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1. Drew Y, Calvert H: The potential of PARP inhibitors in genetic breast and ovarian cancers. Ann N Y Acad Sci; 2008 Sep;1138:136-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The potential of PARP inhibitors in genetic breast and ovarian cancers.
  • The abundant nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1), represents an important novel target in cancer therapy.
  • Inhibitors of PARP-1 have been shown to enhance the cytotoxic effects of ionizing radiation and DNA damaging chemotherapy agents, such as the methylating agents and topoisomerase I inhibitors.
  • Recent in vitro and in vivo evidence suggests that PARP inhibitors could be used not only as chemo/radiotherapy sensitizers, but as single agents to selectively kill cancers defective in DNA repair, specifically cancers with mutations in the breast cancer associated (BRCA) 1 and 2 genes.
  • This theory of selectively exploiting cells defective in one DNA repair pathway by inhibiting another is a major breakthrough in the treatment of cancer.
  • BRCA1/2 mutations are responsible for the majority of genetic breast/ovarian cancers, known as the hereditary breast ovarian cancer syndrome.
  • This review summarizes the preclinical and clinical evidence for the potential of PARP inhibitors in genetic breast and ovarian cancers.
  • [MeSH-major] Breast Neoplasms / drug therapy. Enzyme Inhibitors / therapeutic use. Genetic Predisposition to Disease. Ovarian Neoplasms / drug therapy. Poly(ADP-ribose) Polymerase Inhibitors
  • [MeSH-minor] Female. Genes, BRCA1. Genes, BRCA2. Humans. Mutation


2. Rhiem K, Wappenschmidt B, Bosse K, Köppler H, Tutt AN, Schmutzler RK: Platinum sensitivity in a BRCA1 mutation carrier with advanced breast cancer. Clin Oncol (R Coll Radiol); 2009 Aug;21(6):448-50
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  • [Title] Platinum sensitivity in a BRCA1 mutation carrier with advanced breast cancer.
  • Although BRCA1-associated breast carcinomas are frequently detected in nodal-negative stage, they typically present with an aggressive histopathological phenotype that is reflected by a poor prognosis and an increased risk for distant metastatic spread.
  • Recent in vitro data suggest a high sensitivity of BRCA1-associated carcinomas to platinum-based chemotherapy and a lower sensitivity to anthracyclines and taxanes.
  • This is explained by the key role of BRCA1 in DNA double-strand repair via homologous recombination, thereby leading to a higher sensitivity to DNA intercalating agents, such as platinum.
  • Here we present the case of a woman suffering from BRCA1-associated metastatic breast carcinoma that was resistant to docetaxel, but responded strongly to cisplatin-containing chemotherapy.
  • [MeSH-major] Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Genes, BRCA1. Germ-Line Mutation. Organoplatinum Compounds / therapeutic use

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  • (PMID = 19249193.001).
  • [ISSN] 1433-2981
  • [Journal-full-title] Clinical oncology (Royal College of Radiologists (Great Britain))
  • [ISO-abbreviation] Clin Oncol (R Coll Radiol)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Organoplatinum Compounds
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3. Jahr JS, Walker V, Manoochehri K: Blood substitutes as pharmacotherapies in clinical practice. Curr Opin Anaesthesiol; 2007 Aug;20(4):325-30
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  • [Title] Blood substitutes as pharmacotherapies in clinical practice.
  • RECENT FINDINGS: A pivotal multinational phase III trial of the Biopure product HBOC-201 (Hemopure) has been completed in orthopedic surgery patients.
  • HBOC-201 consists of polymerized bovine hemoglobin and has already been well tolerated in patients undergoing cardiopulmonary bypass and abdominal aortic reconstruction.

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  • (PMID = 17620840.001).
  • [ISSN] 0952-7907
  • [Journal-full-title] Current opinion in anaesthesiology
  • [ISO-abbreviation] Curr Opin Anaesthesiol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Fluorocarbons; 0 / Hemoglobins; S88TT14065 / Oxygen
  • [Number-of-references] 39
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4. Li T, Zhang P, Liu J, Zhou R, Li Q, You Z, Dian K: Protective effects of hemoglobin-based oxygen carrier given to isolated heart during ischemia via attenuation of mitochondrial oxidative damage. Free Radic Biol Med; 2010 Apr 15;48(8):1079-89
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  • This study was designed to investigate the protective effect of a hemoglobin-based oxygen carrier (HBOC) on I/R heart and to elucidate the potential mechanism.
  • The results of our study reveal that HBOC provides a profound protection against cardiac I/R injury as evidenced by significantly improved cardiac function and decreased myocardial infarction, necrosis, and apoptosis.
  • In addition to more oxygen supply to the myocardium, the cardioprotection of HBOC was closely related to well-preserved mitochondrial redox potential, significantly elevated mitochondrial superoxide dismutase activity, and decreased mitochondrial hydrogen peroxide and malondialdehyde formation, which indicated that the I/R-induced mitochondrial oxidative damage was remarkably attenuated.
  • Furthermore, the elevated mitochondrial function and unchanged mitochondrial structure provide additional evidence of the prominent role of HBOC in mitochondrial preservation.
  • In conclusion, our results demonstrate the cardioprotective effect of HBOC on I/R heart and reveal that this protection was mediated in large part by attenuation of mitochondrial oxidative damage.
  • [MeSH-major] Hemoglobins / therapeutic use. Mitochondria, Heart / drug effects. Myocardial Reperfusion Injury / prevention & control. Polymers / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Male. Microscopy, Electron, Transmission. Myocardial Infarction / drug therapy. Myocardial Infarction / pathology. Myocardium / metabolism. Oxidative Stress / drug effects. Rats. Rats, Sprague-Dawley. Ventricular Function, Left / drug effects

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  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20114072.001).
  • [ISSN] 1873-4596
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Polymers
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5. Li T, Liu J, Yang C: Pretreatment with hemoglobin-based oxygen carriers protect isolated rat heart from myocardial infarction. Artif Cells Blood Substit Immobil Biotechnol; 2010 May;38(3):115-8
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  • PolyPHb pretreatment greatly reduced the decreases in left ventricular developed pressure (LVDP), maximum LVDP increase and decrease rate (+/-dp/dt), and the increase in left ventricular end-diastolic pressure (LVEDP) as compared to the control group.
  • [MeSH-major] Blood Substitutes / pharmacology. Hemoglobins / pharmacology. Myocardial Infarction. Pregnancy Proteins. Respiratory Transport / drug effects
  • [MeSH-minor] Animals. Female. Heart / drug effects. Heart / physiopathology. Humans. In Vitro Techniques. Male. Myocardial Reperfusion Injury / physiopathology. Myocardial Reperfusion Injury / therapy. Oxygen / metabolism. Pregnancy. Rats. Rats, Sprague-Dawley. Troponin I / analysis. Troponin I / secretion. Ventricular Function, Left / drug effects. Ventricular Function, Left / physiology

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  • (PMID = 20297921.001).
  • [ISSN] 1532-4184
  • [Journal-full-title] Artificial cells, blood substitutes, and immobilization biotechnology
  • [ISO-abbreviation] Artif Cells Blood Substit Immobil Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Hemoglobins; 0 / Pregnancy Proteins; 0 / Troponin I; S88TT14065 / Oxygen
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6. Ning J, Wong LT, Christoff B, Carmichael FJ, Biro GP: Haemodynamic response following a 10% topload infusion of HemolinkTM in conscious, anaesthetized and treated spontaneously hypertensive rats. Transfus Med; 2000 Mar;10(1):13-22
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  • HemolinkTM (HLK), a haemoglobin-based oxygen carrier (HBOC), is currently undergoing Phase II/III clinical trials in surgical patients.
  • This study suggests that the pressor effect of HemolinkTM can be attenuated in hypertensive animals with general anaesthesia or treatment with antihypertensive agents.
  • [MeSH-major] Blood Pressure / drug effects. Blood Substitutes / adverse effects. Hemoglobins / administration & dosage. Hemoglobins / adverse effects. Raffinose / analogs & derivatives
  • [MeSH-minor] Animals. Blood Transfusion. Humans. Hypertension / drug therapy. Hypertension / physiopathology. Infusions, Intravenous. Nifedipine / pharmacology. Nifedipine / therapeutic use. Rats. Rats, Inbred SHR. Rats, Inbred WKY. Vasodilator Agents / pharmacology. Vasodilator Agents / therapeutic use

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  • (PMID = 10760199.001).
  • [ISSN] 0958-7578
  • [Journal-full-title] Transfusion medicine (Oxford, England)
  • [ISO-abbreviation] Transfus Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Hemoglobins; 0 / O-raffinose cross-linked human hemoglobin; 0 / Vasodilator Agents; I9ZF7L6G2L / Nifedipine; N5O3QU595M / Raffinose
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7. Rabban JT, Barnes M, Chen LM, Powell CB, Crawford B, Zaloudek CJ: Ovarian pathology in risk-reducing salpingo-oophorectomies from women with BRCA mutations, emphasizing the differential diagnosis of occult primary and metastatic carcinoma. Am J Surg Pathol; 2009 Aug;33(8):1125-36
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  • [Title] Ovarian pathology in risk-reducing salpingo-oophorectomies from women with BRCA mutations, emphasizing the differential diagnosis of occult primary and metastatic carcinoma.
  • Risk-reducing salpingo-oophorectomy (RRSO) is an effective prophylactic procedure for women with mutations in BRCA1 or BRCA2 genes, both of which confer an increased lifetime risk for ovarian, tubal, peritoneal, and breast cancer.
  • In addition to lowering this risk, RRSO also offers the opportunity to detect occult early-stage fallopian tube or ovarian carcinoma.
  • The differential diagnosis of occult tubal/ovarian cancer includes a spectrum of benign tubal and ovarian alterations and also occult metastatic breast cancer, although only rare cases of the latter have been reported in RRSO.
  • Neoadjuvant breast cancer chemotherapy may contribute to diagnostic difficulty due to treatment-induced cytologic alterations.
  • With the aim of elucidating features which may help with differential diagnosis, this study reports the incidence and pathologic features of benign ovarian alterations, benign ovarian tumors, and occult primary and metastatic malignancies in prophylactic oophorectomies from 108 women with a BRCA mutation and from 35 women with other strong risk factors for hereditary breast/ovarian carcinoma.
  • We direct particular emphasis on morphologic features of primary ovarian lesions that may mimic occult metastatic breast cancer.
  • We also evaluate histologic alterations due to neoadjuvant breast cancer chemotherapy in the ovary and fallopian tube of patients who received such treatment immediately preceding RRSO.
  • Comparison is made to ovarian metastases of breast cancer in our hospital-based population of breast cancer patients, none of whom underwent RRSO.
  • Overall, 69% of RRSO patients had a personal history of breast cancer.
  • Neoadjuvant breast cancer chemotherapy was administered in 15%.
  • Occult primary carcinoma occurred in 7 (6.5%) BRCA patients (5 in fallopian tube, 1 in fallopian tube and ovary, 1 in ovary).
  • Ovarian metastasis of breast cancer occurred in 1 (1%) BRCA patient undergoing RRSO and in up to a similar proportion (0.8%) of the hospital-based population of breast cancer patients.
  • Abundant foamy, vacuolated cytoplasm due to neoadjuvant chemotherapy exposure was notable.
  • In contrast, ovarian metastases in the non-RRSO population were all clinically detected, bilateral, large, and exhibited well-developed malignant cytologic features.
  • None of the normal cell types in the ovary or tube demonstrated any cytologic alterations in RRSO patients who received neoadjuvant chemotherapy.
  • The main morphologic mimics of metastasis with superimposed chemotherapy-induced alterations in RRSO were stromal hyperthecosis (n=8), nodular hyperthecosis (n=2), adrenal rests (n=3), hilus cell nodules (n=43), and hilus cell hyperplasia (n=4).
  • Occult primary ovarian carcinoma was reliably distinguished from ovarian metastases of breast cancer by WT-1+, p53+, mammaglobin-, GCDPF-immunoprofile.
  • These results demonstrate that evaluation of RRSO specimens requires awareness of a spectrum of ovarian lesions which may mimic occult primary or metastatic carcinoma; awareness of the masquerading effects of neoadjuvant chemotherapy; and awareness of the potential morphologic differences between occult metastatic breast cancer in RRSO and non-RRSO specimens.
  • [MeSH-major] Genes, BRCA1. Genes, BRCA2. Ovarian Neoplasms / genetics. Ovarian Neoplasms / pathology. Ovarian Neoplasms / prevention & control
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Diagnosis, Differential. Fallopian Tubes / surgery. Female. Genetic Predisposition to Disease. Humans. Mutation. Neoplasms, Multiple Primary / genetics. Neoplasms, Multiple Primary / pathology. Neoplasms, Multiple Primary / prevention & control. Ovariectomy. Ovary / drug effects. Ovary / pathology. Risk Factors


8. Lux MP, Fasching PA, Beckmann MW: Hereditary breast and ovarian cancer: review and future perspectives. J Mol Med (Berl); 2006 Jan;84(1):16-28
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  • [Title] Hereditary breast and ovarian cancer: review and future perspectives.
  • Breast cancer (BC) is the most frequent carcinoma in women.
  • The cumulative risk for the disease is 10% up to the age of 80 years.
  • A familial history of BC and ovarian cancer (OC) is a significant risk factor.
  • Some 5-10% of all cases of BC and 25-40% of cases in patients under the age of 35 years have a hereditary origin.
  • BRCA1/BRCA2 mutations are responsible for 3-8% of all cases of BC and 30-40% of familial cases.
  • About 80% of families with a history of OC have BRCA1 mutations, while 15% have BRCA2 mutations.
  • Women at risk can receive counseling from interdisciplinary cancer genetics clinics, while those at high risk can receive genetic testing.
  • Risk calculation programs can define the risks and assist in decision making for genetic testing and clinical options.
  • Clinical options require information on the risks of the disease and its mutation status.
  • It is not currently known whether intensified early cancer detection is individually beneficial, but this is currently the option that is the least invasive and least burdensome to the patient.
  • Although hereditary BC has different pathological characteristics and the BRCA mutation is an independent negative prognostic factor, there are currently no special treatment guidelines.
  • Without adjuvant hormone therapy or chemotherapy, the overall survival in BRCA mutation carriers is reduced.
  • Chemotherapy regimens involving platinum are particularly beneficial in the treatment of hereditary BC.
  • [MeSH-major] Breast Neoplasms / genetics. Genetic Predisposition to Disease. Ovarian Neoplasms / genetics
  • [MeSH-minor] BRCA1 Protein. BRCA2 Protein. Female. Genetic Counseling. Humans. Prognosis. Risk Factors. Syndrome


9. van Iterson M, Siegemund M, Burhop K, Ince C: Hemoglobin-based oxygen carrier provides heterogeneous microvascular oxygenation in heart and gut after hemorrhage in pigs. J Trauma; 2003 Dec;55(6):1111-24
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  • To this end, we tested the influence of the volume of an HBOC on the microcirculatory oxygenation of the heart and the gut serosa and mucosa in a porcine model of hemorrhage.
  • Resuscitation of gut microPO2 with a low volume of DCLHb was as effective as isovolemic resuscitation with HAES.
  • It is concluded that microcirculatory monitoring in this way elucidates the regional behavior of oxygen transport to the tissue by HBOCs, whereas systemic variables were ineffective in describing their response.
  • [MeSH-major] Aspirin / analogs & derivatives. Aspirin / therapeutic use. Disease Models, Animal. Hemoglobins / therapeutic use. Hydroxyethyl Starch Derivatives / administration & dosage. Intestinal Mucosa / metabolism. Microcirculation / drug effects. Pericardium / metabolism. Plasma Substitutes / administration & dosage. Shock, Hemorrhagic / drug therapy
  • [MeSH-minor] Analysis of Variance. Animals. Dose-Response Relationship, Drug. Drug Evaluation, Preclinical. Drug Monitoring. Female. Fluid Therapy / methods. Ileum / blood supply. Ileum / chemistry. Ileum / drug effects. Ileum / metabolism. Oxygen / analysis. Oxygen / metabolism. Oxygen Consumption / drug effects. Resuscitation / methods. Swine. Time Factors

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  • (PMID = 14676658.001).
  • [ISSN] 0022-5282
  • [Journal-full-title] The Journal of trauma
  • [ISO-abbreviation] J Trauma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Hydroxyethyl Starch Derivatives; 0 / Plasma Substitutes; 0 / diaspirin-cross-linked hemoglobin; R16CO5Y76E / Aspirin; S88TT14065 / Oxygen
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10. Prat J, Ribé A, Gallardo A: Hereditary ovarian cancer. Hum Pathol; 2005 Aug;36(8):861-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hereditary ovarian cancer.
  • Family history is the strongest risk factor for ovarian cancer.
  • Three clinical manifestations of hereditary ovarian cancer have been recognized:.
  • (1) "site-specific" ovarian cancer, (2) the breast and ovarian cancer syndrome, and (3) the hereditary nonpolyposis colorectal cancer (HNPCC; Lynch II) syndrome.
  • The first 2 groups are associated with germ line mutations in the BRCA1 and BRCA2 tumor suppressor genes, whereas HNPCC is associated with germ line mutations in the DNA mismatch repair (MMR) genes, primarily hMLH1 and hMSH2.
  • At least 10% of all epithelial ovarian cancers are hereditary, with mutations in the BRCA genes accounting for approximately 90% of cases and most of the remaining 10% attributable to HNPCC.
  • Hereditary ovarian cancers exhibit distinct clinicopathologic features compared with sporadic cancers.
  • The cumulative lifetime risk of ovarian cancer is 40% to 50% for BRCA1 mutation carriers and 20% to 30% for BRCA2 mutation carriers.
  • Mutations of BRCA1 and BRCA2 are mainly of the frameshift or nonsense variety.
  • Most ovarian cancers associated with germ line BRCA mutations are diagnosed at a younger age and are high-grade and advanced-stage serous carcinomas.
  • BRCA mutations do not seem to play a significant role in the development of mucinous or borderline ovarian tumors.
  • Hereditary ovarian cancers have a distinctly better clinical outcome with longer overall survival and recurrence-free interval after chemotherapy than sporadic cancers.
  • Women with a family history including 2 or more first- or second-degree relatives with either ovarian cancer alone or both breast and ovarian cancers should undertake prophylactic oophorectomy immediately after childbearing has been completed to reduce the risk of ovarian cancer.
  • The cumulative risk of ovarian cancer in HNPCC families is more than 12%.
  • Ovarian cancer in HNPCC syndrome is diagnosed at younger age than in the general population.
  • [MeSH-major] Genetic Predisposition to Disease / genetics. Ovarian Neoplasms / genetics
  • [MeSH-minor] Female. Genes, BRCA1. Genes, BRCA2. Humans. Mutation. Risk Factors


11. Kaplan LJ, Philbin N, Arnaud F, Rice J, Dong F, Freilich D: Resuscitation from hemorrhagic shock: fluid selection and infusion strategy drives unmeasured ion genesis. J Trauma; 2006 Jul;61(1):90-7; discussion 97-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Pigs (n = 8/gp) were untreated (NON) or bolused (10 cc/kg bw) with HBOC-201 (HBOC), or 6% Hetastarch (HEX) after 20 minutes of HS.
  • Additional boluses occurred for hypotension (mean arterial pressure [MAP] <60 mm Hg) or tachycardia (heart rate [HR] >baseline) for 4 hours; other therapy was withheld, simulating delayed evacuation.
  • By 30 minutes, MAP was higher with HBOC (63 +/- 8; p = 0.01) versus HEX (37 +/- 5) or NON (35 +/- 4).
  • HBOC required less fluid than HEX (515 +/- 58 versus 830 +/- 45 mL, p = 0.019).
  • pH was highest in HBOC by 180 minutes (p < 0.05).
  • SID was constant in NON, decreased in HEX, but increased in HBOC (p < 0.05 by 60 minutes).
  • SIG remained unchanged in NON and HEX, but declined in HBOC (p < 0.05 by 30 minutes).
  • CONCLUSIONS: HBOC resuscitation required the least fluid.
  • Unmeasured anions were prevalent in HEX and NON (+ SIG), whereas HBOC liberated unmeasured cations (- SIG); differences were inapparent when only evaluating pH.
  • Only HBOC increased the SID, electrochemically promoting alkalosis.
  • [MeSH-major] Acid-Base Equilibrium / drug effects. Blood Substitutes / therapeutic use. Fluid Therapy / methods. Hemoglobins / therapeutic use. Hydroxyethyl Starch Derivatives / therapeutic use. Shock, Hemorrhagic / therapy
  • [MeSH-minor] Animals. Hydrogen-Ion Concentration / drug effects. Infusions, Intravenous / methods. Swine

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  • (PMID = 16832254.001).
  • [ISSN] 0022-5282
  • [Journal-full-title] The Journal of trauma
  • [ISO-abbreviation] J Trauma
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / HBOC 201; 0 / Hemoglobins; 0 / Hydroxyethyl Starch Derivatives
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12. Moon PF, Bliss SP, Posner LP, Erb HN, Nathanielsz PW: Fetal oxygen content is restored after maternal hemorrhage and fluid replacement with polymerized bovine hemoglobin, but not with hetastarch, in pregnant sheep. Anesth Analg; 2001 Jul;93(1):142-50
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  • Fifteen pregnant ewes (132-day gestational age) were hemorrhaged 20 mL/kg over 1 h; they were randomized to receive 20 mL/kg IV of HBOC, hetastarch (HTS), or autologous blood (BLD) (n = 5 each) over 30 min and were monitored for 2 h.
  • Fluid replacement restored maternal blood pressure in all groups, although maternal oxygen content immediately returned to baseline only after BLD or HBOC.
  • Maternal oxygen saturation decreased after HBOC (from 98% to 88%).
  • Fetal oxygen content rapidly returned to baseline with either BLD (7.1 mL/dL) or HBOC (8.0 mL/dL) but was never restored with HTS (4.7 mL/dL), and, 60 min after fluid replacement, it was higher with HBOC (8.3 mL/dL) than with HTS (4.7 mL/dL).
  • Fetal plasma-free hemoglobin did not change after HBOC.
  • In conclusion, maternal fluid replacement with HBOC or BLD effectively restored fetal oxygenation, primarily by restoring maternal oxygen content, whereas HTS did not.
  • [MeSH-major] Fetal Hypoxia / drug therapy. Fetomaternal Transfusion / complications. Fluid Therapy. Hemoglobins / pharmacology. Hydroxyethyl Starch Derivatives / pharmacology. Oxygen Consumption / drug effects. Plasma Substitutes / pharmacology
  • [MeSH-minor] Animals. Blood Gas Analysis. Cattle. Female. Heart Rate, Fetal / drug effects. Hematocrit. Hemodynamics / drug effects. Pregnancy. Sheep

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  • (PMID = 11429355.001).
  • [ISSN] 0003-2999
  • [Journal-full-title] Anesthesia and analgesia
  • [ISO-abbreviation] Anesth. Analg.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / HD 21350
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / Hydroxyethyl Starch Derivatives; 0 / Plasma Substitutes
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13. Verstappen CC, Heimans JJ, Hoekman K, Postma TJ: Neurotoxic complications of chemotherapy in patients with cancer: clinical signs and optimal management. Drugs; 2003;63(15):1549-63
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neurotoxic complications of chemotherapy in patients with cancer: clinical signs and optimal management.
  • Neurotoxic side effects of chemotherapy occur frequently and are often a reason to limit the dose of chemotherapy.
  • Since bone marrow toxicity, as the major limiting factor in most chemotherapeutic regimens, can be overcome with growth factors or bone marrow transplantation, the use of higher doses of chemotherapy is possible, which increases the risk of neurotoxicity.
  • Chemotherapy may cause both peripheral neurotoxicity, consisting mainly of a peripheral neuropathy, and central neurotoxicity, ranging from minor cognitive deficits to encephalopathy with dementia or even coma.
  • The vinca-alkaloids, cisplatin and the taxanes are amongst the most important drugs inducing peripheral neurotoxicity.
  • These drugs are widely used for various malignancies such as ovarian and breast cancer, and haematological cancers.
  • Chemotherapy-induced neuropathy is clearly related to cumulative dose or dose-intensities.
  • Patients who already have neuropathic symptoms due to diabetes mellitus, hereditary neuropathies or earlier treatment with neurotoxic chemotherapy are thought to be more vulnerable for the development of chemotherapy-induced peripheral neuropathy.
  • Risk factors are high doses, frequent administration and radiotherapy preceding methotrexate chemotherapy, which appears to be more neurotoxic than methotrexate as single modality.
  • [MeSH-minor] Dose-Response Relationship, Drug. Drug Administration Schedule. Humans

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  • (PMID = 12887262.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 105
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14. Jahr JS, Weeks DL, Desai P, Lim JC, Butch AW, Gunther R, Driessen B: Does OxyVita, a new-generation hemoglobin-based oxygen carrier, or oxyglobin acutely interfere with coagulation compared with normal saline or 6% hetastarch? An ex vivo thromboelastography study. J Cardiothorac Vasc Anesth; 2008 Feb;22(1):34-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: Because hetastarches have deleterious effects on coagulation that increase with molecular weight (MWt), risk of coagulopathy associated with a high MWt hemoglobin-based oxygen carrier (HBOC) was studied.
  • Coagulopathy related to 1:11, 1:5, 1:2, or 1:1 dilution of whole blood with normal saline, 6% hetastarch (670 kilodaltons [kD]), hemoglobin glutamer-200 (HBOC-200, 200 kD), or OxyVita (OXYVITA Inc, New Windsor, NY) (a new-generation, zero-link polymerized bovine hemoglobin-based oxygen carrier, 33 megadaltons) were analyzed.
  • MEASUREMENTS AND MAIN RESULTS: At 2 lower levels of hemodilution, hetastarch, HBOC-200, and OxyVita produced equivalent reductions in maximum clot strength (TEG-MA and TEG-G) that reached statistical significance compared with whole blood and normal saline.
  • At 2 higher dilutions, OxyVita and HBOC-200 impaired maximum clot strength compared with whole blood, normal saline, and hetastarch.
  • Dilution with hetastarch had a greater effect on clot propagation (K and alpha) than either HBOC.
  • CONCLUSIONS: OxyVita and HBOC-200, HBOCs with different MWt, had similar effects on coagulation as measured by TEG.
  • [MeSH-major] Blood Coagulation / drug effects. Blood Substitutes / pharmacology. Hemoglobins / pharmacology. Thrombelastography / drug effects
  • [MeSH-minor] Dose-Response Relationship, Drug. Humans. Hydroxyethyl Starch Derivatives / administration & dosage. Hydroxyethyl Starch Derivatives / pharmacology. Shock, Hemorrhagic / blood. Shock, Hemorrhagic / therapy. Sodium Chloride / pharmacology

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  • (PMID = 18249328.001).
  • [ISSN] 1532-8422
  • [Journal-full-title] Journal of cardiothoracic and vascular anesthesia
  • [ISO-abbreviation] J. Cardiothorac. Vasc. Anesth.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Hemoglobins; 0 / Hydroxyethyl Starch Derivatives; 0 / OxyVita; 0 / hemoglobin glutamer-200; 451W47IQ8X / Sodium Chloride
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15. Zhou C, Smith JL, Liu J: Role of BRCA1 in cellular resistance to paclitaxel and ionizing radiation in an ovarian cancer cell line carrying a defective BRCA1. Oncogene; 2003 Apr 24;22(16):2396-404
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of BRCA1 in cellular resistance to paclitaxel and ionizing radiation in an ovarian cancer cell line carrying a defective BRCA1.
  • BRCA1, the gene responsible for approximately half of all cases of hereditary breast cancer and almost all cases of combined hereditary breast and ovarian cancer, has been implicated in the maintenance of genomic stability through DNA repair.
  • This function is mediated, at least in part, through two tandem BRCA1 C-terminal (BRCT) repeats.
  • The role of BRCA1 in the development of ovarian cancer is poorly understood, partially owing to the lack of ovarian cancer cell lines with defective BRCA1.
  • The purpose of this study was to further characterize an endometrioid ovarian cancer cell line, SNU-251, which was previously reported to carry a nonsense mutation (from G to A) at amino acid 1815 of BRCA1.
  • In addition, we examined the role of BRCA1 in the cell cycle and in the responses to the chemotherapy drug paclitaxel and ionizing radiation.
  • Loss of the C-terminal 49 amino acids due to this point mutation did not affect the expression of the truncated BRCA1 protein, but caused a loss of transcriptional activation of the endogenous p21(WAF1/CIP1) gene, and could not sustain arrest in the G(2)/M phase of the cell cycle.
  • The BRCA1 mutation in SNU-251 cells inhibited BRCA1 subnuclear assembly for DNA-damage repair and increased cellular sensitivity to ionizing radiation and paclitaxel.
  • This sensitivity was reversed by reintroduction of ectopic wild-type BRCA1.
  • Our results suggest that the deletion of the C-terminal 49 amino acids of BRCA1 results in a loss of BRCA1 function in the SNU-251 cell line.
  • BRCA1 helps to mediate the resistance to both radiation and paclitaxel.
  • Therefore, SNU-251 may be a useful model for studying the molecular mechanism of BRCA1 in the resistance of ovarian cancer to ionizing radiation and chemotherapy treatment and in the development of hereditary human ovarian cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. BRCA1 Protein / metabolism. Ovarian Neoplasms / metabolism. Paclitaxel / pharmacology
  • [MeSH-minor] Cell Line. Drug Resistance, Neoplasm. Female. Humans. In Vitro Techniques. PTEN Phosphohydrolase. Phosphoric Monoester Hydrolases / genetics. Phosphoric Monoester Hydrolases / metabolism. Radiation, Ionizing. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism

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  • (PMID = 12717416.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / BRCA1 Protein; 0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; P88XT4IS4D / Paclitaxel
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16. de Plater L, Laugé A, Guyader C, Poupon MF, Assayag F, de Cremoux P, Vincent-Salomon A, Stoppa-Lyonnet D, Sigal-Zafrani B, Fontaine JJ, Brough R, Lord CJ, Ashworth A, Cottu P, Decaudin D, Marangoni E: Establishment and characterisation of a new breast cancer xenograft obtained from a woman carrying a germline BRCA2 mutation. Br J Cancer; 2010 Oct 12;103(8):1192-200
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Establishment and characterisation of a new breast cancer xenograft obtained from a woman carrying a germline BRCA2 mutation.
  • BACKGROUND: The BRCA2 gene is responsible for a high number of hereditary breast and ovarian cancers, and studies of the BRCA2 biological functions are limited by the lack of models that resemble the patient's tumour features.
  • The aim of this study was to establish and characterise a new human breast carcinoma xenograft obtained from a woman carrying a germline BRCA2 mutation.
  • METHODS: A transplantable xenograft was obtained by grafting a breast cancer sample into nude mice.
  • The biological and genetic profiles of the xenograft were compared with that of the patient's tumour using histology, immunohistochemistry (IHC), BRCA2 sequencing, comparative genomic hybridisation (CGH), and qRT-PCR.
  • RESULTS: Histological profile identified the tumour as a basal-like triple-negative breast cancer.
  • Targeted BRCA2 DNA sequencing of the xenograft showed the presence of the mutation previously identified in the carrier.
  • The therapeutic assessment of the xenograft showed sensitivity to anthracyclin-based chemotherapy and resistance to docetaxel.
  • The xenograft was also highly sensitive to radiotherapy and cisplatin-based treatments.
  • CONCLUSIONS: This study describes a new human breast cancer xenograft obtained from a BRCA2-mutated patient.
  • This xenograft provides a new model for the pre-clinical drug development and for the exploration of the drug response biological basis.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Genes, BRCA2. Germ-Line Mutation
  • [MeSH-minor] Adult. Animals. Anthracyclines / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Culture Techniques. Cell Line, Tumor. Comparative Genomic Hybridization. DNA Mutational Analysis. Female. Heterozygote. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Transplantation, Heterologous. Xenograft Model Antitumor Assays / methods

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  • (PMID = 20877358.001).
  • [ISSN] 1532-1827
  • [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 / Anthracyclines
  • [Other-IDs] NLM/ PMC2967069
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17. Burmeister MA, Rempf C, Standl TG, Rehberg S, Bartsch-Zwemke S, Krause T, Tuszynski S, Gottschalk A, Schulte am Esch J: Effects of prophylactic or therapeutic application of bovine haemoglobin HBOC-200 on ischaemia-reperfusion injury following acute coronary ligature in rats. Br J Anaesth; 2005 Dec;95(6):737-45
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  • [Title] Effects of prophylactic or therapeutic application of bovine haemoglobin HBOC-200 on ischaemia-reperfusion injury following acute coronary ligature in rats.
  • Therefore the effects of HBOC-200 on I-R injury were evaluated in a randomized placebo-controlled animal trial.
  • METHODS: Animals were randomized to receive either placebo i.v. without I-R (sham group, n=9), placebo i.v. with I-R (control group, n=10), HBOC-200 0.4 g kg(-1) i.v. prior to I-R (prophylaxis group, n=12) or HBOC-200 0.4 g kg(-1) i.v. during I-R (therapy group, n=15).
  • RESULTS: Infarct size within the area at risk was 62 (sd 15)% (control), 46 (10)% (prophylaxis, P<0.025 vs control) and 61 (9)% (therapy, P<0.85 vs control).
  • The frequency of DNA single-strand breaks was reduced vs control in the sham (P<0.01) and prophylaxis (P<0.04) groups and was almost the same in the therapy group (P<0.75).
  • The severity of cardiac arrhythmias during ischaemia was lower compared with control in the sham (P<0.001) and prophylaxis (P<0.039) groups, but there was no difference in the therapy group.
  • CONCLUSION: This study demonstrates that neither prophylactic nor therapeutic application of the cell-free haemoglobin solution HBOC-200 aggravates cardiac I-R injury.
  • [MeSH-major] Hemoglobins / therapeutic use. Reperfusion Injury / prevention & control
  • [MeSH-minor] Animals. Arrhythmias, Cardiac / drug therapy. Arrhythmias, Cardiac / prevention & control. Body Temperature / drug effects. DNA Damage. DNA, Single-Stranded / drug effects. Drug Administration Schedule. Hemodynamics / drug effects. Humans. In Situ Nick-End Labeling. Male. Myocardial Infarction / drug therapy. Myocardial Infarction / pathology. Myocardial Infarction / prevention & control. Rats. Rats, Sprague-Dawley


18. Hall C, Malkevich N, Handrigan M, Vandermolen C, Aranaud F, Hong J, Dong F, Rice J, Philbin N, Ahlers S, McCarron R, Freilich D, McGwin G, Flournoy WS, Pearce LB: Innate immune responses in Swine resuscitated from severe traumatic hemorrhagic shock with hemoglobin-based oxygen carrier-201. Artif Cells Blood Substit Immobil Biotechnol; 2007;35(3):259-74
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  • Herein, we evaluated HBOC-201's immune effects in swine with more severe hemorrhagic shock due to soft tissue injury and 55% blood volume catheter withdrawal over 15 minutes followed by fluid resuscitation at 20 minutes with HBOC-201, Hextend, or no treatment (NON) before hospital arrival.
  • Survival rates were similar with HBOC-201 and Hextend (p > 0.05), but were higher than in (p = 0.007).
  • There was a trend to higher plasma IL-10 in HBOC-201 and groups vs. Hextend.
  • We conclude that in swine with severe controlled HS and soft tissue injury, immune responses are similar with resuscitation with HBOC-201 and Hextend.
  • [MeSH-major] Hemoglobins / administration & dosage. Hydroxyethyl Starch Derivatives / administration & dosage. Resuscitation / methods. Shock, Hemorrhagic / immunology. Shock, Hemorrhagic / therapy
  • [MeSH-minor] Animals. Apoptosis / immunology. Blood Pressure / physiology. Blood Substitutes / administration & dosage. Blood Substitutes / pharmacokinetics. Cytokines / immunology. Disease Models, Animal. Drug Evaluation, Preclinical. Emergency Medical Services. Fluid Therapy / methods. Immunity, Innate / drug effects. Swine. Swine, Miniature. T-Lymphocytes / immunology. T-Lymphocytes / pathology

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  • (PMID = 17573626.001).
  • [ISSN] 1073-1199
  • [Journal-full-title] Artificial cells, blood substitutes, and immobilization biotechnology
  • [ISO-abbreviation] Artif Cells Blood Substit Immobil Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Cytokines; 0 / HBOC 201; 0 / Hemoglobins; 0 / Hydroxyethyl Starch Derivatives
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19. Damle SS, Moore EE, Babu AN, Meng X, Fullerton DA, Banerjee A: Hemoglobin-based oxygen carrier induces heme oxygenase-1 in the heart and lung but not brain. J Am Coll Surg; 2009 Apr;208(4):592-8
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  • To date, however, no clinically viable therapy exists to safely induce HO-1.
  • We have recently observed that administration of a hemoglobin-based oxygen carrier (HBOC) attenuates postinjury systemic inflammation.
  • We have further demonstrated that an HBOC can induce HO-1 in vitro.
  • We now explore the tissue-specific induction of heme oxygenase-1 after administration of an HBOC.
  • STUDY DESIGN: Rats were infused with doses of HBOC or saline through femoral vein injection (n=5 per group).
  • Interestingly, brain tissue did not have any significant amount of HO-1, either at baseline or after HBOC therapy.
  • CONCLUSIONS: This study demonstrates that a clinically accessible product, HBOC, can specifically and selectively induce the expression of the protective enzyme HO-1 in vivo.
  • These findings begin to characterize which organ systems may benefit by preischemic treatments with HBOC and further expand potential clinical applications of HBOCs.
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Immunohistochemistry. Infusions, Intravenous. Organ Specificity. Rats. Rats, Sprague-Dawley

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  • (PMID = 19476795.001).
  • [ISSN] 1879-1190
  • [Journal-full-title] Journal of the American College of Surgeons
  • [ISO-abbreviation] J. Am. Coll. Surg.
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / P50GM049222; United States / NIGMS NIH HHS / GM / T32GM008315
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / PolyHeme; EC 1.14.99.3 / Heme Oxygenase-1
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20. Alayash AI, D'Agnillo F, Buehler PW: First-generation blood substitutes: what have we learned? Biochemical and physiological perspectives. Expert Opin Biol Ther; 2007 May;7(5):665-75
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  • Chemically modified or recombinant hemoglobin (Hb)-based oxygen carriers (HBOCs) have been developed as oxygen therapeutics or 'blood substitutes' for use in a variety of clinical settings.
  • [MeSH-major] Blood Substitutes / toxicity. Drug Design. Endothelial Cells / drug effects. Hemoglobins / toxicity
  • [MeSH-minor] Animals. Humans. Molecular Structure. Nitric Oxide / metabolism. Oxidation-Reduction. Oxidative Stress / drug effects. Protein Engineering. Reactive Oxygen Species / metabolism. Recombinant Proteins / toxicity. Structure-Activity Relationship

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  • (PMID = 17477804.001).
  • [ISSN] 1744-7682
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Hemoglobins; 0 / Reactive Oxygen Species; 0 / Recombinant Proteins; 31C4KY9ESH / Nitric Oxide
  • [Number-of-references] 66
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21. Dai M, Yu M, Han J, Li H, Cui P, Liu Q, Xiu R: PEG-conjugated hemoglobin combination with cisplatin enforced the antiangiogeic effect in a cervical tumor xenograft model. Artif Cells Blood Substit Immobil Biotechnol; 2008;36(6):487-97
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  • Hypoxia widely exists in solid tumors due to the abnormal vasculature of tumor tissue and insufficiency of tissue oxygenation.
  • We speculate that hemoglobin-based oxygen carriers (HBOCs) can attenuate tissue hypoxia, thereby suppressing the angiogenesis in solid tumor in the context that HBOCs have the ability to increase tissue oxygenation.
  • In the present study, PEG-conjugated hemoglobin solution (0.3 g/kg i.v. or 0.6 g/kg i.v.) was intravenously administrated to BALB/c nude mice bearing the cervical tumor twice a week with or without the treatment of cisplatin (5mg/kg i.p.) to investigate whether PEG-conjugated hemoglobin has a chemo-sensitization effect though anti-angiogenesis pathway.
  • Anti-angiogenic effect was accessed by detection of mRNA and protein levels of vascular endothelial growth factor (VEGF), the most important angiogenic factor.
  • Collectively, treatment of PEG-conjugated hemoglobin combination with cisplatin has an antiangiogenic effect, but the underlying mechanism should be further studied.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Cisplatin / administration & dosage. Hemoglobins / administration & dosage. Polyethylene Glycols / administration & dosage. Uterine Cervical Neoplasms / drug therapy
  • [MeSH-minor] Animals. Anoxia / prevention & control. Drug Synergism. Drug Therapy, Combination. Female. Humans. Mice. Mice, Inbred BALB C. Neovascularization, Pathologic / drug therapy. Treatment Outcome. Tumor Burden / drug effects. Vascular Endothelial Growth Factor A / biosynthesis. Xenograft Model Antitumor Assays


22. Foulkes WD: BRCA1 and BRCA2: chemosensitivity, treatment outcomes and prognosis. Fam Cancer; 2006;5(2):135-42
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  • [Title] BRCA1 and BRCA2: chemosensitivity, treatment outcomes and prognosis.
  • BRCA1 and BRCA2 are important breast and ovarian cancer susceptibility genes, and mutations in these two genes confer lifetime risks of breast cancer of up to 80% and ovarian cancer risks of up to 40%.
  • Clinico-pathological studies have identified features that are specific to BRCA1-related breast cancer, but this has been more difficult for BRCA2-related breast cancer.
  • Ovarian cancers due to BRCA1 or BRCA2 mutations cannot usually be distinguished from their non-hereditary counterparts on morphological grounds, but micro-array data suggest that differences do exist.
  • Prognostic studies have shown that breast cancer in a BRCA1 mutation carrier is likely to have a similar, or worse, outcome than that occurring in a BRCA2- or non-carrier of the same age.
  • By contrast, most studies indicate that women developing a BRCA1/2-related ovarian cancer have an improved survival compared with non-carriers, particularly if they receive platinum-based therapy.
  • In support of this, in vitro chemo-sensitivity studies have found that human cells lacking BRCA1 may be particularly sensitive to cisplatinum and to other drugs that cause double-strand breaks in DNA.
  • Nevertheless, in breast cancer, little is known regarding clinically important differences in response to chemotherapy between BRCA1/2 mutation carriers and non-carriers, and between different chemotherapeutic regimens within existing series of BRCA1/2 mutation carriers.
  • [MeSH-major] Breast Neoplasms / genetics. Genes, BRCA1. Genes, BRCA2. Ovarian Neoplasms / genetics
  • [MeSH-minor] DNA Methylation. Female. Humans. Mutation. Prognosis. Treatment Outcome

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  • (PMID = 16736282.001).
  • [ISSN] 1389-9600
  • [Journal-full-title] Familial cancer
  • [ISO-abbreviation] Fam. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 85
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23. Rodriguez C, Vitturi DA, He J, Vandromme M, Brandon A, Hutchings A, Rue LW 3rd, Kerby JD, Patel RP: Sodium nitrite therapy attenuates the hypertensive effects of HBOC-201 via nitrite reduction. Biochem J; 2009 Aug 27;422(3):423-32
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  • [Title] Sodium nitrite therapy attenuates the hypertensive effects of HBOC-201 via nitrite reduction.
  • In the present study we tested whether nitrite would attenuate HBOC-mediated hypertension using HBOC-201 (Biopure), a bovine cross-linked, low-oxygen-affinity haemoglobin.
  • In a similar way to unmodified haemoglobin, deoxygenated HBOC-201 reduced nitrite to NO with rates directly proportional to the extent of deoxygenation.
  • The functional importance of HBOC-201-dependent nitrite reduction was demonstrated using isolated aortic rings and a murine model of trauma, haemorrhage and resuscitation.
  • In the former, HBOC-201 inhibited NO-donor and nitrite-dependent vasodilation when oxygenated.
  • However, deoxygenated HBOC-201 failed to affect nitrite-dependent vasodilation but still inhibited NO-donor dependent vasodilation, consistent with a model in which nitrite-reduction by deoxyHBOC-201 counters NO scavenging.
  • Finally, resuscitation using HBOC-201, after trauma and haemorrhage, resulted in mild hypertension ( approximately 5-10 mmHg).
  • Administration of a single bolus nitrite (30-100 nmol) at the onset of HBOC-201 resuscitation prevented hypertension.
  • Nitrite had no effect on mean arterial pressure during resuscitation with LR (lactated Ringer's solution), suggesting a role for nitrite-HBOC reactions in attenuating HBOC-mediated hypertension.
  • Taken together these data support the concept that nitrite can be used as an adjunct therapy to prevent HBOC-dependent hypertension.

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  • (PMID = 19555351.001).
  • [ISSN] 1470-8728
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / GM063490-08; United States / NIGMS NIH HHS / GM / T32 GM063490-08; United States / NIGMS NIH HHS / GM / T32 GM063490; United States / NIGMS NIH HHS / GM / GM063490-09; United States / NIGMS NIH HHS / GM / T32 GM063490-09
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antihypertensive Agents; 0 / Blood Substitutes; 0 / HBOC 201; 0 / Hemoglobins; 0 / Nitric Oxide Donors; 31C4KY9ESH / Nitric Oxide; 9008-02-0 / deoxyhemoglobin; EC 1.7.- / Nitrite Reductases; M0KG633D4F / Sodium Nitrite
  • [Other-IDs] NLM/ NIHMS150230; NLM/ PMC2775055
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24. Rice J, Philbin N, Handrigan M, Hall C, McGwin G, Ahlers S, Pearce LB, Arnaud F, McCarron R, Freilich D: Vasoactivity of bovine polymerized hemoglobin (HBOC-201) in swine with traumatic hemorrhagic shock with and without brain injury. J Trauma; 2006 Nov;61(5):1085-99
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  • [Title] Vasoactivity of bovine polymerized hemoglobin (HBOC-201) in swine with traumatic hemorrhagic shock with and without brain injury.
  • BACKGROUND: We previously reported that bovine polymerized hemoglobin (HBOC- 201) improved outcome in swine with hemorrhagic shock (HS) with and without traumatic brain injury (TBI).
  • METHODS: HBOC-201 versus standard fluid resuscitation was compared in four anesthetized invasively monitored swine models: moderate controlled HS, severe controlled HS, severe uncontrolled HS (liver injury), and severe uncontrolled HS/TBI (liver/parietal brain injuries).
  • The change in mean arterial pressure (DeltaMAP) response severity was stratified and analyzed based on infusion number and HS severity, using Student's t and Fisher's exact tests.
  • RESULTS: HBOC-201 vasoactivity resulted in higher MAP in all studies.
  • Among HBOC-201 pigs, DeltaMAP responses were significant for the first two infusions and inversely related to HS severity.
  • DeltaMAP was higher with HBOC-201 through the first infusion in moderate controlled HS, the fifth in severe uncontrolled HS, and the second in severe uncontrolled HS/TBI; there were no group differences in severe controlled HS.
  • Overall, HBOC-201 improved physiologic parameters and survival without causing hypoperfusion; in severe HS, perfusion improved.
  • CONCLUSIONS: In swine with HS +/- TBI, HBOC-201 had mild to moderate vasoactivity, resulting in significant DeltaMAP responses mainly after initial infusions, no severe/adverse responses, and improved outcome.
  • Our data suggest that use of physiologic parameters (e.g., tachycardia), in addition to hypotension to guide fluid reinfusion during HS resuscitation with HBOC-201, will minimize hypoperfusion risk and maximize potential benefit.
  • [MeSH-major] Blood Pressure / drug effects. Blood Substitutes / therapeutic use. Hemoglobins / therapeutic use. Resuscitation / methods. Shock, Hemorrhagic / drug therapy
  • [MeSH-minor] Animals. Brain Injuries / complications. Disease Models, Animal. Drug Evaluation, Preclinical. Fluid Therapy. Heart Rate / drug effects. Hypotension / drug therapy. Infusions, Intravenous. Isotonic Solutions / therapeutic use. Swine. Tachycardia / drug therapy

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  • (PMID = 17099513.001).
  • [ISSN] 0022-5282
  • [Journal-full-title] The Journal of trauma
  • [ISO-abbreviation] J Trauma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / HBOC 201; 0 / Hemoglobins; 0 / Isotonic Solutions; 8022-63-7 / Ringer's lactate
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25. Pape A, Kleen M, Kemming G, Meisner F, Meier J, Habler O: Fluid resuscitation from severe hemorrhagic shock using diaspirin cross-linked hemoglobin fails to improve pancreatic and renal perfusion. Acta Anaesthesiol Scand; 2004 Nov;48(10):1328-37
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  • BACKGROUND: Fluid resuscitation from hemorrhagic shock is intended to abolish microcirculatory disorders and to restore adequate tissue oxygenation.
  • Diaspirin cross-linked hemoglobin (DCLHb) is a hemoglobin-based oxygen carrier (HBOC) with vasoconstrictive properties.
  • Therefore, fluid resuscitation from severe hemorrhagic shock using DCLHb was expected to improve perfusion pressure and tissue perfusion of kidneys and pancreas.
  • [MeSH-major] Aspirin / analogs & derivatives. Aspirin / therapeutic use. Blood Substitutes / therapeutic use. Fluid Therapy. Hemoglobins / therapeutic use. Pancreas / blood supply. Renal Circulation / drug effects. Shock, Hemorrhagic / physiopathology. Shock, Hemorrhagic / therapy
  • [MeSH-minor] Algorithms. Animals. Female. Male. Microspheres. Regional Blood Flow / drug effects. Resuscitation. Serum Albumin / therapeutic use. Swine

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  • (PMID = 15504197.001).
  • [ISSN] 0001-5172
  • [Journal-full-title] Acta anaesthesiologica Scandinavica
  • [ISO-abbreviation] Acta Anaesthesiol Scand
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Hemoglobins; 0 / Serum Albumin; 0 / diaspirin-cross-linked hemoglobin; R16CO5Y76E / Aspirin
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26. Sakai H, Sou K, Horinouchi H, Kobayashi K, Tsuchida E: Review of hemoglobin-vesicles as artificial oxygen carriers. Artif Organs; 2009 Feb;33(2):139-45
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  • Nevertheless, some problems remain: infection, blood type mismatching, immunological response, short shelf life, and screening test costs.
  • Hb-vesicles (HbV) are a cellular type of HBOC that overcome these issues.
  • [MeSH-major] Blood Substitutes / administration & dosage. Blood Substitutes / therapeutic use
  • [MeSH-minor] Erythrocyte Transfusion. Extracorporeal Circulation. Humans. Ischemia / drug therapy. Liposomes. Shock, Hemorrhagic / drug therapy

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  • (PMID = 19178458.001).
  • [ISSN] 1525-1594
  • [Journal-full-title] Artificial organs
  • [ISO-abbreviation] Artif Organs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Liposomes
  • [Number-of-references] 25
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27. Awasthi V: Pharmaceutical aspects of hemoglobin-based oxygen carriers. Curr Drug Deliv; 2005 Apr;2(2):133-42
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  • Oxygen delivery has evolved as a therapy of widespread interest in the clinical setting, especially in emergency medicine and anesthesiology.
  • Such blood substitutes, defined more correctly as oxygen therapeutics, are particularly valuable in circumstances such as war and trauma situations where properly matched blood may not be immediately available or is not accepted by the recipients for religious reasons.
  • At the same time, properties such as oxygen affinity, hemoglobin content and in vivo efficacy of oxygen carriers are specific to HBOCs.
  • [MeSH-minor] Colloids. Drug Carriers. Drug Contamination. Half-Life. Lipopolysaccharides / toxicity. Osmotic Pressure. Viscosity

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  • (PMID = 16305414.001).
  • [ISSN] 1567-2018
  • [Journal-full-title] Current drug delivery
  • [ISO-abbreviation] Curr Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Colloids; 0 / Drug Carriers; 0 / Hemoglobins; 0 / Lipopolysaccharides; S88TT14065 / Oxygen
  • [Number-of-references] 147
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28. Irwin D, Buehler PW, Alayash AI, Jia Y, Bonventura J, Foreman B, White M, Jacobs R, Piteo B, TissotvanPatot MC, Hamilton KL, Gotshall RW: Mixed S-nitrosylated polymerized bovine hemoglobin species moderate hemodynamic effects in acutely hypoxic rats. Am J Respir Cell Mol Biol; 2010 Feb;42(2):200-9
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  • Hemoglobin (Hb)-based oxygen carriers (HBOCs) are being developed as a potential therapy for increasing tissue oxygenation, yet they have not reached their full potential because of unwanted hemodynamic side effects (vasoconstriction, low cardiac output, and oxygen delivery) due in part to nitric oxide (NO) scavenging by cell-free Hb.
  • It may be possible to overcome the NO scavenging effect by coinfusing S-nitrosylated (SNO) HBOC along with unmodified HBOC.
  • SNO-HBOC, like free Hb, may act as an NO donor in low-oxygen conditions.
  • We hypothesized that an unaltered HBOC, polymerized bovine Hb (PBvHb), coinfused with an SNO-PBvHb, would improve hemodynamics and oxygen delivery during hypoxia.
  • These data support the potential use of HBOC mixed with SNO-HBOC for the treatment of conditions in which acute hypoxia is present, such as tumor oxygenation, wound healing, hemorrhagic trauma, and sickle cell and hemolytic anemia.

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  • (PMID = 19395680.001).
  • [ISSN] 1535-4989
  • [Journal-full-title] American journal of respiratory cell and molecular biology
  • [ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / 5-T32-HL07171
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Hemoglobins; 0 / Nitric Oxide Donors; 0 / Nitrites; 0 / Nitroso Compounds; 0 / Polymers; 0 / polymerized bovine hemoglobin; S88TT14065 / Oxygen
  • [Other-IDs] NLM/ PMC2822981
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29. Hare GM, Harrington A, Liu E, Wang JL, Baker AJ, Mazer CD: Effect of oxygen affinity and molecular weight of HBOCs on cerebral oxygenation and blood pressure in rats. Can J Anaesth; 2006 Oct;53(10):1030-8
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  • Hippocampal cerebral tissue oxygen tension, regional cerebral blood flow (rCBF), MAP, total hemoglobin concentration and arterial blood gases were measured.
  • RESULTS: Hippocampal tissue oxygen tension increased in all HBOC groups following resuscitation.
  • The rCBF remained unchanged after HBOC resuscitation in all groups.
  • Following resuscitation, the peak MAP was higher in the High P50 Poly OR-Hb group (152 +/- 13 mmHg) when compared to either the Low or High P50 large MW, (> 128 kDa) HBOC group (119 +/- 15 mmHg or 127 +/- 18 respectively, P < 0.05 for both).
  • CONCLUSIONS: O-raffinose polymerized HBOC, with or without lower MW components, maintained cerebral tissue oxygen delivery following hemorrhage and resuscitation in rats.
  • No significant effect of oxygen affinity on cerebral tissue oxygen tension or blood flow was observed.
  • [MeSH-major] Blood Pressure / drug effects. Cerebrovascular Circulation / drug effects. Hemoglobins / pharmacology. Raffinose / analogs & derivatives
  • [MeSH-minor] Animals. Hemodilution. Hemorrhage / drug therapy. Hippocampus / blood supply. Male. Models, Animal. Molecular Weight. Rats. Rats, Sprague-Dawley. Resuscitation

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  • (PMID = 16987859.001).
  • [ISSN] 0832-610X
  • [Journal-full-title] Canadian journal of anaesthesia = Journal canadien d'anesthésie
  • [ISO-abbreviation] Can J Anaesth
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Hemoglobins; 0 / O-raffinose cross-linked human hemoglobin; N5O3QU595M / Raffinose
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30. Zhong Y, Sheng XG, Ma ZF, Ma YB, Liu NF, Chen YT, Gao R, Wang YY, Sun L: [Clinicopathological characteristics of hereditary ovarian cancer syndrome]. Zhonghua Fu Chan Ke Za Zhi; 2009 Sep;44(9):676-80
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  • [Title] [Clinicopathological characteristics of hereditary ovarian cancer syndrome].
  • OBJECTIVE: To explore the clinicopathological characteristics of hereditary ovarian cancer syndrome (HOCS).
  • 2007, among 580 cases of primary ovarian cancer, 42 cases (hereditary group), who had a positive family history of ovarian cancer and met the diagnostic criteria of HOCS, were analyzed retrospectively.
  • One hundred cases without a family history of ovarian cancer were enrolled randomizely as control group (sporadic group).
  • There were 90% belong to serous adenocarcinoma in the hereditary group, while 84% in the sporadic group.
  • Fourteen cases (33%,14/42) were previously untreated in the hereditary group, while 40 cases (40%, 40/100) in the sporadic group.
  • There were 15 cases (36%, 15/42) underwent secondary surgery and 15 cases (36%, 15/42) underwent third surgery or more in hereditary group, while 50 cases (50%,50/100) and 27 cases (27%, 27/100) in the sporadic group.
  • The mean number of chemotherapy cycles received in two groups was 13.3 and 11.8 (P > 0.05).
  • The 3-year and 5-year survival rate in hereditary group were 73.6% and 54.9% respectively, compared with 47.4% and 21.2% (P < 0.05) in sporadic group.
  • CONCLUSION: Hereditary ovarian cancer mostly from maternal lineage are featuring in early age of onset, serous adenocarcinoma, advanced stage (stage III), and better prognosis after the comprehensive treated by cytoreductive surgery plus with chemotherapy.
  • [MeSH-major] Cystadenocarcinoma, Serous / genetics. Cystadenocarcinoma, Serous / pathology. Ovarian Neoplasms / genetics. Ovarian Neoplasms / pathology
  • [MeSH-minor] Adult. Age of Onset. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / genetics. Cisplatin / administration & dosage. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Female. Genetic Diseases, Inborn / pathology. Genetic Diseases, Inborn / therapy. Genetic Predisposition to Disease. Humans. Middle Aged. Neoplasm Staging. Pedigree. Prognosis. Retrospective Studies. Risk Factors


31. Mullan PB, Gorski JJ, Harkin DP: BRCA1--a good predictive marker of drug sensitivity in breast cancer treatment? Biochim Biophys Acta; 2006 Dec;1766(2):205-16
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  • [Title] BRCA1--a good predictive marker of drug sensitivity in breast cancer treatment?
  • There are currently only two predictive markers of response to chemotherapy for breast cancer in routine clinical use, namely the Estrogen receptor-alpha and the HER2 receptor.
  • The breast and ovarian cancer susceptibility gene BRCA1 is an important genetic factor in hereditary breast and ovarian cancer and there is increasing evidence of an important role for BRCA1 in the sporadic forms of both cancer types.
  • Our group and numerous others have shown in both preclinical and clinical studies that BRCA1 is an important determinant of chemotherapy responses in breast cancer.
  • In this review we will outline the current understanding of the role of BRCA1 as a determinant of response to DNA damaging and microtubule damaging chemotherapy.
  • We will then discuss how the known functions of this multifaceted protein may provide mechanistic explanations for its role in chemotherapy responses.
  • [MeSH-major] BRCA1 Protein / genetics. BRCA1 Protein / metabolism. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Breast Neoplasms / genetics. DNA Repair / genetics. Drug Resistance, Neoplasm / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Humans. Microtubules / drug effects


32. Indraccolo S, Tisato V, Agata S, Moserle L, Ferrari S, Callegaro M, Persano L, Palma MD, Scaini MC, Esposito G, Fassina A, Nicoletto O, Plebani M, Chieco-Bianchi L, Amadori A, D'Andrea E, Montagna M: Establishment and characterization of xenografts and cancer cell cultures derived from BRCA1 -/- epithelial ovarian cancers. Eur J Cancer; 2006 Jul;42(10):1475-83
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  • [Title] Establishment and characterization of xenografts and cancer cell cultures derived from BRCA1 -/- epithelial ovarian cancers.
  • The BRCA1 gene is responsible for a high number of hereditary breast and ovarian cancers that cluster in families with a strong genetic predisposition.
  • Despite intense investigation, the accumulating findings on BRCA1 biological functions have not yet been translated into specific therapeutic approaches, also due to the lack of suitable experimental models.
  • The purpose of this study was to establish and characterize cell cultures and xenografts from patients with BRCA1 -/- ovarian cancers.
  • We derived two ovarian cancer cell lines, termed PD-OVCA1 and PD-OVCA2, both from patients previously treated with chemotherapy, that propagate in SCID mice as well as in vitro for a limited number of passages.
  • A detailed molecular characterization highlighted both constitutive and somatic genetic events that abrogate BRCA1 gene function.
  • Both cell lines were shown to lose the wild type BRCA1 allele; intriguingly, these deletions were apparently accompanied by gain of one or more copies of the mutant alleles.
  • The PD-OVCA1 and PD-OVCA2 ovarian cancer cell lines will provide a valuable tool for new experimental models for the study of BRCA1-associated tumour biology.
  • [MeSH-major] Genes, BRCA1. Ovarian Neoplasms / pathology. Tumor Cells, Cultured / pathology


33. Levine DA, Federici MG, Reuter VE, Boyd J: Cell proliferation and apoptosis in BRCA-associated hereditary ovarian cancer. Gynecol Oncol; 2002 Jun;85(3):431-4
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  • [Title] Cell proliferation and apoptosis in BRCA-associated hereditary ovarian cancer.
  • OBJECTIVE: The goal was to test the hypothesis that cellular growth properties differ between hereditary and sporadic ovarian cancers.
  • METHODS: Cell proliferation and apoptosis were assessed in 67 tumors associated with deleterious germline BRCA mutations (hereditary) and 69 tumors without BRCA mutations (sporadic).
  • RESULTS: The mean number of Ki-67-immunopositive nuclei was significantly higher in ovarian cancers from the hereditary group compared with those from the sporadic group (P = 0.017).
  • Cell proliferation did not differ significantly between BRCA1- and BRCA2-associated hereditary tumors, and apoptosis did not differ significantly between the hereditary and sporadic tumors.
  • CONCLUSION: These data indicate that ovarian carcinomas associated with germline BRCA mutations have a significantly higher growth fraction than sporadic cancers.
  • This property may contribute to an improved response to cytotoxic chemotherapy, partially accounting for the longer recurrence-free interval and overall survival observed in the hereditary group.
  • [MeSH-major] Apoptosis / genetics. Genes, BRCA1. Genes, BRCA2. Ovarian Neoplasms / genetics. Ovarian Neoplasms / pathology
  • [MeSH-minor] Cell Division / genetics. Cell Nucleus / metabolism. Cohort Studies. Disease-Free Survival. Female. Germ-Line Mutation. Humans. Jews / genetics. Ki-67 Antigen / metabolism. Middle Aged. Neoplasm Staging. Retrospective Studies


34. Wu W, Yang Q, Li T, Zhang P, Zhou R, Yang C: Hemoglobin-based oxygen carriers combined with anticancer drugs may enhance sensitivity of radiotherapy and chemotherapy to solid tumors. Artif Cells Blood Substit Immobil Biotechnol; 2009;37(4):163-5
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  • [Title] Hemoglobin-based oxygen carriers combined with anticancer drugs may enhance sensitivity of radiotherapy and chemotherapy to solid tumors.
  • The aberrant vascular architecture in solid tumors is the key limiting factor known to ameliorate hypoxia and increase circulating anticancer drugs, thus resulting in resistance to radiotherapy and chemotherapy in tumor treatment.
  • Herein, we draw the hypothesis that HBOCs combined with an anticancer drug may increase oxygen bioavailability and anticancer drug retention in solid tumors and in turn contribute to enhanced sensitivity of radiotherapy and chemotherapy.
  • This novel drug will bring a new breakthrough in the field of the development of anticancer drugs and reveal the alternative clinical use of HBOCs in tumor treatment.
  • [MeSH-major] Antineoplastic Agents / metabolism. Blood Substitutes / chemistry. Blood Substitutes / metabolism. Hemoglobins / chemistry. Hemoglobins / metabolism. Neoplasms / drug therapy. Neoplasms / radiotherapy. Oxygen / metabolism

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  • (PMID = 19548133.001).
  • [ISSN] 1532-4184
  • [Journal-full-title] Artificial cells, blood substitutes, and immobilization biotechnology
  • [ISO-abbreviation] Artif Cells Blood Substit Immobil Biotechnol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Blood Substitutes; 0 / Hemoglobins; S88TT14065 / Oxygen
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35. Murray MM, Mullan PB, Harkin DP: Role played by BRCA1 in transcriptional regulation in response to therapy. Biochem Soc Trans; 2007 Nov;35(Pt 5):1342-6
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  • [Title] Role played by BRCA1 in transcriptional regulation in response to therapy.
  • BRCA1 (breast-cancer susceptibility gene 1) is a tumour suppressor, implicated in the hereditary predisposition to breast and ovarian cancer.
  • BRCA1 has been implicated in a number of cellular processes including DNA repair and recombination, cell cycle checkpoint control, chromatin remodelling and ubiquitination.
  • In addition, substantial data now exist to suggest a role for BRCA1 in transcriptional regulation; BRCA1 has been shown to interact with the Pol II holoenzyme complex and to interact with multiple transcription factors, such as p53 and c-Myc.
  • We have previously identified a range of BRCA1 transcriptional targets and have linked these to specific cellular pathways, including cell cycle checkpoint activation and apoptosis.
  • Current research is focused on the transcriptional mechanisms that underpin the association of BRCA1 deficiency with increased sensitivity to DNA damage-based chemotherapy and resistance to spindle poisons.
  • [MeSH-major] Breast Neoplasms / therapy. Genes, BRCA1. Transcription, Genetic / genetics
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. DNA Damage. DNA Repair. Genes, cdc. Humans. Spindle Apparatus / drug effects

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  • (PMID = 17956347.001).
  • [ISSN] 0300-5127
  • [Journal-full-title] Biochemical Society transactions
  • [ISO-abbreviation] Biochem. Soc. Trans.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0200103
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 39
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36. Patel MB, Feinstein AJ, Saenz AD, Majetschak M, Proctor KG: Prehospital HBOC-201 after traumatic brain injury and hemorrhagic shock in swine. J Trauma; 2006 Jul;61(1):46-56
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  • [Title] Prehospital HBOC-201 after traumatic brain injury and hemorrhagic shock in swine.
  • This study evaluates neurotoxicity, vasoactivity, cardiac toxicity, and inflammatory activity of HBOC-201 (Biopure, Cambridge, Mass.) resuscitation in a TBI model.
  • After 30 minutes, resuscitation was initiated with 10 mL/kg normal saline (NS), followed by either HBOC-201 (6 mL/kg, n = 10) or NS control (n = 10).
  • The control group received mannitol (1 g/kg) and blood (10 mL/kg) at 90 minutes and half (n = 5) received CPP directed phenylephrine (PE) therapy after 120 minutes.
  • RESULTS: With HBOC administration, MAP, CPP, and brain tissue PO2 were restored within 30 minutes and maintained until 300 minutes.
  • In contrast, with control, MAP and brain tissue PO2 did not correct until 120 minutes, after mannitol, transfusion and 40% more crystalloid.
  • CONCLUSIONS: After TBI, a single HBOC-201 bolus with minimal supplements provided rapid resuscitation, while maintaining CPP and improving brain oxygenation, without causing cardiac dysfunction, coagulopathy, cytokine release, or brain structural changes.
  • [MeSH-major] Blood Substitutes / toxicity. Brain Injuries / therapy. Fluid Therapy / methods. Hemoglobins / toxicity. Shock, Hemorrhagic / therapy
  • [MeSH-minor] Analysis of Variance. Animals. Blood Coagulation / drug effects. Brain / drug effects. Brain / pathology. Cerebrovascular Circulation / drug effects. Cytokines / blood. Drug-Related Side Effects and Adverse Reactions. Female. Hemodynamics / drug effects. Male. Swine

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  • (PMID = 16832248.001).
  • [ISSN] 0022-5282
  • [Journal-full-title] The Journal of trauma
  • [ISO-abbreviation] J Trauma
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM08749-01
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Cytokines; 0 / HBOC 201; 0 / Hemoglobins
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37. Habler O, Pape A, Meier J, Zwissler B: [Artificial oxygen carriers as an alternative to red blood cell transfusion]. Anaesthesist; 2005 Aug;54(8):741-54
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  • The expected cost-explosion in transfusion medicine (increasing imbalance between donors and recipients, treatment of transfusion-associated complications) increases the socio-economic significance of the development of safe and effective synthetic oxygen carriers as an alternative to the transfusion of allogeneic red blood cells.
  • Currently two types of artificial oxygen carriers have been tested for safety and efficacy in cases of severe anemia otherwise requiring transfusion.
  • Solutions based on human or bovine hemoglobin (HBOC) possess vasoconstrictor properties in addition to their oxygen transport capacity.
  • The impact of vasoconstriction on tissue perfusion and organ function is however not yet fully understood.
  • Nevertheless, in 2001 the bovine HBOC Hemopure was approved in South Africa for treatment of acutely anemic surgical patients.
  • Although reduction of perioperative allogeneic blood transfusion has already been demonstrated for HBOC and PFC, the global clinical establishment of artificial oxygen carriers is not to be expected in the near future.
  • [MeSH-major] Blood Substitutes / therapeutic use. Blood Transfusion
  • [MeSH-minor] Animals. Cattle. Emulsions. Fluorocarbons / therapeutic use. Humans. Perioperative Care. Shock, Hemorrhagic / drug therapy

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  • (PMID = 16021390.001).
  • [ISSN] 0003-2417
  • [Journal-full-title] Der Anaesthesist
  • [ISO-abbreviation] Anaesthesist
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Emulsions; 0 / Fluorocarbons
  • [Number-of-references] 99
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38. Roukos DH, Briasoulis E: Individualized preventive and therapeutic management of hereditary breast ovarian cancer syndrome. Nat Clin Pract Oncol; 2007 Oct;4(10):578-90
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  • [Title] Individualized preventive and therapeutic management of hereditary breast ovarian cancer syndrome.
  • Life-saving, risk-reducing medical interventions are required for women with a BRCA1/2 mutation.
  • Genetic counseling should be offered at specialized familial breast-cancer clinics and gene-mutation analysis should be recommended on the basis of personal and family-history-based risk criteria.
  • Tamoxifen is an alternative approach only for BRCA2 mutation carriers.
  • The comprehensive, clinical decision-making Ioannina algorithm provided here can facilitate the complex preventive strategic approach.
  • Newly diagnosed BRCA1/2 carriers might benefit from extensive surgery and a specific pharmacological treatment, but data to support this strategy are limited.
  • Microarray gene-expression studies show that breast tumors from BRCA1 carriers are predominantly of basal subtype (i.e. triple negative) and BRCA2 carriers are of luminal subtype (i.e. estrogen-receptor-positive).
  • Although optimum management of women with familial susceptibility to breast and ovarian cancer has not yet been prospectively validated, data indicate substantial benefits when an individualized evidence-based prevention strategy is provided by an experienced team.
  • [MeSH-major] Breast Neoplasms / genetics. Genetic Predisposition to Disease. Neoplastic Syndromes, Hereditary / prevention & control. Ovarian Neoplasms / genetics
  • [MeSH-minor] Female. Genes, BRCA1. Genes, BRCA2. Genetic Counseling. Genetic Testing. Humans. Mastectomy. Ovariectomy. Tamoxifen / therapeutic use


39. Levy JH: The use of haemoglobin glutamer-250 (HBOC-201) as an oxygen bridge in patients with acute anaemia associated with surgical blood loss. Expert Opin Biol Ther; 2003 Jun;3(3):509-17
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  • [Title] The use of haemoglobin glutamer-250 (HBOC-201) as an oxygen bridge in patients with acute anaemia associated with surgical blood loss.
  • For the treatment of substantial blood loss in surgery, allogeneic blood is transfused to maintain stability and organ perfusion and function.
  • Multi-centre, randomised, Phase III, controlled trials have demonstrated the safety and efficacy of haemoglobin glutamer-250 (bovine) (Hemopure), Biopure Corporation, Cambridge, MA, USA), also known as HBOC-201.
  • HBOC-201 is bovine-derived, modified haemoglobin that has been ultrapurified to remove any plasma proteins, RBC stroma and potential pathogenic material.
  • During the manufacturing process, crosslinking and polymerisation stabilise the haemoglobin molecule, which increases its vascular persistence as well as the efficiency of oxygen transport to tissue.
  • Results from clinical trials indicate that HBOC-201 can be used as an oxygen 'bridge' for patients experiencing anaemia due to surgical blood loss, until their own red blood cells are replenished or have regenerated (haematinic effect).
  • HBOC-201 is generally well-tolerated and is approved for use in South Africa, where it is indicated for use in adult surgical patients who are acutely anaemic, and is used to eliminate, delay or reduce the need for allogeneic RBCs.
  • A Biologics License Application for HBOC-201 is currently under review by the US FDA.
  • [MeSH-major] Anemia / drug therapy. Blood Loss, Surgical. Blood Substitutes / therapeutic use. Oxygen Consumption / drug effects
  • [MeSH-minor] Acute Disease. Animals. Anoxia / blood. Anoxia / drug therapy. Hemoglobins. Humans. Postoperative Complications / blood. Postoperative Complications / prevention & control

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  • [ErratumIn] Expert Opin Biol Ther. 2003 Sep;3(6):1017
  • (PMID = 12783619.001).
  • [ISSN] 1471-2598
  • [Journal-full-title] Expert opinion on biological therapy
  • [ISO-abbreviation] Expert Opin Biol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / HBOC 201; 0 / Hemoglobins
  • [Number-of-references] 40
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40. Trainer AH, Lewis CR, Tucker K, Meiser B, Friedlander M, Ward RL: The role of BRCA mutation testing in determining breast cancer therapy. Nat Rev Clin Oncol; 2010 Dec;7(12):708-17
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  • [Title] The role of BRCA mutation testing in determining breast cancer therapy.
  • Landmark discoveries in the field of breast cancer research include the identification of germline BRCA mutations as a cause of hereditary disease, and the use of gene-expression profiling to identify distinct subtypes of breast cancer.
  • These findings, coupled with the availability of rapid germline testing, make it possible to identify a BRCA mutation carrier contemporaneous with a diagnosis of breast cancer.
  • For the first time, testing for a germline mutation that predisposes to cancer has the potential to influence the immediate surgical, radiotherapeutic, and drug treatment choices of an individual with a new diagnosis of breast cancer.
  • In this Review, we examine the implications of moving germline BRCA mutation testing from highly specialized family cancer clinics to mainstream settings.
  • [MeSH-major] Breast Neoplasms / genetics. Genes, BRCA1. Genes, BRCA2. Genetic Testing. Germ-Line Mutation. Neoplastic Syndromes, Hereditary / genetics
  • [MeSH-minor] Adult. Age of Onset. Case Management. Ethnic Groups / genetics. Female. Gene Expression Profiling. Genes, Dominant. Genetic Counseling. Genetic Predisposition to Disease. Humans. Mastectomy / psychology. Neoplasm Proteins / analysis. Neoplasm Proteins / genetics. Neoplasms, Second Primary / epidemiology. Neoplasms, Second Primary / prevention & control. Ovarian Neoplasms / epidemiology. Ovarian Neoplasms / genetics. Precision Medicine. Prognosis. Risk

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  • (PMID = 21060331.001).
  • [ISSN] 1759-4782
  • [Journal-full-title] Nature reviews. Clinical oncology
  • [ISO-abbreviation] Nat Rev Clin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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41. Beiner ME, Finch A, Rosen B, Lubinski J, Moller P, Ghadirian P, Lynch HT, Friedman E, Sun P, Narod SA, Hereditary Ovarian Cancer Clinical Study Group: The risk of endometrial cancer in women with BRCA1 and BRCA2 mutations. A prospective study. Gynecol Oncol; 2007 Jan;104(1):7-10
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  • [Title] The risk of endometrial cancer in women with BRCA1 and BRCA2 mutations. A prospective study.
  • OBJECTIVE: To evaluate the risk of endometrial cancer in women who carry a deleterious mutation in the BRCA1 or BRCA2 genes.
  • PATIENTS AND METHODS: Women known to carry a BRCA1 or BRCA2 mutation, aged 45 to 70, were identified from an international registry and were followed prospectively.
  • Study subjects were followed until diagnosis of endometrial cancer, ovarian cancer, death or the date of completion of the last questionnaire.
  • RESULTS: After an average follow-up period of 3.3 years, six women were diagnosed with endometrial cancer, compared to 1.13 cancers expected (SIR=5.3, p=0.0011).
  • The risk among women who were never exposed to tamoxifen treatment was not significantly elevated (SIR=2.7, p=0.17), but among the 226 participants who had used tamoxifen (220 as treatment and six for the primary prevention of breast cancer) the relative risk for endometrial cancer was 11.6 (p=0.0004).
  • CONCLUSION: The main contributor to the increased risk of endometrial cancer among BRCA carriers is tamoxifen treatment for a previous breast cancer.
  • The risk and benefits of prophylactic hysterectomy should be discussed with women with a BRCA mutation considering tamoxifen therapy.
  • [MeSH-major] Endometrial Neoplasms / genetics. Genes, BRCA1. Genes, BRCA2. Germ-Line Mutation
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents, Hormonal / adverse effects. Breast Neoplasms / drug therapy. Female. Follow-Up Studies. Humans. Middle Aged. Prospective Studies. Tamoxifen / adverse effects


42. Goldman M, O'Hair K: Women's health, breast health: a review of the gynecologic effects of breast cancer. Obstet Gynecol Surv; 2009 Jul;64(7):469-80; quiz 499
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  • [Title] Women's health, breast health: a review of the gynecologic effects of breast cancer.
  • Breast cancer is very common and seen in both premenopausal and postmenopausal women.
  • Research into prevention, better screening, and more effective treatments is occurring continually, and changes are translated into clinical practice relatively quickly.
  • It is important for women's health care providers to have an understanding of breast cancer treatments and the gynecologic side effects.
  • For premenopausal women interested in fertility, options should be discussed prior to chemotherapy.
  • Issues pertaining to pregnancy after breast cancer should be discussed in a multidisciplinary fashion, involving the obstetrician/gynecologist, breast surgeon, and oncologist.
  • Ovarian suppression is often used as part of breast cancer treatment in premenopausal women with hormone positive disease, and menopausal symptoms may be severe.
  • Hormonal therapies including tamoxifen and the aromatase inhibitors are used in the treatment of hormone positive breast cancers.
  • Each of these drugs has a variety of gynecologic implications.
  • Understanding the options for treatment for menopausal complaints in breast cancer patients is important for women's health providers.
  • Although most breast cancers are sporadic, a small percentage will be due to mutations in the BRCA genes.
  • It is important for women's health providers to take an appropriate family history and refer to genetic counselors for possible testing when hereditary cancer is suspected.
  • This review focuses on the various women's health issues pertaining to breast cancer and treatment.
  • [MeSH-major] Breast Neoplasms / complications. Genital Diseases, Female / etiology. Pregnancy Complications, Neoplastic / etiology

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  • (PMID = 19545455.001).
  • [ISSN] 1533-9866
  • [Journal-full-title] Obstetrical & gynecological survey
  • [ISO-abbreviation] Obstet Gynecol Surv
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 125
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43. Ganz PA: Breast cancer, menopause, and long-term survivorship: critical issues for the 21st century. Am J Med; 2005 Dec 19;118 Suppl 12B:136-41
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Breast cancer, menopause, and long-term survivorship: critical issues for the 21st century.
  • Breast cancer accounts for 33% of all incident cancers in women in North America, and there are an estimated >2 million breast cancer survivors in the United States today.
  • Ovarian hormones are intimately involved in the initiation and promotion of breast cancer development, with targeted endocrine therapies being the most widely used as anticancer treatment.
  • It is not surprising that these treatments frequently cause persistent menopausal symptoms in breast cancer survivors.
  • In addition, adjuvant chemotherapy often induces premature menopause in younger patients with breast cancer.
  • Some women at high risk for the development of breast cancer (e.g., precancerous breast disease, carriers of deleterious hereditary predisposition genes) experience vasomotor symptoms as a result of tamoxifen therapy or preventive oophorectomy.
  • Clinical management of menopausal symptoms in these settings is complicated by the relative prohibition of hormonal therapies and the fact that breast cancer-directed therapies often exacerbate these menopausal symptoms.
  • [MeSH-major] Breast Neoplasms. Menopause / physiology. Survivors
  • [MeSH-minor] Antineoplastic Agents / adverse effects. Female. Humans. Menopause, Premature. Primary Ovarian Insufficiency / chemically induced. Primary Ovarian Insufficiency / drug therapy. Risk


44. Caswell JE, Strange MB, Rimmer DM 3rd, Gibson MF, Cole P, Lefer DJ: A novel hemoglobin-based blood substitute protects against myocardial reperfusion injury. Am J Physiol Heart Circ Physiol; 2005 Apr;288(4):H1796-801
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  • HBOC-201 (Biopure; Cambridge, MA) is a glutaraldehyde-polymerized bovine hemoglobin (Hb) solution that is stroma free, has lower viscosity than blood, and promotes O(2) unloading.
  • We investigated the effects of HBOC-201 in a canine model of myocardial ischemia-reperfusion injury.
  • HBOC-201 or 0.9% saline vehicle equivalent to 10% total blood volume was infused 30 min before myocardial ischemia.
  • In addition, myocardial blood flow (as measured by radioactive microspheres) in the ischemic zone was similar between the vehicle and HBOC-201 groups.
  • HBOC-201-infused dogs demonstrated a significant (P < 0.01) 56% reduction in Inf/AAR.
  • Analysis of blood samples taken at 4 h of reperfusion showed a significant (P < 0.05) reduction in creatine kinase MB isoform for the HBOC-201 group.
  • Histological analysis of the myocardium demonstrated significant (P < 0.01) reductions in neutrophil infiltration in the HBOC-201 group.
  • These data indicate that treatment with HBOC-201 before myocardial ischemia-reperfusion reduces the extent of myocardial inflammation and ischemia-reperfusion injury in the canine myocardium.
  • [MeSH-major] Blood Substitutes / pharmacology. Hemoglobins / pharmacology. Myocardial Reperfusion Injury / drug therapy
  • [MeSH-minor] Animals. Blood Pressure. Coronary Circulation / drug effects. Creatine Kinase / metabolism. Creatine Kinase, MB Form. Dogs. Female. Heart Rate. Isoenzymes / metabolism. Leukocyte Count. Male. Myocardial Infarction / drug therapy. Myocardial Infarction / pathology. Neutrophils / cytology. Platelet Count. Ventricular Pressure

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  • (PMID = 15772335.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P01 DK 43785; United States / NHLBI NIH HHS / HL / R01 HL 60849
  • [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 / Blood Substitutes; 0 / HBOC 201; 0 / Hemoglobins; 0 / Isoenzymes; EC 2.7.3.2 / Creatine Kinase; EC 2.7.3.2 / Creatine Kinase, MB Form
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