Gene-modified bone marrow cell therapy for prostate cancer

Wang, H; Thompson, Timothy C.

doi:10.1038/gt.2008.37

Cited by 6 publications

(4 citation statements)

References 116 publications

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“…Unfortunately, very little information is available in the literature regarding bone marrow cell therapy that targets metastatic prostate cancer. Wang and Thompson, 2008 summarized the importance of developing gene-modified bone marrow cell therapy for advanced prostate cancer [ 120 ]. A previous study has demonstrated that IL-12-gene-modified bone marrow cell therapy suppressed the development of experimental prostate cancer metastasis in a preclinical mouse model [ 121 ].…”

Section: Bone Marrow Cell Therapy For Metastatic Prostate Cancermentioning

confidence: 99%

Bone Health Management in the Continuum of Prostate Cancer Disease

Boopathi

Birbe

Shoyele

et al. 2022

Cancers

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Prostate cancer (PCa) is the second-leading cause of cancer-related deaths in men. PCa cells require androgen receptor (AR) signaling for their growth and survival. Androgen deprivation therapy (ADT) is the preferred treatment for patients with locally advanced and metastatic PCa disease. Despite their initial response to androgen blockade, most patients eventually will develop metastatic castration-resistant prostate cancer (mCRPC). Bone metastases are common in men with mCRPC, occurring in 30% of patients within 2 years of castration resistance and in >90% of patients over the course of the disease. Patients with mCRPC-induced bone metastasis develop lesions throughout their skeleton; the 5-year survival rate for these patients is 47%. Bone-metastasis-induced early changes in the bone that proceed the osteoblastic response in the bone matrix are monitored and detected via modern magnetic resonance and PET/CT imaging technologies. Various treatment options, such as targeting osteolytic metastasis with bisphosphonates, prednisone, dexamethasone, denosumab, immunotherapy, external beam radiation therapy, radiopharmaceuticals, surgery, and pain medications are employed to treat prostate-cancer-induced bone metastasis and manage bone health. However, these diagnostics and treatment options are not very accurate nor efficient enough to treat bone metastases and manage bone health. In this review, we present the pathogenesis of PCa-induced bone metastasis, its deleterious impacts on vital organs, the impact of metastatic PCa on bone health, treatment interventions for bone metastasis and management of bone- and skeletal-related events, and possible current and future therapeutic options for bone management in the continuum of prostate cancer disease.

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Section: Bone Marrow Cell Therapy For Metastatic Prostate Cancermentioning

confidence: 99%

Bone Health Management in the Continuum of Prostate Cancer Disease

Boopathi

Birbe

Shoyele

et al. 2022

Cancers

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“…13,14 Alternative approaches have been tested, including gene-modified cell-therapy approaches that focus on the delivery of therapeutic genes to the PCa, such as interleukin 12 (IL-12) gene-modified macrophage therapy. 15 The results of that study demonstrated suppression of tumor growth and spontaneous lung metastasis, induction of systemic antitumor immune response, and prolongation of survival in mouse orthotopic models of metastatic PCa.…”

Section: Introductionmentioning

confidence: 99%

Tumor growth and metastasis suppression by Glipr1 gene-modified macrophages in a metastatic prostate cancer model

et al. 2011

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We previously identified the mouse and human Glipr1 and GLIPR1/RTVP-1 (respectively) genes as direct p53 targets with proapoptotic activities in various cancer cell lines, including prostate cancer. Intratumoral injection of an adenoviral vector capable of efficient transduction and expression of Glipr1 (AdGlipr1) yielded promising therapeutic results in an orthotopic, metastatic mouse model of prostate cancer. AdGlipr1-transduced macrophages (Mϕ/Glipr1) generated greater surface expression of CD40, CD80, and MHC class II molecules and greater production of interleukin (IL)-12 and IL-6 in vitro than control macrophages did. Mechanistic analysis indicated that increased production of IL-12 in Mϕ/Glipr1 depends on activation of the p38 signaling cascade. Mϕ/Glipr1 injected into orthotopic 178-2BMA tumors in vivo resulted in significantly suppressed prostate tumor growth and spontaneous lung metastases and longer survival relative to those observed in control-treated mice. Furthermore, these preclinical data indicate the generation of systemic natural killer-cell activity and tumor-specific cytotoxic T-lymphocyte responses. Trafficking studies confirmed that intratumorally injected Mϕ/Glipr1 could migrate to draining lymph nodes. Overall, our data suggest that this novel gene-modified cell approach is an effective treatment avenue that induces antitumor immune responses in preclinical studies.

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“…Almost one in six men will be diagnosed with prostate cancer during their lifetime. Although the second leading cause of death from cancer, prostate cancer is a relatively slow-growing malignancy that may be amenable to the applications of cellular therapy [17]. CEPs are increased in the peripheral blood of prostate cancer patients [18], and TAMs also play a crucial role in the development and metastasis of prostate tumors [9].…”

Section: Introductionmentioning

confidence: 99%

Adenoviral-Mediated Endothelial Precursor Cell Delivery of Soluble CD115 Suppresses Human Prostate Cancer Xenograft Growth in Mice

et al. 2009

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Prostate cancer tumor growth and neovascularization is promoted by an interplay between migratory tumor stromal cells such as specialized tumor-associated macrophages (TAMs) and circulating endothelial precursor cells (CEPs). As vehicles for tumor therapy, human CEPs are relatively easy to isolate from peripheral blood, are able to proliferate long-term in vitro, are amenable to viral manipulation, and preferentially home to regions of ischemia found in growing tumors. We show here that human peripheral blood CEPs expanded ex vivo migrate to prostate cancer cells in vitro and efficiently home to human prostate tumor xenografts in vivo. Infection of precursors ex vivo with an adenovirus constructed to secrete a soluble form of the colony-stimulating factor-1 receptor CD115 that inhibits macrophage viability and migration in vitro significantly decreases the number of TAMs in xenografts (p < .05), reduces proliferation (p < .01) and vascular density (p < .03), and suppresses the growth of xenografts (p < .03). These data show for the first time that targeting stromal cell processes with cellular therapy has the potential to retard prostate tumor growth.

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Gene-modified bone marrow cell therapy for prostate cancer

Cited by 6 publications

References 116 publications

Bone Health Management in the Continuum of Prostate Cancer Disease

Bone Health Management in the Continuum of Prostate Cancer Disease

Tumor growth and metastasis suppression by Glipr1 gene-modified macrophages in a metastatic prostate cancer model

Adenoviral-Mediated Endothelial Precursor Cell Delivery of Soluble CD115 Suppresses Human Prostate Cancer Xenograft Growth in Mice

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