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T Browder

Publications and source records attributed to T Browder.

15 recordsLinked to original sources
PubMed2001

Computed tomographic scan can be used for surgical decision making in zone II penetrating neck injuries.

BACKGROUND: Controversy surrounds the evaluation of zone II penetrating neck injuries. Current literature supports mandatory exploration or selective management. Computed tomographic (CT) scanning provides high-resolution images that are used for trauma in other body regions. The purpose of this study is to prospectively evaluate the utility of CT scanning in the evaluation of zone II penetrating neck injuries. METHODS: From July 1998 to November 1999, 14 stable patients were studied who sustained zone II penetrating neck injuries. All patients had a physical examination, infusion CT scan of the neck, and an operative exploration. Before surgery, the trauma surgeon evaluated the CT scan and interpreted it as demonstrating either "high" or "low" probability for significant injury. Surgical findings were compared with the surgeon's preoperative interpretation of the CT scan. RESULTS: Three of 14 patients had five significant injuries. All these patients had high probability of injury CT scans, with four of the five injuries specifically diagnosed by CT scan. Sensitivity, specificity, positive predictive value, and negative predictive value were 100%, 91%, 75%, and 100% (p < 0.02), respectively. CONCLUSION: This small prospective study demonstrates that zone II penetrating neck injuries can be accurately evaluated by CT scan. In addition, the CT scan can be used for surgical decision making. This will eliminate the need for mandatory exploration and limit the role of angiography, esophagography, and endoscopy in zone II penetrating neck injuries.

Adult↗
PubMed2001

Angiogenesis research: guidelines for translation to clinical application.

Angiogenesis research is being translated to the clinic. Certain guidelines may facilitate this effort. Recruitment of endothelial cells by a tumor is an early event in angiogenesis, a process regulated at genetic and epigenetic levels. The microvascular endothelial cell has become an important second target in cancer therapy. Angiogenesis inhibitors are either "direct" or "indirect" and their optimal dosing depends on a different logic than conventional chemotherapy. Conversely, antiangiogenic scheduling of chemotherapy can by-pass drug resistance. Like all solid tumors, hematologic malignancies are angiogenesis-dependent. Further, angiogenesis is modulated by proteins and cells from the hematopoietic and hemostatic systems. Clinical testing of angiogenesis inhibitors has accentuated the need for surrogate markers of tumor angiogenesis activity. Microvessel density, so valuable as a prognostic indicator of metastatic risk, cannot determine efficacy of an angiogenesis inhibitor. In the future, angiogenesis inhibitors may be added to chemotherapy or to radiotherapy, or to other modalities. Also, combinations of angiogenesis inhibitors may be administered together.

Angiogenesis Inhibitors↗
PubMed2000

Antiangiogenic scheduling of chemotherapy improves efficacy against experimental drug-resistant cancer.

To reveal the antiangiogenic capability of cancer chemotherapy, we developed an alternative antiangiogenic schedule for administration of cyclophosphamide. We show here that this antiangiogenic schedule avoided drug resistance and eradicated Lewis lung carcinoma and L1210 leukemia, an outcome not possible with the conventional schedule. When Lewis lung carcinoma and EMT-6 breast cancer were made drug resistant before therapy, the antiangiogenic schedule suppressed tumor growth 3-fold more effectively than the conventional schedule. When another angiogenesis inhibitor, TNP-470, was added to the antiangiogenic schedule of cyclophosphamide, drug-resistant Lewis lung carcinomas were eradicated. Each dose of the antiangiogenic schedule of cyclophosphamide induced the apoptosis of endothelial cells within tumors, and endothelial cell apoptosis preceded the apoptosis of drug-resistant tumor cells. This antiangiogenic effect was more pronounced in p53-null mice in which the apoptosis of p53-null endothelial cells induced by cyclophosphamide was so vigorous that drug-resistant tumors comprising 4.5% of body weight were eradicated. Thus, by using a dosing schedule of cyclophosphamide that provided more sustained apoptosis of endothelial cells within the vascular bed of a tumor, we show that a chemotherapeutic agent can more effectively control tumor growth in mice, regardless of whether the tumor cells are drug resistant.

Animals↗
PubMed1997

Antiangiogenic therapy of experimental cancer does not induce acquired drug resistance.

Acquired drug resistance is a major problem in the treatment of cancer. Of the more than 500,000 annual deaths from cancer in the United States, many follow the development of resistance to chemotherapy. The emergence of resistance depends in part on the genetic instability, heterogeneity and high mutational rate of tumour cells. In contrast, endothelial cells are genetically stable, homogeneous and have a low mutational rate. Therefore, antiangiogenic therapy directed against a tumour's endothelial cells should, in principle, induce little or no drug resistance. Endostatin, a potent angiogenesis inhibitor, was administered to mice bearing Lewis lung carcinoma, T241 fibrosarcoma or B16F10 melanoma. Treatment was stopped when tumours had regressed. Tumours were then allowed to re-grow and endostatin therapy was resumed. After 6, 4 or 2 treatment cycles, respectively, no tumours recurred after discontinuation of therapy. These experiments show that drug resistance does not develop in three tumour types treated with a potent angiogenesis inhibitor. An unexpected finding is that repeated cycles of antiangiogenic therapy are followed by prolonged tumour dormancy without further therapy.

Animals↗