29,863 research outputs found

    Targeted therapy for breast cancer prevention.

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    With a better understanding of the etiology of breast cancer, molecularly targeted drugs have been developed and are being testing for the treatment and prevention of breast cancer. Targeted drugs that inhibit the estrogen receptor (ER) or estrogen-activated pathways include the selective ER modulators (tamoxifen, raloxifene, and lasofoxifene) and aromatase inhibitors (AIs) (anastrozole, letrozole, and exemestane) have been tested in preclinical and clinical studies. Tamoxifen and raloxifene have been shown to reduce the risk of breast cancer and promising results of AIs in breast cancer trials, suggest that AIs might be even more effective in the prevention of ER-positive breast cancer. However, these agents only prevent ER-positive breast cancer. Therefore, current research is focused on identifying preventive therapies for other forms of breast cancer such as human epidermal growth factor receptor 2 (HER2)-positive and triple-negative breast cancer (TNBC, breast cancer that does express ER, progesterone receptor, or HER2). HER2-positive breast cancers are currently treated with anti-HER2 therapies including trastuzumab and lapatinib, and preclinical and clinical studies are now being conducted to test these drugs for the prevention of HER2-positive breast cancers. Several promising agents currently being tested in cancer prevention trials for the prevention of TNBC include poly(ADP-ribose) polymerase inhibitors, vitamin D, and rexinoids, both of which activate nuclear hormone receptors (the vitamin D and retinoid X receptors). This review discusses currently used breast cancer preventive drugs, and describes the progress of research striving to identify and develop more effective preventive agents for all forms of breast cancer

    The effects of menopausal vasomotor symptoms and changes in anthropometry on breast cancer etiology

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    One of the strongest predictors of breast cancer risk is mammographic density; however, incomplete understanding of the mechanisms relating density to risk has limited its use as a marker for breast cancer susceptibility. Hormone fluctuations during the menopausal transition may influence declines in mammographic density and may also trigger the onset of menopausal vasomotor symptoms (VMS), which have been associated with lower breast cancer risk. The effects of hormone changes on density, VMS, and breast cancer risk are complicated by external factors such as changing body mass and hormone therapy use during the menopausal transition. We evaluated the association between change in BMI and change in mammographic density using volumetric measurement methods. We found that an annual increase in BMI was associated with a decrease in absolute dense volume and percent dense volume. Longitudinal studies of density and breast cancer, or those using density to reflect breast cancer risk, should consider controlling for BMI gain/loss to understand the independent relationship between density and risk. We further investigated the association of VMS and percent mammographic density. We observed no overall association, but found some evidence of an inverse relationship among perimenopausal women and those using hormone therapies. This suggests that an association between VMS and breast cancer risk is not strongly mediated by changes in breast density. Finally, we evaluated VMS and incident breast cancer risk. VMS were associated with a 38% reduction in risk. Adjustment for endogenous hormone levels did not alter our results, suggesting that endogenous hormones play a lesser role in the association between VMS and breast cancer risk than previously hypothesized. These studies further our understanding of breast cancer etiology. If confirmed, the association between VMS and breast cancer risk could propose VMS as an easily measured factor that could enhance risk prediction. Our findings that this association is not strongly mediated through breast density nor endogenous hormone levels raise provocative questions regarding the mechanisms that link VMS to breast cancer risk. Extending our knowledge of breast cancer etiology through new measurement methods and risk factors may lead to improved risk prediction and opportunities for disease prevention

    Diagnosis and treatment of paraneoplastic neurological disorders

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    In about two thirds of cases, patients with paraneoplastic neurological disorders present to the neurologist without a known tumor. Due to the ongoing immune response, this tumor tends to stay biologically relatively benign, and therefore difficult to diagnose. In patients with a known tumor, the neurological symptoms often precede a tumor recurrence. In both scenarios, anti-neuronal antibodies are an invaluable diagnostic help to the clinician, and may be supplemented by other diagnostic tests such as MRI, CSF, and electrophysiology. Tumor therapy remains the mainstay of therapeutic options, although early immune therapy must be started in parallel. It is hoped that the recent fundamental advances in understanding the autoimmune pathology of these disorders, especially the role of cytotoxic T cells, will eventually lead to more effective treatment options

    Molecular Genetics of Metastatic Breast Cancer

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    Breast cancer is the most common form of cancer in women. Breast cancer has a heterogeneous etiology. Genetic and environmental factors contribute to the pathogenesis and progression of breast cancer. Various genes as proliferation and nuclear factors have been identified in breast cancer. Therefore, the genetic component of patients is important in determining disease behavior, response to anticancer therapeutics, and patient survival. Prognosis of breast cancer is associated with potential metastatic properties of primary breast tumors. Metastasis is the leading cause of death in patients with breast cancer. Therefore, it is important to understand the mechanisms underlying the development of distant metastases to specific regions and has clinical value. Metastasis shows an organ-specific spread pattern and occurs with a series of complex and multistep events associated with each other, such as angiogenesis, invasion, migration-motility, extravasation, and proliferation. Breast cancer often metastasizes to the bone, liver, brain, and lungs. Metastasis may develop years after successful primary treatment. The metastatic process will become clear, as information about molecules and genes associated with metastases increases, and this is extremely important for cancer treatment