Dr. Malvika  Sagar  Md image

Dr. Malvika Sagar Md

1 Medical Ctr Blvd Pob 1, Suite 402
Chester PA 19013
610 476-6680
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #: MT-192448
NPI: 1164660304
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Nonaccidental trauma presenting with respiratory distress and pleural effusion. - Pediatric emergency care
Nonaccidental trauma (NAT) is common and presents with varied symptoms. Pleural effusion as a complication of physical abuse has not been described in the past. We report the case of a 10-week-old infant who presented with multiple nonspecific complaints that included respiratory distress, refusal to feed, constipation, and lethargy. Sepsis was the working diagnosis on admission, but a massive pleural effusion and rib fractures seen on chest imaging ultimately led to the diagnosis of nonaccidental trauma. This interesting case highlights the importance of maintaining a high index of suspicion for abuse irrespective of atypical presenting signs.
HER receptor signaling confers resistance to the insulin-like growth factor-I receptor inhibitor, BMS-536924. - Molecular cancer therapeutics
We have reported previously the activity of the insulin-like growth factor-I (IGF-IR)/insulin receptor (InsR) inhibitor, BMS-554417, in breast and ovarian cancer cell lines. Further studies indicated treatment of OV202 ovarian cancer cells with BMS-554417 increased phosphorylation of HER-2. In addition, treatment with the pan-HER inhibitor, BMS-599626, resulted in increased phosphorylation of IGF-IR, suggesting a reciprocal cross-talk mechanism. In a panel of five ovarian cancer cell lines, simultaneous treatment with the IGF-IR/InsR inhibitor, BMS-536924 and BMS-599626, resulted in a synergistic antiproliferative effect. Furthermore, combination therapy decreased AKT and extracellular signal-regulated kinase activation and increased biochemical and nuclear morphologic changes consistent with apoptosis compared with either agent alone. In response to treatment with BMS-536924, increased expression and activation of various members of the HER family of receptors were seen in all five ovarian cancer cell lines, suggesting that inhibition of IGF-IR/InsR results in adaptive up-regulation of the HER pathway. Using MCF-7 breast cancer cell variants that overexpressed HER-1 or HER-2, we then tested the hypothesis that HER receptor expression is sufficient to confer resistance to IGF-IR-targeted therapy. In the presence of activating ligands epidermal growth factor or heregulin, respectively, MCF-7 cells expressing HER-1 or HER-2 were resistant to BMS-536924 as determined in a proliferation and clonogenic assay. These data suggested that simultaneous treatment with inhibitors of the IGF-I and HER family of receptors may be an effective strategy for clinical investigations of IGF-IR inhibitors in breast and ovarian cancer and that targeting HER-1 and HER-2 may overcome clinical resistance to IGF-IR inhibitors.

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1 Medical Ctr Blvd Pob 1, Suite 402 Chester, PA 19013
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