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Biomedical subjects

Gerald M Higa

Publications and source records attributed to Gerald M Higa.

8 recordsLinked to original sources
PubMed2006

5-Hydroxyindoleacetic acid and substance P profiles in patients receiving emetogenic chemotherapy.

BACKGROUND: Even though direct cause and effect has not been proved, clinical evidence suggests serotonin and substance P (SP) are involved in the emetic response following chemotherapy. Because of several parallels, we hypothesized that SP release, like serotonin, may be propagated by chemotherapy and both substances can be measured in biological fluids, and correlated with a particular phase of emesis. METHODS: Urinary 5-hydroxyindoleacetic acid (5-HIAA) was assessed by HPLC; serum and urine SP were measured by immunoassay. In addition to construction of neurotransmitter profiles, all SP data were grouped according to cisplatin dosages, = or >75 mg/m(2) versus <75 mg/m(2), and phase of emesis, acute versus delayed. Analyses of these data were performed by repeated measures analysis of variance. RESULTS: Samples were collected over a 72-hour period from 26 adult patients who received cisplatin- (n = 13) or non-cisplatin-containing (n = 13) chemotherapy. Mean baseline 5-HIAA: creatinine ratios were 5.23 and 5.16 in females and males, respectively; mean baseline SP levels were 392 and 181 pg/mL in females and males, respectively. Comparisons between SP data stratified by cisplatin dosage and emetic phase were significantly different, P < 0.0001. CONCLUSIONS: Laboratory studies provide additional evidence that serotonin and SP are involved primarily, though not exclusively, in acute and delayed vomiting, respectively.

Adult↗
PubMed2005

Actinic keratosis and capecitabine therapy.

Topical application of 5-fluorouracil (5-FU) is one of the most effective clinical strategies available to treat actinic keratosis (AK). During treatment, an apparent toxic skin reaction occurs before dermal quiescence ensues. We report a case of a typical flare of AK in a woman treated with capecitabine for advanced breast cancer.

Aged↗
PubMed2004

Targeted therapies in oncology: in the crosshairs or at the crossroads?

Normal cellular behavior depends on functional integration of extracellular stimuli with intracellular signal transduction pathways. Coupling cell surface message reception to nuclear gene expression is no longer a linear model constructed with molecular components acting merely as conduits to relay signals that cascade toward the nucleus. What has emerged instead is a highly integrated circuit comprised of numerous molecular components harmoniously programmed to communicate a multitude of internal signals that controls cellular response. Despite increasing understanding of cell signaling, mutinous elements embedded in these pathways have defied complete resolution. Research indicates that propagation of signals emanating from the extracellular environment to the cell nucleus follows a complex internal circuit equipped with sophisticated molecular components that provide rigid control over a variety of cellular responses. Although increasing understanding of genetic aberrations and signaling pathway transgressions can lead to novel strategies for targeting cancer cells, the disappointing results from clinical trials suggest that the occult processes responsible for neoplastic transformation remain largely unexplained.

Antineoplastic Agents↗
PubMed2004

Signaling multiplex of the epidermal growth factor receptor.

Cells must be able to not only internalize extracellular signals, but also decipher these messages that ultimately result in a variety of cell-specific outcomes. Physiologically, transmembrane receptor tyrosine kinases play an important role in normal development. Pathologically, these receptors are implicated in deregulation of growth displayed by cancer cells. Over the past 30 years, the mechanistic understanding of cell signaling through receptor tyrosine kinases has become quite sophisticated. This review focuses primarily on the epidermal growth factor receptor and cetuximab, the only monoclonal antibody approved for targeting this receptor.

Antibodies, Monoclonal↗
PubMed2002

Exemestane: treatment of breast cancer with selective inactivation of aromatase.

The mechanism of action, pharmacology, and clinical efficacy and safety of exemestane in the treatment of metastatic breast cancer are reviewed. Endocrine strategies that deprive tumor cells of estrogens are effective therapeutic modalities for patients with hormone-dependent breast cancer. The efficacy and toxicities associated with tamoxifen and aminoglutethimide have contributed to the development of agents that selectively target aromatase, the enzyme responsible for conversion of androgens to estrogens. Exemestane, an orally active irreversible inhibitor of aromatase, was recently approved as second-line endocrine therapy of advanced hormone-sensitive postmenopausal breast cancer. Compared with megestrol acetate in patients with disease progressing on tamoxifen, a number of clinical endpoints, including a survival advantage, were significantly better in the exemestane-treated group. Preliminary data also indicate that cross-resistance is incomplete between exemestane and the reversible aromatase inhibitors. Even though suppression of aromatase activity is quantitatively similar regardless of the interactive mechanism between drug and enzyme, clinically relevant differences may become apparent with further application of these two types of aromatase inhibitors. Exemestane is effective as a second- or third-line treatment of advanced, estrogen-receptor positive breast cancer in postmenopausal patients.

Androstadienes↗