonary metastasis was detected.
  • Chemotherapy was planned but as sudden vaginal bleeding began she was referred to the Gynecology Department.
  • CONCLUSION: Although chemotherapy is the cornerstone of treatment for choriocarcinoma, optimal treatment results may depend on the addition of surgery in selected circumstances.

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  • (PMID = 19115703.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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15. Ni Z, Bikadi Z, Rosenberg MF, Mao Q: Structure and function of the human breast cancer resistance protein (BCRP/ABCG2). Curr Drug Metab; 2010 Sep;11(7):603-17
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  • BCRP is capable of transporting non-chemotherapy drugs and xenobiotiocs as well, including nitrofurantoin, prazosin, glyburide, and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine.
  • BCRP is also highly expressed in normal human tissues including the small intestine, liver, brain endothelium, and placenta.
  • Therefore, BCRP has been increasingly recognized for its important role in the absorption, elimination, and tissue distribution of drugs and xenobiotics.
  • At present, little is known about the transport mechanism of BCRP, particularly how it recognizes and transports a large number of structurally and chemically unrelated drugs and xenobiotics.
  • Here, we review current knowledge of structure and function of this medically important ABC efflux drug transporter.
  • [MeSH-major] ATP-Binding Cassette Transporters / chemistry. ATP-Binding Cassette Transporters / physiology. Drug Resistance, Multiple / physiology. Drug Resistance, Neoplasm / physiology. Neoplasm Proteins / chemistry. Neoplasm Proteins / physiology

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  • (PMID = 20812902.001).
  • [ISSN] 1875-5453
  • [Journal-full-title] Current drug metabolism
  • [ISO-abbreviation] Curr. Drug Metab.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM073715; United States / NIGMS NIH HHS / GM / GM073715; United States / NIGMS NIH HHS / GM / R01 GM073715-05; United Kingdom / Wellcome Trust / / 081406/Z/06/Z; United Kingdom / Wellcome Trust / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / Antineoplastic Agents; 0 / Mutant Proteins; 0 / Neoplasm Proteins; 0 / Xenobiotics
  • [Other-IDs] NLM/ NIHMS229269; NLM/ PMC2950214
  •  go-up   go-down


16. Rutland CS, Jiang K, Soff GA, Mitchell CA: Maternal administration of anti-angiogenic agents, TNP-470 and Angiostatin4.5, induces fetal microphthalmia. Mol Vis; 2009;15:1260-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Agents specifically targeting the vasculature as a mode of therapy are finding increasing use in the clinic, primarily in the treatment of colon cancer (Avastin) and age-related macular degeneration (Lucentis).
  • We have previously shown that maternal administration of angiogenic inhibitors (TNP-470 [O-[chloroacetyl-carbamoyl]fumagillol, initially called AGM-1470], the first angiogenic inhibitor to undergo clinical trials, and Angiostatin(4.5), currently in phase I-III clinical trials) cause fetal growth restriction and/or placental abnormalities.
  • During a rapid growth phase of ocular development in the mouse (embryonic days 12 to 19 [E12-E19]), the placenta mediates the metabolic requirements of the fetus and consequently may impact upon the growth of the highly oxygen sensitive fetal eye.
  • METHODS: We injected pregnant dams (between E10.5 - E18.5) with anti-angiogenic agents, which caused either a placental insufficiency type of IUGR (intrauterine growth restriction; i.e., TNP-470) or frank placental pathology (Angiostatin(4.5) [AS(4.5)]), and assessed changes in absolute ocular dimensions, tissue types, and vascular profiles using stereological techniques.
  • CONCLUSIONS: These experiments support the hypothesis that the angiogenic inhibitors (specifically TNP-470 and AS(4.5)) induce microphthalmia either indirectly by their known effects on placental morphology (and/or function) or directly via altering microvascular growth in the fetus.
  • These results also warrant further investigation of a new experimental paradigm linking placental pathology-related fetal growth restriction and microphthalmia.
  • [MeSH-minor] Animals. Eye / blood supply. Eye / pathology. Female. Fetal Development / drug effects. Fetal Growth Retardation / chemically induced. Histocytochemistry. Male. Mice. Mice, Inbred C57BL. Organ Size. Placenta / pathology. Pregnancy. Random Allocation

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  • (PMID = 19572040.001).
  • [ISSN] 1090-0535
  • [Journal-full-title] Molecular vision
  • [ISO-abbreviation] Mol. Vis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cyclohexanes; 0 / Sesquiterpenes; 0 / Teratogens; 0 / angiostatin4.5, human; 129298-91-5 / O-(chloroacetylcarbamoyl)fumagillol; 86090-08-6 / Angiostatins
  • [Other-IDs] NLM/ PMC2704144
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17. Kashimura Y, Tanaka M, Harada N, Shinmoto M, Morishita T, Morishita H, Kashimura M: Twin pregnancy consisting of 46, XY heterozygous complete mole coexisting with a live fetus. Placenta; 2001 Apr;22(4):323-7
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  • Molar tissues are cytogenetically divided into two types, homozygous and heterozygous.
  • The molar tissue of our case showed a 46, XY heterozygous complete mole.
  • The patient developed persistent trophoblastic disease (PTD) with lung metastasis.
  • Nine of the 16 CMCF cases before 21 weeks of gestation and seven of the 12 CMCF cases after 22 weeks of gestation developed PTD.
  • Two of six homozygous and three of four heterozygous moles in CMCF cases developed PTD.
  • [MeSH-major] Hydatidiform Mole / diagnosis
  • [MeSH-minor] Adult. Antineoplastic Agents / therapeutic use. Chorionic Gonadotropin, beta Subunit, Human / blood. DNA / analysis. Female. Genotype. Gestational Age. Heterozygote. Humans. Karyotyping. Lung Neoplasms / diagnosis. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary. Male. Methotrexate / therapeutic use. Polymerase Chain Reaction. Pregnancy. Pregnancy, Multiple. Tomography, X-Ray Computed. Trophoblastic Neoplasms / etiology. Twins. Ultrasonography, Prenatal. Uterine Neoplasms / etiology

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  • [Copyright] Copyright 2001 Harcourt Publishers Ltd.
  • (PMID = 11286568.001).
  • [ISSN] 0143-4004
  • [Journal-full-title] Placenta
  • [ISO-abbreviation] Placenta
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chorionic Gonadotropin, beta Subunit, Human; 9007-49-2 / DNA; YL5FZ2Y5U1 / Methotrexate
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18. Kondraganti S, Gondi CS, Gujrati M, McCutcheon I, Dinh DH, Rao JS, Olivero WC: Restoration of tissue factor pathway inhibitor inhibits invasion and tumor growth in vitro and in vivo in a malignant meningioma cell line. Int J Oncol; 2006 Jul;29(1):25-32
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  • [Title] Restoration of tissue factor pathway inhibitor inhibits invasion and tumor growth in vitro and in vivo in a malignant meningioma cell line.
  • Tissue factor pathway inhibitor 2 (TFPI-2) is a 32-kDa extracellular matrix-associated kunitz-type serine proteinase inhibitor.
  • It is secreted by all vascular cells and plays a role in tumor invasion and metastasis, presumably by plasmin-mediated matrix remodeling.
  • Previous studies have shown high expression of TFPI-2 by benign tumors and low or absent expression in highly malignant tumors.
  • Malignant meningiomas constitute 10-15% of all meningiomas and our previous studies revealed loss of expression of TFPI-2 in malignant gliomas.
  • To investigate the role of TFPI-2 in the invasiveness of malignant meningiomas, we stably transfected the human meningioma cell line, IOMM-Lee, with a vector capable of expressing a transcript complementary to the full length of TFPI-2 mRNA in a sense orientation.
  • Finally, TFPI-2 overexpression inhibited intracranial tumor formation in nude mice.
  • Our data substantiate our previous observation that TFPI-2 plays an important role in tumor progression and has potential in anti-cancer therapy.

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  • (PMID = 16773181.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / NS47699; United States / NCI NIH HHS / CA / R01 CA075557; United States / NCI NIH HHS / CA / CA75557; United States / NCI NIH HHS / CA / CA116708; United States / NCI NIH HHS / CA / CA95058; United States / NCI NIH HHS / CA / R01 CA116708; United States / NINDS NIH HHS / NS / R01 NS047699; United States / NCI NIH HHS / CA / R01 CA095058; United States / NCI NIH HHS / CA / R01 CA092393; United States / NCI NIH HHS / CA / CA92393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Glycoproteins; 0 / Laminin; 0 / Lipoproteins; 0 / Proteoglycans; 0 / bcl-2-Associated X Protein; 0 / lipoprotein-associated coagulation inhibitor; 0 / tissue-factor-pathway inhibitor 2; 119978-18-6 / matrigel; 9007-34-5 / Collagen; 9007-43-6 / Cytochromes c; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS9141; NLM/ PMC1479607
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19. Sebzda T, Hanczyc P, Saleh Y, Akinpelumi BF, Siewinski M, Rudnicki J: Effect of vitamin E and human placenta cysteine peptidase inhibitor on expression of cathepsins B and L in implanted hepatoma Morris 5123 tumor model in Wistar rats. World J Gastroenterol; 2005 Jan 28;11(4):587-92
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  • [Title] Effect of vitamin E and human placenta cysteine peptidase inhibitor on expression of cathepsins B and L in implanted hepatoma Morris 5123 tumor model in Wistar rats.
  • AIM: To examine the effectiveness of human placental inhibitors, by injecting vitamin E to rats with transplanted Morris-5123 hepatoma, on the expression of cathepsins B and L in tumor, liver, lung and blood sera after transplantation of Morris 5123 hepatoma.
  • METHODS: Animals were divided into 10 groups receiving three different concentrations of vitamin E and inhibitors along or in combination and compared with negative control (healthy rats) and positive control (tumor rats).
  • Effectiveness of treatment was evaluated with regard to survival time, tumor response and determination of the activities of proteolytic enzymes and their inhibitors using flurogenic substrates.
  • RESULTS: Cathepsins B and L activities were elevated by 16-fold in comparison with negative control tissues, and their endogenous inhibitor activity decreased by 1.2-fold before treatment.
  • In several cases, tumors completely disappeared following vitamin E plus human placental cyteine protease inhibitor (CPI) compared with controls.
  • The number of complete tumor responses was higher when 20 m/kg vitamin E plus 400 microg of CPI was used, i.e.
  • Cathepsins B and L were expressed significantly in tumor, liver, lung tissues and sera in parallel to the increasing of the endogenous inhibitor activity compared with the controls after treatment (P<0.0001).
  • CONCLUSION: The data indicate formation of metastasis significantly reduced in treated rats, which might provide a therapeutic basis for anti-cancer therapy.
  • [MeSH-major] Antioxidants / pharmacology. Cathepsin B / metabolism. Cathepsins / metabolism. Cysteine Proteinase Inhibitors / pharmacology. Liver Neoplasms, Experimental / drug therapy. Vitamin E / pharmacology
  • [MeSH-minor] Animals. Cathepsin L. Cysteine Endopeptidases. Disease Models, Animal. Female. Humans. Liver / metabolism. Lung / metabolism. Male. Neoplasm Transplantation. Placenta / metabolism. Rats. Rats, Wistar

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  • (PMID = 15641152.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Cysteine Proteinase Inhibitors; 1406-18-4 / Vitamin E; EC 3.4.- / Cathepsins; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.22.1 / Cathepsin B; EC 3.4.22.15 / CTSL1 protein, human; EC 3.4.22.15 / Cathepsin L; EC 3.4.22.15 / Ctsl protein, rat
  • [Other-IDs] NLM/ PMC4250817
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20. Deprimo SE, Bello CL, Smeraglia J, Baum CM, Spinella D, Rini BI, Michaelson MD, Motzer RJ: Circulating protein biomarkers of pharmacodynamic activity of sunitinib in patients with metastatic renal cell carcinoma: modulation of VEGF and VEGF-related proteins. J Transl Med; 2007;5:32
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  • [Title] Circulating protein biomarkers of pharmacodynamic activity of sunitinib in patients with metastatic renal cell carcinoma: modulation of VEGF and VEGF-related proteins.
  • BACKGROUND: Sunitinib malate (SUTENT) is an oral, multitargeted tyrosine kinase inhibitor, approved multinationally for the treatment of advanced RCC and of imatinib-resistant or - intolerant GIST.
  • The purpose of this study was to explore potential biomarkers of sunitinib pharmacological activity via serial assessment of plasma levels of four soluble proteins from patients in a phase II study of advanced RCC: VEGF, soluble VEGFR-2 (sVEGFR-2), placenta growth factor (PlGF), and a novel soluble variant of VEGFR-3 (sVEGFR-3).
  • METHODS: Sunitinib was administered at 50 mg/day on a 4/2 schedule (4 weeks on treatment, 2 weeks off treatment) to 63 patients with metastatic RCC after failure of first-line cytokine therapy.
  • These levels tended to return to near-baseline after 2 weeks off treatment, indicating that these effects were dependent on drug exposure.
  • Overall, significantly larger changes in VEGF, sVEGFR-2, and sVEGFR-3 levels were observed in patients exhibiting objective tumor response compared with those exhibiting stable disease or disease progression (P < 0.05 for each analyte; analysis not done for PlGF).
  • CONCLUSION: Sunitinib treatment in advanced RCC patients leads to modulation of plasma levels of circulating proteins involved in VEGF signaling, including soluble forms of two VEGF receptors.
  • This panel of proteins may be of value as biomarkers of the pharmacological and clinical activity of sunitinib in RCC, and of angiogenic processes in cancer and other diseases.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Biomarkers, Tumor / blood. Carcinoma, Renal Cell / blood. Indoles / pharmacology. Kidney Neoplasms / blood. Neoplasm Proteins / blood. Pyrroles / pharmacology. Vascular Endothelial Growth Factors / blood
  • [MeSH-minor] Cluster Analysis. Humans. Membrane Proteins / blood. Middle Aged. Solubility / drug effects. Time Factors. Vascular Endothelial Growth Factor Receptor-2 / blood. Vascular Endothelial Growth Factor Receptor-3 / blood

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  • (PMID = 17605814.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Indoles; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / PIGF protein, human; 0 / Pyrroles; 0 / Vascular Endothelial Growth Factors; 0 / sunitinib; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
  • [Other-IDs] NLM/ PMC1939830
  • [General-notes] NLM/ Original DateCompleted: 20070810
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21. Luttun A, Autiero M, Tjwa M, Carmeliet P: Genetic dissection of tumor angiogenesis: are PlGF and VEGFR-1 novel anti-cancer targets? Biochim Biophys Acta; 2004 Mar 4;1654(1):79-94
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  • [Title] Genetic dissection of tumor angiogenesis: are PlGF and VEGFR-1 novel anti-cancer targets?
  • Genetic studies have been very helpful in unraveling the cellular and molecular players in pathological blood vessel formation and have provided opportunities to reduce tumor growth and metastasis.
  • The fact that tumor vessels and normal blood vessels have distinct properties may help in designing more specific--and therefore safer--anti-angiogenic strategies.
  • Some anti-angiogenic drugs, i.e., vascular endothelial growth factor (VEGF) antibodies and VEGF receptor-2 (VEGFR-2) inhibitors, have progressed into clinical cancer trials.
  • While the results of these trials support the potential of anti-angiogenic therapy to treat cancer, they also demonstrate the need for more effective and safer alternatives.
  • Targeting placental growth factor (PlGF) or VEGFR-1 may constitute such an alternative since animal studies have proven their pleiotropic working mechanism and attractive safety profile.
  • Together, these insights may bring anti-angiogenic drugs closer from bench to bedside.
  • [MeSH-minor] Angiogenesis Inducing Agents / metabolism. Animals. Blood Coagulation Factors / metabolism. Drug Delivery Systems. Extracellular Matrix Proteins / metabolism. Growth Substances / metabolism. Humans

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  • (PMID = 14984769.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Blood Coagulation Factors; 0 / Extracellular Matrix Proteins; 0 / Growth Substances; 0 / Pregnancy Proteins; 144589-93-5 / placenta growth factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1
  • [Number-of-references] 212
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22. Wen XY, Bai Y, Stewart AK: Adenovirus-mediated human endostatin gene delivery demonstrates strain-specific antitumor activity and acute dose-dependent toxicity in mice. Hum Gene Ther; 2001 Mar 1;12(4):347-58
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  • To develop a clinical gene therapy strategy with endostatin, we cloned the cDNA of human endostatin by RT-PCR from human placenta.
  • After systemic delivery of 2 x 10(9) PFU of AdENDO-YFP into 129/J mice, human endostatin expression was achieved at a mean value of 1.34 +/- 0.42 microg/ml of serum (n = 6) and inhibition of lung metastasis was observed in an EOMA tumor model.
  • [MeSH-major] Adenoviridae / genetics. Angiogenesis Inhibitors / genetics. Collagen / genetics. Genetic Therapy / methods. Lung Neoplasms / therapy. Melanoma, Experimental / therapy. Peptide Fragments / genetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Antineoplastic Agents / metabolism. Antineoplastic Agents / toxicity. Base Sequence. Cell Division. Endostatins. Endothelium, Vascular / drug effects. Gene Transfer Techniques. Humans. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Nude. Molecular Sequence Data. Neovascularization, Pathologic / prevention & control. Reverse Transcriptase Polymerase Chain Reaction. Sequence Homology, Amino Acid

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  • (PMID = 11242527.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / Endostatins; 0 / Peptide Fragments; 9007-34-5 / Collagen
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23. Sen CK: Wound healing essentials: let there be oxygen. Wound Repair Regen; 2009 Jan-Feb;17(1):1-18
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  • From a diagnostic standpoint, measurements of wound oxygenation are commonly used to guide treatment planning such as amputation decision.
  • Importantly, approaches to correct wound pO(2) favorably influence outcomes of other therapies such as responsiveness to growth factors and acceptance of grafts.
  • Primarily based on the tumor literature, hypoxia is generally viewed as being angiogenic.
  • Extreme near-anoxic hypoxia, as commonly noted in problem wounds, is not compatible with tissue repair.
  • Adequate wound tissue oxygenation is required but may not be sufficient to favorably influence healing outcomes.
  • In considering approaches to oxygenate the wound tissue it is important to recognize that both too little as well as too much may impede the healing process.
  • Therapeutic approaches targeting the oxygen sensing and redox signaling pathways are promising.

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  • (PMID = 19152646.001).
  • [ISSN] 1524-475X
  • [Journal-full-title] Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
  • [ISO-abbreviation] Wound Repair Regen
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM 077185; United States / NHLBI NIH HHS / HL / R01 HL073087; United States / NIGMS NIH HHS / GM / R01 GM077185-01A2; United States / NIGMS NIH HHS / GM / GM069589-01A1; United States / NIGMS NIH HHS / GM / GM077185-01A2; United States / NIGMS NIH HHS / GM / GM 069589; United States / NIGMS NIH HHS / GM / R01 GM069589-01A1; United States / NCRR NIH HHS / RR / UL1 RR025755; United States / NIGMS NIH HHS / GM / R01 GM069589; United States / NIGMS NIH HHS / GM / R01 GM077185
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.6.3.1 / NADPH Oxidase; S88TT14065 / Oxygen
  • [Number-of-references] 280
  • [Other-IDs] NLM/ NIHMS95304; NLM/ PMC2704021
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24. Suzuki N, Aoki D, Orikawa K, Suzuki A, Susumu N, Tamada Y, Sakayori M, Tsukazaki K, Mukai M, Kikuchi H, Ishida I, Nozawa S: 8-1A, a human monoclonal antibody that reacts with intact human chorionic gonadotropin. Placenta; 2006 Feb-Mar;27(2-3):333-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The incidence of choriocarcinoma has decreased over time and therapeutic results have improved about 90% complete remission in patients without extensive metastasis.
  • However, some choriocarcinomas metastasize to other organs and show resistance to chemotherapy, having a poor prognosis despite multidisciplinary treatment.
  • Better methods of early diagnosis for recurrence or micrometastasis, and treatment against cases with intractable gestational trophoblastic neoplasia (GTN) are needed to improve the prognosis.
  • Human chorionic gonadotropin (hCG) is a glycoprotein hormone composed of two dissimilar subunits and a tumor marker to make a diagnosis and monitor therapeutic effect in GTN.
  • Residual trophoblast cells may cause symptoms such as bleeding or undergo malignant transformation to choriocarcinoma.
  • Since most monoclonal antibodies developed so far are murine, administration creates human anti-mouse antibodies, resulting in clinical failure.
  • In the future, new diagnostic techniques and treatments for chorionic diseases may be developed using this kind of human monoclonal antibody.

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  • (PMID = 16338478.001).
  • [ISSN] 0143-4004
  • [Journal-full-title] Placenta
  • [ISO-abbreviation] Placenta
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 8-1A monoclonal antibody, human; 0 / Antibodies, Monoclonal; 0 / Chorionic Gonadotropin
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25. Ding Y, Huang Y, Song N, Gao X, Yuan S, Wang X, Cai H, Fu Y, Luo Y: NFAT1 mediates placental growth factor-induced myelomonocytic cell recruitment via the induction of TNF-alpha. J Immunol; 2010 Mar 1;184(5):2593-601
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NFAT1 mediates placental growth factor-induced myelomonocytic cell recruitment via the induction of TNF-alpha.
  • Recruitment of bone marrow-derived myelomonocytic cells plays a fundamental role in tumor angiogenesis and metastasis.
  • Placental growth factor (PlGF) is a potent cytokine that can attract myelomonocytic cells to the tumor.
  • In this study, we demonstrate that tumor-derived PlGF activates NFAT1 via vascular endothelial growth factor receptor 1 in both murine and human myelomonocytic cells.
  • Activation of NFAT1 is crucial for PlGF-induced myelomonocytic cell recruitment as shown by the in vitro transwell migration assay, transendothelial migration assay, and PlGF-overexpressing tumor models in mice, respectively.
  • Our present studies discover a novel role of the NFAT1-TNF-alpha pathway in tumor inflammation, which may provide potential targets to diversify current cancer therapy.
  • [MeSH-major] Monocytes / metabolism. Myeloid Cells / metabolism. NFATC Transcription Factors / metabolism. Pregnancy Proteins / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Cell Line. Cell Line, Tumor. Cell Movement / drug effects. Cyclosporine / pharmacology. Fluorescent Antibody Technique. Humans. Immunoblotting. Mice. Mice, Inbred C57BL. Neoplasms, Experimental / genetics. Neoplasms, Experimental / metabolism. Neoplasms, Experimental / pathology. Oligopeptides / pharmacology. RNA Interference. Transfection. Transplantation, Heterologous. Vascular Endothelial Growth Factor Receptor-1 / genetics. Vascular Endothelial Growth Factor Receptor-1 / metabolism

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  • (PMID = 20097868.001).
  • [ISSN] 1550-6606
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NFATC Transcription Factors; 0 / Oligopeptides; 0 / Pregnancy Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / VIVIT peptide; 144589-93-5 / placenta growth factor; 83HN0GTJ6D / Cyclosporine; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-1
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26. Holtan SG, Creedon DJ, Haluska P, Markovic SN: Cancer and pregnancy: parallels in growth, invasion, and immune modulation and implications for cancer therapeutic agents. Mayo Clin Proc; 2009 Nov;84(11):985-1000
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cancer and pregnancy: parallels in growth, invasion, and immune modulation and implications for cancer therapeutic agents.
  • In addition to the shared capacity for invading through normal tissues, both cancer cells and cells of the developing placenta create a microenvironment supportive of both immunologic privilege and angiogenesis.
  • Systemic alterations in immunity are also detectable, particularly with respect to a helper T cell type 2 polarization evident in advanced cancers and midtrimester pregnancy.
  • The knowledge gained from analyzing similarities and differences between the physiologic state of pregnancy and the pathologic state of cancer could lead to identification of new potential targets for cancer therapeutic agents.
  • [MeSH-major] Antineoplastic Agents / immunology. Cell Transformation, Neoplastic / immunology. Neoplasm Invasiveness / immunology. Neoplasms / drug therapy. Neoplasms / immunology. Pregnancy / immunology
  • [MeSH-minor] Academic Medical Centers. Cell Movement / immunology. Cell Proliferation. Drug Delivery Systems. Female. Humans. Immune System Phenomena / immunology. Immune System Phenomena / physiology. Immunologic Factors. Minnesota. Neovascularization, Pathologic / immunology. Pregnancy Trimester, Third

  • Genetic Alliance. consumer health - Pregnancy.
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  • (PMID = 19880689.001).
  • [ISSN] 1942-5546
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors
  • [Number-of-references] 263
  • [Other-IDs] NLM/ PMC2770910
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27. Chung C, Kao MS, Gersell D: Incidental placental choriocarcinoma in a term pregnancy: a case report. J Med Case Rep; 2008;2:330

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Incidental placental choriocarcinoma in a term pregnancy: a case report.
  • Of all forms of gestational choriocarcinoma, placental choriocarcinoma is the most rare.
  • Maternal choriocarcinoma is usually diagnosed in symptomatic patients with metastases.
  • The incidental finding of a choriocarcinoma confined to the placenta with no evidence of dissemination to the mother, or infant is the least common scenario.
  • Her placenta revealed intraplacental choriocarcinoma.
  • No chemotherapy was initiated.
  • Metastasis was ruled out by chest x-ray and whole body computed tomography scan.
  • CONCLUSION: Due to the potential fatal outcome of placental choriocarcinoma, careful evaluation of both mother and infant after the diagnosis is made is important.
  • The incidence of placental choriocarcinoma may actually be higher than expected since it is not routine practice to send placentas for pathological evaluation after a normal spontaneous delivery.
  • The obstetrician, pathologist, and pediatrician should have an increased awareness of placental choriocarcinoma and its manifestations.

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  • (PMID = 18922186.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2577684
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28. Karbowski B, Jackisch C: [Malignant melanoma and pregnancy]. Z Geburtshilfe Neonatol; 2000 Jul-Aug;204(4):158-61
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Malignant melanoma and pregnancy].
  • BACKGROUND: Incidence of malignant melanoma has more than doubled in the past 10 years.
  • Two thirds of malignant melanoma arise from melanocytes, the pigmented cells of epidermis and dermis, in one third of the cases from preexisting nevi.
  • CASE REPORT: We report on a 39 year-old pregnant woman with liver metastases after surgical removal of a malignant melanoma two years before.
  • The mother died in the course of progredient liver insufficiency, a male baby had been delivered with a gestational age of 26 weeks + 4 days via cesarean section 11 days before and developed normally.
  • RESULTS: Early diagnosis and operative excision are decisive for survival, in advanced stages chemotherapy does not prolong survival.
  • [MeSH-major] Liver Neoplasms / secondary. Melanoma / secondary. Pregnancy Complications, Neoplastic / diagnosis. Skin Neoplasms / diagnosis
  • [MeSH-minor] Adult. Cesarean Section. Fatal Outcome. Female. Humans. Infant, Newborn. Lymph Nodes / pathology. Lymphatic Metastasis. Male. Placenta / pathology. Pregnancy






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