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  1. Article ; Online: Gabapentin toxicity in patients with chronic kidney disease: a preventable cause of morbidity.

    Zand, Ladan / McKian, Kevin P / Qian, Qi

    The American journal of medicine

    2010  Volume 123, Issue 4, Page(s) 367–373

    Abstract: ... mL and 58.8+/-10.22 microL/mL, respectively) than in group I (5.52+/-0.32 microL/mL, P<.01). Toxicity ...

    Abstract Background: Gabapentin is frequently used as an analgesic in patients with chronic kidney disease. Although gabapentin is well known for its favorable pharmacokinetics, it is exclusively eliminated renally, and patients with chronic kidney disease are at risk for toxicity. Existing literature on such risk is lacking.
    Methods: We examined the Mayo Clinic Rochester database from 1998 to 2007 in patients with serum gabapentin measurements and known medical outcomes. A total of 729 patients were stratified according to their estimated glomerular filtration rate: group I, 126 individuals with estimated glomerular filtration greater than 90 mL/min/1.72 mm(2) [corrected]

    group II, 594 individuals with estimated glomerular filtration less than 90 mL/min/1.72 mm(2) [corrected] without dialysis; group III, 9 individuals with chronic dialysis.
    Results: Patients in groups II and III had higher serum gabapentin levels (8.39+/-0.32 microL/mL and 58.8+/-10.22 microL/mL, respectively) than in group I (5.52+/-0.32 microL/mL, P<.01). Toxicity occurred exclusively in groups II (5.56%) and III (77.8%); toxic manifestations were more severe in group III than in group II. Elderly individuals with multiple comorbidities were overrepresented in those with toxic manifestations. Gabapentin toxicity was suspected initially in only 41.5% of symptomatic cases.
    Conclusion: Gabapentin toxicity in patients with chronic kidney disease is underrecognized. Patients with chronic kidney disease often receive inappropriately high gabapentin dosage for their kidney function, occasioning overt toxicity; advanced age and comorbidity predispose these patients for toxicity. Heightened awareness of such preventable risk, amid the chronic kidney disease epidemic, would be cost-effective and improve healthcare quality.
    MeSH term(s) Adult ; Age Distribution ; Amines/adverse effects ; Amines/blood ; Amines/therapeutic use ; Anticonvulsants/adverse effects ; Anticonvulsants/blood ; Anticonvulsants/therapeutic use ; Cyclohexanecarboxylic Acids/adverse effects ; Cyclohexanecarboxylic Acids/blood ; Cyclohexanecarboxylic Acids/therapeutic use ; Female ; Glomerular Filtration Rate ; Humans ; Kidney Failure, Chronic/complications ; Male ; Middle Aged ; Renal Dialysis ; Retrospective Studies ; gamma-Aminobutyric Acid/adverse effects ; gamma-Aminobutyric Acid/blood ; gamma-Aminobutyric Acid/therapeutic use
    Chemical Substances Amines ; Anticonvulsants ; Cyclohexanecarboxylic Acids ; gamma-Aminobutyric Acid (56-12-2) ; gabapentin (6CW7F3G59X)
    Language English
    Publishing date 2010-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80015-6
    ISSN 1555-7162 ; 1873-2178 ; 0002-9343 ; 1548-2766
    ISSN (online) 1555-7162 ; 1873-2178
    ISSN 0002-9343 ; 1548-2766
    DOI 10.1016/j.amjmed.2009.09.030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cixutumumab.

    McKian, Kevin P / Haluska, Paul

    Expert opinion on investigational drugs

    2009  Volume 18, Issue 7, Page(s) 1025–1033

    Abstract: The IGF pathway plays a major role in cancer cell proliferation, survival and resistance to antineoplastic therapies in many human malignancies. As such, interference with this pathway is the target of many investigational pharmacologic agents. ... ...

    Abstract The IGF pathway plays a major role in cancer cell proliferation, survival and resistance to antineoplastic therapies in many human malignancies. As such, interference with this pathway is the target of many investigational pharmacologic agents. Cixutumumab, a monoclonal antibody to IGF-1R, utilizes this concept. In this review, we summarize preclinical, pharmacologic and early clinical data regarding this agent and discuss the impact this drug might have on the future treatment of human cancers.
    MeSH term(s) Animals ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Clinical Trials as Topic/methods ; Humans ; Neoplasms/immunology ; Neoplasms/therapy ; Receptor, IGF Type 1/immunology ; Signal Transduction/immunology
    Chemical Substances Antibodies, Monoclonal ; Antineoplastic Agents ; Receptor, IGF Type 1 (EC 2.7.10.1)
    Language English
    Publishing date 2009-06-23
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1182884-5
    ISSN 1744-7658 ; 0967-8298 ; 1354-3784
    ISSN (online) 1744-7658
    ISSN 0967-8298 ; 1354-3784
    DOI 10.1517/13543780903055049
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Novel breast tissue feature strongly associated with risk of breast cancer.

    McKian, Kevin P / Reynolds, Carol A / Visscher, Daniel W / Nassar, Aziza / Radisky, Derek C / Vierkant, Robert A / Degnim, Amy C / Boughey, Judy C / Ghosh, Karthik / Anderson, Stephanie S / Minot, Douglas / Caudill, Jill L / Vachon, Celine M / Frost, Marlene H / Pankratz, V Shane / Hartmann, Lynn C

    Journal of clinical oncology : official journal of the American Society of Clinical Oncology

    2009  Volume 27, Issue 35, Page(s) 5893–5898

    Abstract: ... a step-wise increase in breast cancer risk with increasing numbers of acini per lobule (P = .0004 ... of breast cancer (P = .03). We examined the individual accuracy of these measures using the concordance (c ...

    Abstract Purpose: Accurate, individualized risk prediction for breast cancer is lacking. Tissue-based features may help to stratify women into different risk levels. Breast lobules are the anatomic sites of origin of breast cancer. As women age, these lobular structures should regress, which results in reduced breast cancer risk. However, this does not occur in all women.
    Methods: We have quantified the extent of lobule regression on a benign breast biopsy in 85 patients who developed breast cancer and 142 age-matched controls from the Mayo Benign Breast Disease Cohort, by determining number of acini per lobule and lobular area. We also calculated Gail model 5-year predicted risks for these women.
    Results: There is a step-wise increase in breast cancer risk with increasing numbers of acini per lobule (P = .0004). Adjusting for Gail model score, parity, histology, and family history did not attenuate this association. Lobular area was similarly associated with risk. The Gail model estimates were associated with risk of breast cancer (P = .03). We examined the individual accuracy of these measures using the concordance (c) statistic. The Gail model c statistic was 0.60 (95% CI, 0.50 to 0.70); the acinar count c statistic was 0.65 (95% CI, 0.54 to 0.75). Combining acinar count and lobular area, the c statistic was 0.68 (95% CI, 0.58 to 0.78). Adding the Gail model to these measures did not improve the c statistic.
    Conclusion: Novel, tissue-based features that reflect the status of a woman's normal breast lobules are associated with breast cancer risk. These features may offer a novel strategy for risk prediction.
    MeSH term(s) Adult ; Age Factors ; Biopsy ; Breast/pathology ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Case-Control Studies ; Cell Proliferation ; Female ; Genetic Predisposition to Disease ; Humans ; Hyperplasia ; Logistic Models ; Middle Aged ; Parity ; Pedigree ; Precancerous Conditions/genetics ; Precancerous Conditions/pathology ; Predictive Value of Tests ; Pregnancy ; Reproducibility of Results ; Risk Assessment ; Risk Factors ; Time Factors
    Language English
    Publishing date 2009-10-05
    Publishing country United States
    Document 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.
    ZDB-ID 604914-x
    ISSN 1527-7755 ; 0732-183X
    ISSN (online) 1527-7755
    ISSN 0732-183X
    DOI 10.1200/JCO.2008.21.5079
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Structure-function relationships of the raloxifene-estrogen receptor-alpha complex for regulating transforming growth factor-alpha expression in breast cancer cells.

    Liu, Hong / Park, Woo-Chan / Bentrem, David J / McKian, Kevin P / Reyes, Alexander De Los / Loweth, Jessica A / Schafer, Jennifer MacGregor / Zapf, James W / Jordan, V Craig

    The Journal of biological chemistry

    2001  Volume 277, Issue 11, Page(s) 9189–9198

    Abstract: Amino acid Asp-351 in the ligand binding domain of estrogen receptor alpha (ERalpha) plays an important role in regulating the estrogen-like activity of selective estrogen receptor modulator-ERalpha complexes. 4-Hydroxytamoxifen is a full agonist at a ... ...

    Abstract Amino acid Asp-351 in the ligand binding domain of estrogen receptor alpha (ERalpha) plays an important role in regulating the estrogen-like activity of selective estrogen receptor modulator-ERalpha complexes. 4-Hydroxytamoxifen is a full agonist at a transforming growth factor alpha target gene in situ in MDA-MB-231 human breast cancer cells stably transfected with the wild-type ERalpha. In contrast, raloxifene (Ral), which is also a selective estrogen receptor modulator, is a complete antiestrogen in this system. Because D351G ERalpha allosterically silences activation function-1 activity in the 4-hydroxytamoxifen-ERalpha complex with the complete loss of estrogen-like activity, we examined the converse interaction of amino acid 351 and the piperidine ring of the antiestrogen side chain of raloxifene to enhance estrogen-like action. MDA-MB-231 cells were either transiently or stably transfected with Asp-351 (the wild type), D351E, D351Y, or D351F ERalpha expression vectors. Profound differences in the agonist and antagonist actions of Ralcenter dotERalpha complexes were noted only in stable transfectants. The agonist activity of the Ralcenter dotERalpha complex was enhanced with D351E and D351Y ERalpha, but raloxifene lost its agonist activity with D351F ERalpha. The distance between the piperidine nitrogen of raloxifene and the negative charge of amino acid 351 was critical for estrogen-like actions. The role of the piperidine ring in neutralizing Asp-351 was addressed using compound R1h, a raloxifene derivative replacing the nitrogen on its piperidine ring with a carbon to form cyclohexane. The derivative was a potent agonist with wild type ERalpha. These results support the concept that the side chain of raloxifene shields and neutralizes the Asp-351 to produce an antiestrogenic ERalpha complex. Alteration of either the side chain or its relationship with the negative charge at amino acid 351 controls the estrogen-like action at activating function 2b of the selective estrogen receptor modulator ERalpha complex.
    MeSH term(s) Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Estrogen Antagonists/pharmacology ; Estrogen Receptor alpha ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Nuclear Receptor Coactivator 2 ; Proteins/genetics ; Raloxifene Hydrochloride/chemistry ; Raloxifene Hydrochloride/pharmacology ; Receptors, Estrogen/analysis ; Receptors, Estrogen/drug effects ; Receptors, Estrogen/physiology ; Selective Estrogen Receptor Modulators/pharmacology ; Structure-Activity Relationship ; Tamoxifen/analogs & derivatives ; Tamoxifen/pharmacology ; Transcription Factors/analysis ; Transfection ; Transforming Growth Factor alpha/genetics ; Trefoil Factor-1 ; Tumor Cells, Cultured ; Tumor Suppressor Proteins
    Chemical Substances Estrogen Antagonists ; Estrogen Receptor alpha ; Nuclear Receptor Coactivator 2 ; Proteins ; Receptors, Estrogen ; Selective Estrogen Receptor Modulators ; TFF1 protein, human ; Transcription Factors ; Transforming Growth Factor alpha ; Trefoil Factor-1 ; Tumor Suppressor Proteins ; Tamoxifen (094ZI81Y45) ; afimoxifene (17197F0KYM) ; Raloxifene Hydrochloride (4F86W47BR6)
    Language English
    Publishing date 2001-12-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M108335200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Apoptotic action of 17beta-estradiol in raloxifene-resistant MCF-7 cells in vitro and in vivo.

    Liu, Hong / Lee, Eun-Sook / Gajdos, Csaba / Pearce, Sandra Timm / Chen, Bin / Osipo, Clodia / Loweth, Jessica / McKian, Kevin / De Los Reyes, Alexander / Wing, Laura / Jordan, V Craig

    Journal of the National Cancer Institute

    2003  Volume 95, Issue 21, Page(s) 1586–1597

    Abstract: ... cells (0.8 U, 95% CI = 0.4 to 1.1 U; P =.004). When cultured with 1 microM raloxifene, MCF-7/Ral cells ... grew statistically significantly (P<.001) faster than MCF-7 cells. Estradiol treatment of MCF-7/Ral ... 2 to 0.3 U; P<.001), increased expression of Fas protein and mRNA (4.5-fold, 95% CI = 2.8- to 6.3 ...

    Abstract Background: Resistance to tamoxifen, a selective estrogen receptor modulator (SERM), involves changes that prevent apoptosis and enhance cell proliferation and survival. Paradoxically, estrogen treatment inhibits the growth of long-term tamoxifen-treated breast tumors. Because of the increasing use of raloxifene, another SERM, to prevent osteoporosis and potentially reduce breast cancer risk, some women will develop raloxifene-resistant breast cancer. We developed a raloxifene-resistant MCF-7 cell model (MCF-7/Ral) and investigated the nature of raloxifene-resistant breast cancer and its response to estradiol.
    Methods: Raloxifene resistance and hormone responsiveness were assessed by proliferation assays and cell cycle analysis in parental MCF-7 and MCF-7/Ral cells. Nuclear factor kappaB (NF-kappaB) activity was investigated with a transient transfection assay. Apoptosis was investigated by annexin V staining, mRNA was measured by real-time polymerase chain reaction, and protein was measured by western blotting. Tumorigenesis was studied by injecting MCF-7 or MCF-7/Ral cells into ovariectomized athymic mice (10 per group) and monitoring tumor size weekly. All statistical tests were two-sided.
    Results: Basal NF-kappaB activity was higher in MCF-7/Ral cells (1.6 U, 95% confidence interval [CI] = 1.2 to 2.0 U) than in MCF-7 cells (0.8 U, 95% CI = 0.4 to 1.1 U; P =.004). When cultured with 1 microM raloxifene, MCF-7/Ral cells grew statistically significantly (P<.001) faster than MCF-7 cells. Estradiol treatment of MCF-7/Ral cells arrested cells in G(2)/M phase of the cell cycle, decreased NF-kappaB activity (0.2 U, 95% CI = 0.2 to 0.3 U; P<.001), increased expression of Fas protein and mRNA (4.5-fold, 95% CI = 2.8- to 6.3-fold versus 0.5-fold, 95% CI = 0.3- to 0.8-fold for control treatment; P<.001), and induced apoptosis. Treatment with either raloxifene or tamoxifen stimulated MCF-7/Ral tumor growth, suggesting that such tumors were resistant to both drugs. When a 9-week raloxifene or tamoxifen treatment was followed by a 5-week estradiol treatment, estradiol statistically significantly reduced the size of tumors stimulated by raloxifene or tamoxifen (at week 14, P =.004 for raloxifene and P<.001 for tamoxifen).
    Conclusions: Growth of raloxifene-resistant MCF-7/Ral cells in vitro and in vivo is repressed by estradiol treatment by a mechanism involving G2/M-phase arrest, decreased NF-kappaB activity, and increased Fas expression to induce apoptosis.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Blotting, Western ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Drug Resistance, Neoplasm ; Estradiol/pharmacology ; Female ; Humans ; Mice ; Mice, Nude ; NF-kappa B/analysis ; Ovariectomy ; Polymerase Chain Reaction/methods ; RNA, Messenger/analysis ; RNA, Neoplasm/analysis ; Raloxifene Hydrochloride/pharmacology ; Selective Estrogen Receptor Modulators/pharmacology
    Chemical Substances Antineoplastic Agents ; NF-kappa B ; RNA, Messenger ; RNA, Neoplasm ; Selective Estrogen Receptor Modulators ; Raloxifene Hydrochloride (4F86W47BR6) ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2003-07-11
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2992-0
    ISSN 1460-2105 ; 0027-8874 ; 0198-0157
    ISSN (online) 1460-2105
    ISSN 0027-8874 ; 0198-0157
    DOI 10.1093/jnci/djg080
    Database MEDical Literature Analysis and Retrieval System OnLINE

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