Treating tumor-bearing mice with vitamin D3 diminishes tumor-induced myelopoiesis and associated immunosuppression, and reduces tumor metastasis and recurrence

Young, Matthew R.; Ihm, Joe; Lozano, Yvonne; Wright, M. A.; Prechel, Margaret

doi:10.1007/bf01788958

Cited by 40 publications

(28 citation statements)

References 35 publications

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“…35,36 Since then, studies in animals have shown the beneficial effects of 1,25(OH 2 )D 3 in reducing cancer progression. [37][38][39][40] However, the associations between Vitamin D and sunshine exposure and colorectal cancer are mixed, with inverse associations generally observed, although often not reaching statistical significance. 10,13 In our study, we observed stronger associations with vitamin D intake and sunshine exposure for colon cancer in men if they also had 23 or more CAG repeats of the AR gene.…”

Section: Discussionmentioning

confidence: 99%

Associations between vitamin D, vitamin D receptor gene and the androgen receptor gene with colon and rectal cancer

Slattery

Sweeney

Murtaugh

et al. 2006

Intl Journal of Cancer

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The transcriptional activity of the vitamin D receptor (VDR) gene is regulated, at least in part, by the androgen receptor (AR) gene. We evaluate how the number of polyglutamine (CAG) repeats of the AR gene influence colorectal cancer in conjunction with vitamin D, sunshine exposure and VDR. Studies of colon (1,580 cases and 1,968 controls) and rectal (797 cases and 1,016 controls) cancer were used. Vitamin D intake and average hours of sunshine exposure interacted with AR genotype in men. Men with low vitamin D intake or low levels of sunshine exposure who had 231 CAG repeats of the AR gene had the greatest risk of colon cancer. ORs for men with 23 or more CAG repeats of the AR gene and in the lowest tertile of vitamin D intake or sunshine exposure were 1.71 (95% CI 1.14, 2.56) and 1.51 (95% CI 1.09, 2.09). Men with high levels of sunshine exposure were at reduced risk of developing rectal cancer if they had 23 or more CAG repeats (OR 0.62 95% CI 0.39, 0.97) than if they had fewer than 23 CAG repeats. The FF genotype of the Fok1 VDR gene was associated with reduced risk of colon cancer among women with any allele of 231 CAG repeats (OR 0.62 95% CI 0.44, 0.88), whereas men with the LL/bb VDR genotypes were at reduced risk of rectal cancer if they also had 231 CAG repeats (OR 0.71 95% CI 0.48, 1.05) relative to men with fewer than 23 CAG repeats of the AR gene. These data provide support for the role of vitamin D and sunshine exposure in the etiology of colorectal cancer and suggest that AR gene may modulate the association. Vitamin D has been associated inconsistently with colorectal cancer. 10 Differences in relative risk could stem from many sources, including sunshine, a major source of vitamin D, not being considered as part of the risk factor equation. Several investigators have studied sunshine exposure independently to better understand the associations between vitamin D and colorectal cancer. 11-13 Polymorphisms of the VDR gene have also been studied in conjunction with colorectal cancer and adenomas, since it may play a key role in vitamin D signaling, which could further influence colorectal cancer risk. [14][15][16][17][18][19] Polymorphisms of the VDR gene that have been studied include a poly A repeat at the 3 0 untranslated region (3 0 UTR) of the gene, 2 polymorphisms at intron 8 (Bsm I and Apa I) and 1 in exon 9 (Taq I) that are in linkage-disequilibrium with each other. 17,20 These polymorphisms, either alone or in combination, have been associated with increased mRNA expression of the VDR gene and increased serum levels of 1,25-dihydroxy vitamin D. 21,22 At the start site of the gene, a polymorphism detected with a Fok I digest has also been studied and has been shown to be not in linkage disequilibrium with the other variants. 17 A study conducted in human fibroblast cell lines found higher vitamin D hormone activity for the F allele than for the f allele. 23 One study showed that the ff genotype of the Fok I polymorphism increased risk of colorectal cancer, 18 whereas another showed that it w...

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Section: Discussionmentioning

confidence: 99%

Associations between vitamin D, vitamin D receptor gene and the androgen receptor gene with colon and rectal cancer

Slattery

Sweeney

Murtaugh

et al. 2006

Intl Journal of Cancer

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“…In both clinical and experimental settings, vitamin D 3 decreases the levels of MDSC and increases the effectiveness of tumor immunotherapy. 67,[73][74][75] Vitamin A stimulates the differentiation of myeloid progenitors into myeloid DCs and macrophages. 10,90 Mice with vitamin A deficiency, 91 or those treated with a pan-retinoic acid receptor antagonist, 92 show accumulation of MDSCs in bone marrow and spleen cells.…”

Section: Nagaraj and Gabrilovichmentioning

confidence: 99%

Myeloid-Derived Suppressor Cells in Human Cancer

Nagaraj

Gabrilovich²

2010

The Cancer Journal

206

191

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“…In fact, the anti-metastatic effect of Vitamin D has been discussed in many articles. Vitamin D3 treatment has been shown in the metastatic Lewis lung carcinoma (LLC-LN7) tumor model to reduce granulocyte/macrophage-colony-stimulating factor (GM-CSF) secreted by the tumor and interrupt the myelopoiesis-associated immunosuppressor cascade stimulated by GM-CSF, leading to a prominent reduction in tumor metastasis [156]. 1,25-Dihydroxycholecalciferol (1,25-D3) has also been shown to reduce the number and size of lung metastases in highly metastatic Mat-lylu prostate cancer rat model [157].…”

Section: Vitamin D3mentioning

confidence: 99%

Phytochemicals: cancer chemoprevention and suppression of tumor onset and metastasis

Shu

Cheung

Khor

et al. 2010

Cancer Metastasis Rev

216

155

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Carcinogenesis is a multi-step process which could be prevented by phytochemicals. Phytochemicals from dietary plants and other plant sources such as herbs are becoming increasingly important sources of anticancer drugs or compounds for cancer chemoprevention or adjuvant chemotherapy. Phytochemicals can prevent cancer initiation, promotion, and progression by exerting anti-inflammatory and anti-oxidative stress effects which are mediated by integrated Nrf2, NF-kappaB, and AP-1 signaling pathways. In addition, phytochemicals from herbal medicinal plants and/or some dietary plants developed in recent years have been shown to induce apoptosis in cancer cells and inhibition of tumor growth in vivo. In advanced tumors, a series of changes involving critical signaling molecules that would drive tumor cells undergoing epithelial-mesenchymal transition and becoming invasive. In this review, we will discuss the potential molecular targets and signaling pathways that mediate tumor onset and metastasis. In addition, we will shed light on some of the phytochemicals that are capable of targeting these signaling pathways which would make them potentially applicable to cancer chemoprevention, treatment and control of cancer progression.

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Treating tumor-bearing mice with vitamin D3 diminishes tumor-induced myelopoiesis and associated immunosuppression, and reduces tumor metastasis and recurrence

Cited by 40 publications

References 35 publications

Associations between vitamin D, vitamin D receptor gene and the androgen receptor gene with colon and rectal cancer

Associations between vitamin D, vitamin D receptor gene and the androgen receptor gene with colon and rectal cancer

Myeloid-Derived Suppressor Cells in Human Cancer

Phytochemicals: cancer chemoprevention and suppression of tumor onset and metastasis

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