What causes cancer? Reports from sixth-grade girls.

Background: We evaluated students' perception of cancer causation among sixth-grade girls living in Wisconsin.

Method: We asked female students to list up to 3 causes of cancer in a cross-sectional health survey.

Results: A total of 141 answers were given by 53 students.

The identification of senescence-specific genes during the induction of senescence in prostate cancer cells.

Classic mechanisms of tumor response to chemotherapy include apoptosis and mitotic catastrophe. Recent studies have suggested that cellular senescence, a terminal proliferation arrest seen in vitro, may be invoked during the exposure of cancer cells to chemotherapeutic agents. To identify markers associated specifically with the cellular senescence phenotype, we utilized expression data from cDNA microarray experiments identifying transcripts whose expression levels increased as human prostate epithelial cells progressed to senescence.

Medullary thyroid cancer: the functions of raf-1 and human achaete-scute homologue-1.

Medullary thyroid cancer (MTC) is a prototypic neuroendocrine tumor of the thyroid C cells. Other than surgery, there are no curative therapies for MTC. In this review, we detail recent studies that suggest that targeting specific signaling pathways may be a viable strategy to control MTC tumor progression.

The role of human achaete-scute homolog-1 in medullary thyroid cancer cells.

Background: Human achaete-scute homolog-1 (hASH1) is a transcription factor that is expressed highly in neuroendocrine tumors such as medullary thyroid cancer (MTC). Thyroid C-cells do not develop in hASH1 knockout mice, which suggests that hASH1 is essential for normal C-cell development.

Methods: To determine the effect of raf-1 induction on hASH1 and hormone production, we used an estrogen inducible raf-1 construct in MTC cell line (TT) cells (TT-raf cells).

Preclinical and clinical development of immunocytokines.

Advances in preclinical and clinical development have demonstrated that monoclonal antibodies and immuno-activating cytokines have a beneficial role in certain clinical oncology settings. Genetic engineering has now been used to create 'immunocytokines (ICs)'. These are fusion proteins that consist of an immune-activating cytokine linked to a tumor-reactive monoclonal antibody.

The effects of tamoxifen on the vaginal epithelium in postmenopausal women.

Although increased vaginal discharge occurs with treatment, clinicians often presume the effects of tamoxifen on the vaginal epithelium are antiestrogenic. We studied 16 postmenopausal women before they began tamoxifen treatment, at 6 months, and then at annual intervals for up to 6 years. Vaginal scrapings for cytology smears and maturation values (MV) for these were performed.

Structure of the human glutamate-L-cysteine ligase catalytic (GLCLC) subunit gene.

Glutamate-L-cysteine ligase (GLCL [EC 6.3.2.

Symptoms associated with oophorectomy and tamoxifen treatment for breast cancer in premenopausal Vietnamese women.

There are very few data about the efficacy and toxicity of adjuvant systemic therapies for breast cancer in non-western populations. In 1993 in Vietnam we began a randomized controlled clinical trial on premenopausal women with operable breast cancer comparing adjuvant surgical oophorectomy plus tamoxifen with observation and this same combined hormonal treatment on recurrence. We evaluated the symptoms reported at regular follow-up visits by the first 482 premenopausal women entered in this clinical trial and treated with surgical oophorectomy plus tamoxifen or observation.

Induction of apoptosis in MCF-7:WS8 breast cancer cells by beta-lapachone.

Beta-lapachone (beta-lap) affects a number of enzymes in vitro, including type I topoisomerase (Topo I); however, its exact intracellular target(s) and mechanism of cell killing remain unknown. We compared the cytotoxic responses of MCF-7:WS8 (MCF-7) human breast cancer cells after 4-h pulses of beta-lap or camptothecin (CPT), a known Topo I poison. A direct correlation between loss of survival and apoptosis was seen after beta-lap treatment (LD50 = 2.