Cancer Bone Metastases (cancer + bone_metastase)

Distribution by Scientific Domains
Medical Sciences50%

Kinds of Cancer Bone Metastases

  • prostate cancer bone metastase
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    Selected Abstracts

    Usefulness of single photon emission computed tomography imaging in the detection of lumbar vertebral metastases from prostate cancer

    INTERNATIONAL JOURNAL OF UROLOGY, Issue 6 2008
    Tetsuo Nozaki
    Objective: To determine whether single photon emission computed tomography (SPECT) is useful in the detection of prostate cancer bone metastases in the lumbar vertebrae. Methods: Thirty-nine patients (12 with benign prostatic hyperplasia, 27 with prostate cancer) were considered and submitted to bone SPECT. All of them had increased uptake in lumbar vertebrae on bone scintigraphy. In those with prostate cancer, definitive diagnosis of bone metastases was established by magnetic resonance imaging (MRI). SPECT axial images were classified into five accumulation patterns: mosaic, large hot, diffuse, peripheral, and articular (or pediculate). Sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of bone SPECT were calculated. Results: Overall, 116 vertebral lesions (49 metastatic, 67 degenerative) were studied. Mosaic, large hot and diffuse patterns were more frequently associated with metastatic lesions (84.2%, 70.3%, and 63.1% of the cases, respectively). On the other hand, peripheral and articular (or pediculate) patterns were mostly ascribed to degenerative lesions (100% and 87.5% of the cases, respectively). Sensitivity, specificity, PPV and NPV of bone SPECT were 95.9% (47/49), 73.1% (49/67), 72.3% (47/65), and 96.1% (49/51), respectively. Conclusions: Bone SPECT provides better accuracy than bone scintigraphy in differential diagnosis of lumbar vertebral lesions from prostate cancer. [source]

    A paradigm for the treatment of prostate cancer bone metastases based on an understanding of tumor cell,microenvironment interactions

    JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2005
    Robert D. Loberg
    Abstract The pliability of cancer cells to mutate into several different phenotypes in an attempt to find one that will survive and colonize at the metastatic site is a tremendous "hurdle" to overcome in designing novel cancer therapeutics. New targets of therapy are essential if we are to effectively overcome the evasiveness of cancer. The interaction between the tumor cell and the surrounding microenvironment creates a vicious cycle that perpetuates disease survival and progression. The future of cancer therapy resides in the ability to focus on the recruited and exploited relationships of the cancer cell with the host environment. These therapies target cancer cell growth early and interrupt the vicious cycle that is created by the tumor cells interacting with bone components by inhibiting osteoclasts, osteoblasts, stromal cells, and endothelial cells. They alter the bone microenvironment, creating a hostile "soil" that prevents the "seed" from developing into bone metastases and represent a potential new platform for the development of prostate cancer therapeutics. © 2005 Wiley-Liss, Inc. [source]

    A Bayesian hierarchical mixture model for platelet-derived growth factor receptor phosphorylation to improve estimation of progression-free survival in prostate cancer

    JOURNAL OF THE ROYAL STATISTICAL SOCIETY: SERIES C (APPLIED STATISTICS), Issue 1 2010
    Satoshi Morita
    Summary., Advances in understanding the biological underpinnings of many cancers have led increasingly to the use of molecularly targeted anticancer therapies. Because the platelet-derived growth factor receptor (PDGFR) has been implicated in the progression of prostate cancer bone metastases, it is of great interest to examine possible relationships between PDGFR inhibition and therapeutic outcomes. We analyse the association between change in activated PDGFR (phosphorylated PDGFR) and progression-free survival time based on large within-patient samples of cell-specific phosphorylated PDGFR values taken before and after treatment from each of 88 prostate cancer patients. To utilize these paired samples as covariate data in a regression model for progression-free survival time, and be cause the phosphorylated PDGFR distributions are bimodal, we first employ a Bayesian hierarchical mixture model to obtain a deconvolution of the pretreatment and post-treatment within-patient phosphorylated PDGFR distributions. We evaluate fits of the mixture model and a non-mixture model that ignores the bimodality by using a supnorm metric to compare the empirical distribution of each phosphorylated PDGFR data set with the corresponding fitted distribution under each model. Our results show that first using the mixture model to account for the bimodality of the within-patient phosphorylated PDGFR distributions, and then using the posterior within-patient component mean changes in phosphorylated PDGFR so obtained as covariates in the regression model for progression-free survival time, provides an improved estimation. [source]

    Pathogenesis of osteoblastic bone metastases from prostate cancer,

    CANCER, Issue 6 2010
    Toni Ibrahim MD
    Abstract Prostate cancer is the second leading cause of cancer-related death in men. A typical feature of this disease is its ability to metastasize to bone. It is mainly osteosclerotic, and is caused by a relative excess of osteoblast activity, leading to an abnormal bone formation. Bone metastases are the result of a complex series of steps that are not yet fully understood and depend on dynamic crosstalk between metastatic cancer cells, cellular components of the bone marrow microenvironment, and bone matrix (osteoblasts and osteoclasts). Prostate cancer cells from primary tissue undergo an epithelial-mesenchymal transition to disseminate and acquire a bone-like phenotype to metastasize in bone tissue. This review discusses the biological processes and the molecules involved in the progression of bone metastases. Here we focus on the routes of osteoblast differentiation and activation, the crosstalk between bone cells and tumor cells, and the molecules involved in these processes that are expressed by both osteoblasts and tumor cells. Furthermore, this review deals with the recently elucidated role of osteoclasts in prostate cancer bone metastases. Certainly, to better understand the underlying mechanisms of bone metastasis and so improve targeted bone therapies, further studies are warranted to shed light on the probable role of the premetastatic niche and the involvement of cancer stem cells. Cancer 2010. © 2010 American Cancer Society. [source]