Search tips
Search criteria

Results 1-5 (5)

Clipboard (0)

Select a Filter Below

Year of Publication
Document Types
1.  The Development of a Minority Recruitment Plan for Cancer Clinical Trials 
Cancer does not occur in all ethnic and racial groups at similar rates. In addition, responses to treatment also vary in certain ethnic and racial groups. For Hispanics, the overall cancer incidence is generally lower yet for some specific tumor types, the incidence rates are higher compared to other populations.
Although disparities are recognized for treatment outcomes and prevention methodologies for Hispanics and other minority populations, specific recruiting and reporting of minorities remains a challenge. In order to circumvent this problem, the Cancer Therapy and Research Center (CTRC) has developed a new minority recruitment plan for all cancer related clinical trials at this Institute. The overall goal of this initiative is to increase the accrual of minorities in cancer clinical trials by implementing several key interventions.
The Cancer Therapy & Research Center (CTRC) at the University of Texas Health Science Center at San Antonio established the Clinical Trials Accrual Task Force to develop and monitor interventions designed to increase accrual to cancer clinical trials, specifically the accrual of minorities with a focus on the Hispanic population that makes up 68% of the CTRC's catchment area.
A Minority Accrual Plan (MAP) was implemented in March 2013 as part of the process for initiating and conducting cancer-related clinical trials at the CTRC. The Minority Accrual Plan focuses on Hispanic enrollment due to the characteristics of the South Texas population served by the CTRC but could be easily adapted to other populations.
The CTRC has designed a process to prospectively address the challenge of deliberately enrolling minority subjects and accurately accounting for the results by implementing a Minority Accrual Plan for every cancer-related clinical trial at CTRC.
PMCID: PMC4141778  PMID: 25152846
Minority; Disparities; Cancer; Clinical trials enrollment; Barriers; Accrual
2.  Temporal Changes in the Clinical Approach to Diagnosing Prostate Cancer 
The diagnosis and detection of prostate cancer has undergone profound changes over the past three decades, due primarily to the development and widespread clinical use of prostate-specific antigen (PSA) testing. These changes have led to substantial differences in the prostate cancer phenotype. It is important to understand these changes to develop appropriate treatment options for contemporarily diagnosed prostate cancer. We explored a group of four temporal changes in prostate cancer detection that occurred after the advent of PSA testing. Through changes in the use of PSA testing, performance of prostate biopsy, application of PSA testing in different age groups, and pathologic tumor grading, a significant increase in detection of potentially inconsequential prostate cancers has occurred. The prostate cancer of 2011 is generally a smaller, lower-grade tumor and more often observed in younger men. These changes in detection will allow for increased use of active surveillance for prostate cancer.
PMCID: PMC3540883  PMID: 23271768
3.  TGF-β promotion of Gli2-induced expression of parathyroid hormone-related protein, an important osteolytic factor in bone metastasis, is independent of canonical Hedgehog signaling 
Cancer research  2010;71(3):822-831.
Breast cancer frequently metastasizes to bone, where tumor cells receive signals from the bone marrow microenvironment. One relevant factor is TGF-β, which up regulates expression of the Hedgehog (Hh) signaling molecule Gli2 which in turn increases secretion of important osteolytic factors such as parathyroid hormone-related protein (PTHrP). PTHrP inhibition can prevent tumor-induced bone destruction, whereas Gli2 over expression in tumor cells can promote osteolysis. In this study, we tested the hypothesis that Hh inhibition in bone metastatic breast cancer would decrease PTHrP expression and therefore osteolytic bone destruction. However, when mice engrafted with human MDA-231 breast cancer cells were treated with the Hh receptor antagonist cyclopamine, we observed no effect on tumor burden or bone destruction. In vitro analyses revealed that osteolytic tumor cells lack expression of the Hh receptor, Smoothened, suggesting an Hh-independent mechanism of Gli2 regulation. Blocking Gli signaling in metastatic breast cancer cells with a Gli2-Repressor gene (Gli2-Rep) reduced endogenous and TGF-β-stimulated PTHrP mRNA expression, but did not alter tumor cell proliferation. Furthermore, mice inoculated with Gli2-Rep-expressing cells exhibited a decrease in osteolysis, suggesting that Gli2 inhibition may block TGF-β propagation of a vicious osteolytic cycle in this MDA-231 model of bone metastasis. Accordingly, in the absence of TGF-β signaling, Gli2 expression was down regulated in cells, whereas enforced over expression ofGli2 restored PTHrP activity. Taken together, our findings suggest that Gli2 is required for TGF-β to stimulate PTHrP expression, and that blocking Hh-independent Gli2 activity will inhibit tumor-induced bone destruction.
PMCID: PMC3077118  PMID: 21189326
Gli; PTHrP; Osteolysis; Breast cancer; Hedgehog; Cyclopamine; Bone Metastasis
4.  Caspase-2 Deficiency Enhances Aging-Related Traits in Mice 
Alteration of apoptotic activity has been observed in a number of tissues in aging mammals, but it remains unclear whether and/or how apoptosis may affect aging. Caspase-2 is a member of the cysteine protease family that plays a critical role in apoptosis. To understand the impact of compromised apoptosis function on mammalian aging, we conducted a comparative study on caspase-2 deficient mice and their wild-type littermates with a specific focus on the aging-related traits at advanced ages. We found that caspase-2 deficiency enhanced a number of traits commonly seen in premature aging animals. Loss of caspase-2 was associated with shortened maximum lifespan, impaired hair growth, increased bone loss, and reduced body fat content. In addition, we found that the livers of caspase-2 deficient mice had higher levels of oxidized proteins than those of age-matched wild-type mice, suggesting that caspase-2 deficiency compromised the animal's ability to clear oxidatively damaged cells. Collectively, these results suggest that caspase-2 deficiency affects aging in the mice. This study thus demonstrates for the first time that disruption of a key apoptotic gene has a significant impact on aging.
PMCID: PMC1828128  PMID: 17188333
caspase-2; maximum lifespan; bone; hair growth; fat
5.  The role of bisphosphonates in breast cancer: Actions of bisphosphonates in animal models of breast cancer 
Breast Cancer Research  2001;4(1):35-41.
The skeleton is the most common site of breast cancer metastases. These bone metastases are usually osteolytic and cause significant morbidity. Bisphosphonates, potent inhibitors of bone resorption, reduce skeletal morbidity in breast cancer patients with bone metastases. Animal studies with bisphosphonates are crucial to understanding the mechanisms by which these compounds affect bone and tumor cells in vivo. Such animal models of breast cancer that are used to test the efficacy of bisphosphonates are discussed. These studies may offer insight into the treatment of other tumor types that frequently metastasize to bone.
PMCID: PMC138714  PMID: 11879558
animal models; bisphosphonate; breast cancer; metastases; skeletal metastases

Results 1-5 (5)