Management of advanced prostate cancer

Kaliks, Rafael Aliosha; Giglio, Auro del

doi:10.1590/s0104-42302008000200025

Cited by 10 publications

(7 citation statements)

References 22 publications

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“…It often develops in patients over the age of 50. This type of cancer is subject to metastasis, particularly in the bones and lymph nodes [61]. "Colorectal cancer" was also retrieved by DAVID [36,37].…”

Section: Resultsmentioning

confidence: 99%

Meta-analysis of archived DNA microarrays identifies genes regulated by hypoxia and involved in a metastatic phenotype in cancer cells

et al. 2010

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BackgroundMetastasis is a major cancer-related cause of death. Recent studies have described metastasis pathways. However, the exact contribution of each pathway remains unclear. Another key feature of a tumor is the presence of hypoxic areas caused by a lack of oxygen at the center of the tumor. Hypoxia leads to the expression of pro-metastatic genes as well as the repression of anti-metastatic genes. As many Affymetrix datasets about metastasis and hypoxia are publicly available and not fully exploited, this study proposes to re-analyze these datasets to extract new information about the metastatic phenotype induced by hypoxia in different cancer cell lines.MethodsAffymetrix datasets about metastasis and/or hypoxia were downloaded from GEO and ArrayExpress. AffyProbeMiner and GCRMA packages were used for pre-processing and the Window Welch t test was used for processing. Three approaches of meta-analysis were eventually used for the selection of genes of interest.ResultsThree complementary approaches were used, that eventually selected 183 genes of interest. Out of these 183 genes, 99, among which the well known JUNB, FOS and TP63, have already been described in the literature to be involved in cancer. Moreover, 39 genes of those, such as SERPINE1 and MMP7, are known to regulate metastasis. Twenty-one genes including VEGFA and ID2 have also been described to be involved in the response to hypoxia. Lastly, DAVID classified those 183 genes in 24 different pathways, among which 8 are directly related to cancer while 5 others are related to proliferation and cell motility. A negative control composed of 183 random genes failed to provide such results. Interestingly, 6 pathways retrieved by DAVID with the 183 genes of interest concern pathogen recognition and phagocytosis.ConclusionThe proposed methodology was able to find genes actually known to be involved in cancer, metastasis and hypoxia and, thus, we propose that the other genes selected based on the same methodology are of prime interest in the metastatic phenotype induced by hypoxia.

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Section: Resultsmentioning

confidence: 99%

Meta-analysis of archived DNA microarrays identifies genes regulated by hypoxia and involved in a metastatic phenotype in cancer cells

et al. 2010

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“…Hormone therapy is the standard treatment for advanced prostate cancer [6,14]. Nonetheless, the timing of hormonal treatment in advanced prostate cancer remains controversial [6].…”

Section: Discussionmentioning

confidence: 99%

Clinical Significance of Free-to-Total Prostate-Specific Antigen (PSA) Ratio in Advanced Prostate Cancer Patients with PSA Less than 0.1 ng/ml after Hormone Treatment

2012

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PurposeWe analyzed the pattern of change in the free-to-total prostate-specific antigen (f/t PSA) ratio and the progression to castration-resistant prostate cancer (CRPC) in patients with advanced prostate cancer who received hormone treatment and whose PSA nadir was below 0.1 ng/ml.Materials and MethodsWe retrospectively analyzed the medical records of 52 patients with advanced prostate cancer. All patients were treated with maximum androgen blockade (gonadotrophin-releasing hormone agonist and anti-androgen agents). The patients were divided into two groups: those with a nadir f/t PSA ratio above 60% and those with a nadir f/t PSA ratio of 60% or below. Age, initial PSA, clinical stage, lymph node metastasis, bone metastasis, and follow-up data, including PSA, free PSA, and f/t PSA ratio, were collected. The Mann-Whitney U-test, Fisher exact test, chi-square test, Kaplan-Meier survival analysis, and log rank test were used.ResultsThere were 24 patients in the group with a nadir f/t PSA ratio above 60% and 28 patients in the group with a nadir f/t PSA ratio of 60% or below. After hormone therapy, the median f/t PSA ratio in each group increased from 37% and 34% at 3 months to 75% and 60% at 6 months, respectively. At 9 months, however, the f/t PSA ratio increased to 80% in the group with a nadir f/t PSA ratio above 60%, whereas it decreased to 31% in the group with a nadir f/t PSA ratio of 60% or below. From 9 to 15 months, the f/t PSA ratio showed a tendency to decrease (75 to 37% and 27 to 20%, respectively). The progression to CRPC was significantly different between the two groups (10 vs. 24).ConclusionsProgression to CRPC was significantly higher in the group with a lower f/t PSA ratio. Additionally, the pattern of change in the f/t PSA ratio was significantly different after 9 months. Collectively, the f/t PSA ratio can be used as an additional marker for prognosis of hormone treatment.

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“…Unfortunately, despite the effectivity of such procedures during the initial period, PCa eventually progresses to the androgen-independent stage and resists additional androgen withdrawal [14]. It is known that hormoneindependent PCa cells are only modestly sensitive to chemotherapy and to radiation therapy [15]. No curative and durable therapeutic methods are available for AI and metastatic PCa.…”

Section: Discussionmentioning

confidence: 99%

The radiation response of androgen-refractory prostate cancer cell line C4-2 derived from androgen-sensitive cell line LNCaP

Xie¹,

Zhang²,

Lan³

et al. 2010

Asian J Androl

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Radiation therapy is a relatively effective therapeutic method for localized prostate cancer (PCa) patients. However, radioresistance occurs in nearly 30% of patients treated with potentially curative doses. Therapeutic synergy between radiotherapy and androgen ablation treatment provides a promising strategy for improving the clinical outcome. Accordingly, the androgen deprivation-induced signaling pathway may also mediate radiosensitivity in PCa cells. The C4-2 cell line was derived from the androgen-sensitive LNCaP parent line under androgen-depleted condition and had acquired androgen-refractory characteristics. In our study, the response to radiation was evaluated in both LNCaP and C4-2. Results showed that C4-2 cells were more likely to survive from irradiation and appeared more aggressive in their resistance to radiation treatment compared with LNCaP, as measured by clonogenic assays and cell viability and cell cycle analyses. Gene expression analyses revealed that a set of genes involved in cell cycle arrest and DNA repair were differentially regulated in LNCaP and C4-2 in response to radiation, which was also consistent with the radiation-resistant property observed in C4-2 cells. These results strongly suggested that the radiation-resistant property may develop with progression of PCa to androgen-independent status. Not only can the LNCaP and C4-2 PCa progression model be applied for investigating androgen-refractory progression, but it can also be used to explore the development of radiation resistance in PCa.

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Management of advanced prostate cancer

Cited by 10 publications

References 22 publications

Meta-analysis of archived DNA microarrays identifies genes regulated by hypoxia and involved in a metastatic phenotype in cancer cells

Meta-analysis of archived DNA microarrays identifies genes regulated by hypoxia and involved in a metastatic phenotype in cancer cells

Clinical Significance of Free-to-Total Prostate-Specific Antigen (PSA) Ratio in Advanced Prostate Cancer Patients with PSA Less than 0.1 ng/ml after Hormone Treatment

The radiation response of androgen-refractory prostate cancer cell line C4-2 derived from androgen-sensitive cell line LNCaP

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