Vitamin D and lymphoid cancers: A review

Received: 05-Apr-2024, Manuscript No. OAR-24-133546; Accepted: 25-Jun-2024, Pre QC No. OAR-24-133546(PQ); Editor assigned: 10-May-2024, Pre QC No. OAR-24-133546(PQ); Reviewed: 19-Jun-2024, QC No. OAR-24-133546(Q); Revised: 23-Jun-2024, Manuscript No. OAR-24-133546(R); Published: 29-Jun-2024

Introduction

Lymphoid Cancer (LC) is heterogeneous spectrum of monoclonal disorder with accumulation of abnormal of lymphocytes in the blood, bone marrow and reticuloendothelial This ranges from the B and T -cell, Hodgkin to Non-Hodgkin Lymphomas disorders, and its spectrum [1-3].

Epidemiologically lymphoid malignancies differ from one geographical region to another. Jaffe et al in is study on understanding the new WHO classification reported, that the most common hematological malignancies were Non-Hodgins’s Lymphoma (NHL) and it makes up 3% of cancer diagnoses and deaths [4]. Another study by Omoti et al reported a high prevalence of 61.1% of NHL in an oil rich region of Niger-delta [5]. Furthermore, another study, reported a prevalence of 76.81% of lymphoid malignancies at cross river state, south-south of Nigeria [6]. Similarly, salawu in ife southwest of Nigeria reported a high prevalence of 69% moreso another study by Mounia et al in morocco North Africa, reported predominantly NHL with a prevalence of 29.7% [7, 8]. Vitamin D is a fat-soluble vitamin and plays a majorly role in calcium homeostasis, and mineralization of the bone [8, 9]. It can be acquired through exposure to sunlight, ingestion of vitamin D rich diets and other supplement. Several studies have reported low level of vitamin D in high grade B- lymphoma and chronic lymphocytic leukemia, patients, treated with immunotherapy [10, 11]. Similarly, a nest case-controlled study conducted in Finland by Lim U et al, show no likely relationship between serum vitamin D and lymphoid malignancies, rather provides a potential protective risk of non-Hodgkin Lymphoma (NHL) [12]. However similar studies conducted by Kricker et al., reported no statistically significant change with the downtrend in risk with total sun exposure and Vander Rhee et al., respectively reported no changes in the level of vitamin D level among lymphoid malignancies [13, 14]. This shows that there is dearth and inconsistency of information on vitamin D in lymphoid cancer. Hence this study seeks to review the role and level of vitamin D in lymphoid cancer.

Literature Review

Vitamin D structure, source, function and metabolism

It regulates calcium metabolism; it is one of the fat-soluble vitamins. It is synthesized from the skin.

Vitamin D is derived from its precursor cholesterol. It exists in two forms: vitamin D₂ , (Ergocalciferol) which is synthesize from plants, while the second form is vitamin D₃ , and derive from animal tissues and also termed cholecalciferol. These inactive precursors are converted to active precursor in the liver which is termed calcidiol (25-hydroxyvitamin D) (Figure 1). Calcitriol, transported to the renal tubules, where it is converted to the active and potent calcitriol, via vitamin D binding proteins in the blood [15].

Figure 1: Calcitriol x (1,25 dihydroxyvitamin D)

Vitamin D is essential in so many physiological activities in the body such as immune modulation, calcium regulation and cell differentiation [16, 17]. Calcitriol gets activated through the attachment to the vitamin D receptor, a receptor located in nuclear and it is found in most organs [18]. During activation, the vitamin D receptor heterodimerize with retinoid x receptor, there by stimulating the target genes to regulate their transcription, increasing the concern of the potential biological impact of vitamin D in cancer prevention and treatment [19-22].

Vitamin D is synthesis mainly from the skin with dietary contributing less because foods rich in vitamin D are not routine dietary pattern. Hence supplementation of vitamin D to persons with its deficiency because of inadequate sun exposure is important (Figure 2).

Figure 2: Calcidiol (25-hydroxyvitamin)

Vitamin D and lymphoid cancer

Vitamin D, regulate several cancers associated cellular processes, which include differentiation, proliferation, angiogenesis, apoptosis and spread of cancer cells [23, 24]. Calcitriol impaired the growth of cancer cells by activating cell cycle arrest through the stimulation of cyclin-dependent kinase inhibitors, such as p21 and p27, and the downregulation of cyclins, thereby impairing the progression of the cell cycle [25, 26]. Furthermore, vitamin D causes continuous and uncontrolled differentiation of cancer cell [27, 28]. Moreso in many cancer cell lines, calcitriol has shown to increase the expression of markers of differentiation and activate morphological changes. Also, its merit in the treatment of acute myeloid leukaemia with analogues of vitamin D [21, 29].

Programmed cell death, also called apoptosis is a mechanism in the body for removal of abnormal cells, such as cancer cells. Calcitriol turn-on apoptosis via the appearance of antiapoptotic and proapoptotic proteins, such as B-Cell Leukaemia/Lymphoma 2 protein (BCL-2) family members and caspases [30, 31]. Thus, apoptosis generated by vitamin D may contribute to its antitumor activity and hamper angiogenesis in developing tumours by obstructing the production of proangiogenic molecules, such as matrix metalloproteinase and vascular endothelial growth factors [32]. Calcitriol has anti-inflammatory effects, which is significance for cancer prevention by hampering the production of chemokines and proinflammatory cytokines, which may accord to its anticancer properties [32]. Another study also reported a lower level in follicular lymphoma and it is associated with inferior survivor [33]. Furthermore, another study by Nath K et al, also reported that vitamin D insufficiency is associated with an inferior outcome with chimeric antigen receptor in diffuse Large B-cell lymphoma [34]. Moreso, Bitten bring et al also reported reduce of vitamin D level in patients among Diffuse Large B Cell Lymphoma (DLBCL) and reduce rituximab activity mediated [35]. Drake et al., also reported that in insufficient level of Vitamin D is associated with inferior event free survival and T cell Lymphoma [36]. Furthermore, another study conducted by Vasko and Veselin also reported a low of serum vitamin D level in Non–Hodgkin lymphomas and multiple myeloma [37]. However, Tracy et al, reported a clinical failure and adverse outcome with vitamin D insufficiency among those treated with therapies other than im-munochemotherapy [38]. Furthermore, similar studies with slight variation by Vasko and Veselin, show that there was reduce level of vitamin D in Non-Hodgkin Lymphoma except Burkitt Lym-phoma [37]. Renne et al also reported an upward regulation of vi-tamin D receptor in Hodgkin’s Lymphoma but reduce in B-NHL subtype [39]. Another study by Luczynska showed association between increase Vitamin D level and lower risk of Chronic Lymphocytic Leukaemia (CLL) however does not adduce to it protec-tive role in lymphoid cancers [40].

Conclusion

The role of Vitamin D, in lymphoid cancer has been underscore with so paucity and inconsistency of information, this calls for further research to bridge the gaps of the so many unanswered questions on its role in lymphoid cancers. Authors declared that

Ethical Issue

Not applicable.

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