Search

Adequate vitamin B12 levels in infancy are crucial for normal psychomotor and cognitive development of infants. Our aim was to examine serum vitamin B12, folate and ferritin levels in exclusively breastfed healthy full-term infants (age group: 1-6 months), and also investigate their correlation with maternal markers.A cross-sectional study was conducted on 100 exclusively breastfed healthy full-term infants (age group: 1-6 months) along with their lactating mothers. Serum vitamin B12, folate and ferritin levels were determined for each mother-infant dyad using enzyme-linked immunosorbent assay.The mean serum vitamin B12, folate and ferritin levels were 512 vs. 535 pg/mL, 15 vs. 12 ng/mL and 313 vs. 114 ng/mL in infants and mothers, respectively. Among 100 infants, 26 (26%) had lower vitamin B12 levels and 5 (5%) had inadequate folate levels. In addition, 22 (22%) of 100 lactating mothers were deficient in vitamin B12 levels and 14 (14%) had inadequate folate levels. We found a statistically significant positive correlation between infant and maternal vitamin B12 (r = 0.659, P 0.001) and folate levels (r = 0.51, P 0.001).Vitamin B12 deficiency was observed in 26% of infants and 22% of lactating mothers. Vitamin B12 and folate levels of infants were positively correlated with maternal levels in the state of Punjab, North-West India. Our findings support that maternal vitamin B12 status can be used as a valuable predictor of infant vitamin B12 status.

Male Breast Cancer (MBC) has a familial component thus identification of polymorphic risk alleles of candidate genes and/or cytogenetic anomalies may help to predict the risk for the offspring of MBC patients. The conventional metaphase cytogenetics can indicate loci that are hotspots while analysis by single nucleotide polymorphism arrays (SNP-A) can identify chromosomal defects which may play a role in the etiology of cancer. A cumulative genotype risk due to each allele of candidate genes of the signaling pathways regulating c-MYC, HIF1A, TP53 and BRCA1 may be a factor facilitating cancer development. Cancer risk was assessed in a 35-year-old healthy son of a 60-year-old MBC patient with a family history of cancer by metaphase cytogenetics, SNP-A and analysis of 25 polymorphisms in six genes TP53, MDM2, VEGF, VEGFR1, HIF1A, and BRCA1. The risk genotype GG-TT of MDM2 309T > G and VEGF-417C/T polymorphisms along with chromosomal instability shown by cytogenetic analysis and SNP-A, rare de novo duplication Yp, deletion in 7q pericentromeric region indicate an increased risk of cancer in the healthy son of an MBC patient.

Abstract Background Angiogenesis is a complex and coordinated process regulated by different growth factors and is one of the hallmark features of cancer. VEGF is one of the most important endothelial cell mitogen and has a critical role in normal physiological and tumor angiogenesis. The objective of this study was to investigate the potential association of haplotypes of six VEGF polymorphisms with breast cancer risk in North-West Indians. Methods Samples of 250 breast cancer patients and 250 age and sex matched controls were genotyped for VEGF −2578C/A, −2549I/D, −460T/C, +405C/G, −7C/T and +936C/T polymorphisms. Haplotypes were generated to determine the better contribution of VEGF polymorphisms to breast cancer risk. Results Haplotypes CDTCCC (OR = 0.56, 95%CI, 0.38–0.81; p = 0.003) and CDTGCC (OR = 0.63, 95%CI, 0.44–0.92; p = 0.018) of VEGF −2578C/A, −2549I/D, −460T/C, +405C/G, −7C/T and +936C/T polymorphisms were significantly associated with decreased risk of breast cancer. CDTCCC haplotype was also significantly associated with reduced risk of breast cancer in pre and post menopausal as well as both obese and non obese patients. Haplotype CDTGCC was marginally associated (p = 0.07) with reduced risk of breast cancer in non-obese patients as compared with non-obese controls where as haplotype AICGTC was marginally associated (p = 0.09) with reduced risk of breast cancer in obese patients when compared with non-obese patients. The CDTGCC haplotype was significantly associated with increased risk of breast cancer in premenopausal obese patients (OR = 1.98, 95%CI, 1.10–3.56; p = 0.02). Conclusions Our data indicated that CDTCCC and CDTGCC haplotypes of VEGF −2578C/A, −2549I/D, −460T/C, +405C/G, −7C/T and +936C/T polymorphisms were significantly associated with breast cancer risk in North-West Indians. Further studies on multiethnic groups with larger sample size are required to confirm our results.

BACKGROUND Monocyte chemoattractant protein-1 (MCP-1) is a major chemokine thought to be responsible for monocyte and T-lymphocyte recruitment in acute inflammatory conditions and recruitment of macrophages in tumors. It is also implicated in cardiovascular disease, rheumatoid arthritis and chronic obstructive pulmonary disease. The aim of the present study was to investigate the correlation between MCP-1 -2518 A/G polymorphism and breast cancer risk in patients from Amritsar city of Punjab state in North-West India. MATERIALS AND METHODS We screened DNA samples of 200 sporadic breast cancer patients and 200 age and gender matched unrelated healthy individuals for MCP-1 -2518 A/G polymorphism using the PCR-RFLP method. RESULTS A significantly increased frequency of the GG genotype was observed in patients as compared to controls. Individuals carrying the MCP1 -2518GG genotype had a two fold risk for breast cancer (OR=2.06, 95%CI, 1.06-3.98; p=0.03). Genetic models analysis revealed a significant association between MCP-1 -2518 A/G polymorphism and cancer risk in homozygous co-dominant (OR=2.06, 95%CI, 1.06-3.98; p=0.03) and recessive (OR=1.97, 95%CI, 1.05-3.70; p=0.03) models. CONCLUSIONS We conclude that the GG genotype of the MCP-1-2518 A/G polymorphism is associated with increased risk to breast cancer in Punjab, North-West India.

BACKGROUND Vascular endothelial growth factor (VEGF), an endothelial cell specific mitogen, has been implicated as a critical factor influencing tumor related angiogenesis. The aim of present study was to evaluate the relationship between VEGF +936C>T and +405C>G polymorphisms of VEGF with risk of breast cancer in Punjab, India. MATERIALS AND METHODS We screened DNA samples of 192 sporadic breast cancer patients and 192 unrelated healthy, gender and age matched control individuals for VEGF +936C>T and +405C>G polymorphisms using the PCR-RFLP method. RESULTS For the VEGF +405C>G polymorphism, we observed significantly increased frequency of GG genotype in cases as compared to controls and strong association of +405GG genotype was observed with three fold risk for breast cancer (OR=3.07; 95%CI 1.41-6.65; p=0.003). For the +936C>T polymorphism, significant associations of CT and combined CT+TT genotypes were observed with elevated risk of breast cancer (p=0.021; 0.023). The combined genotype combinations of GG-CC and GG- CT of +405C>G and +936C>T polymorphisms were found to be significantly associated with increased risk of breast cancer (p=0.04; 0.0064). CONCLUSIONS The findings of the present study indicated significant associations of VEGF +936C>T and +405C>G polymorphisms with increased breast cancer risk in patients from Punjab, North India.

Aims: The aim of the present study was to assess the role of the vascular endothelial growth factor (VEGF) −2549 insertion/deletion (I/D) polymorphism in susceptibility to sporadic breast cancer. Methods: DNA samples of 94 breast cancer patients and 94 unrelated healthy control individuals with matched age and gender from the same geographical region of Punjab, North West India were screened for the −2549 I/D polymorphism. Serum VEGF-C (sVEGF-C) levels of breast cancer patients and healthy controls were measured using an enzyme-linked immunosorbent assay. Results: The frequency of the II, ID, and DD genotype was 23.40 versus 10.64%, 48.94 versus 52.13%, and 27.66 versus 37.23%, in patients and controls, respectively. A statistically significant difference was observed for genotype distribution among the patients and controls (χ2=6.039, p=0.049). There was a significant increase in the I allele frequency in the patients as compared with controls (47.86 versus 36.70%, p=0.028). The sVEGF-C levels were also considerably higher in patients as compared to healthy controls (p

The aim of present study was to evaluate the relationship between vascular endothelial growth factor (VEGF) −2578C/A, −2549I/D, −460T/C and −7C/T and VEGFR1 −710C/T polymorphisms with risk to breast cancer in North Indians. A total of 204 sporadic breast cancer patients and 204 controls were recruited for this case-control study. Significantly increased frequency of II genotype of −2549I/D polymorphism was observed in patients as compared to control individuals (odds ratio (OR) = 2.76, 95 % confidence interval (CI), 1.55–4.92; p = 0.0005). VEGF −2578AA genotype (OR = 2.87; 95 % CI, 1.61–5.10; p = 0.0003) and A allele (OR = 1.65, 95 % CI, 1.25–2.18; p = 0.0004) were found to be associated with increased risk for breast cancer. Individuals carrying CC genotype (OR = 2.23, 95 % CI, 1.25–3.97) and C allele (OR = 1.42, 95 % CI, 1.07–1.87) of VEGF −460T/C polymorphism were at higher risk of breast cancer. There was no significant difference in genotype and allele distribution of VEGF −7C/T and VEGFR1 −710C/T polymorphisms between cases and control individuals (p > 0.05). Linkage disequilibrium analysis showed a strong linkage between VEGF −2549I/D and −2578C/A polymorphisms (Lewontin’s $$ \overset{^{\prime }}{D} $$ = 0.99; r 2 = 0.97), −2549I/D and −460T/C ( $$ \overset{^{\prime }}{D} $$ = 0.94; r 2 = 0.84), and −2578C/A and −460T/C polymorphisms ( $$ \overset{^{\prime }}{D} $$ = 0.93; r 2 = 0.83). In the present study, we concluded that VEGF −2549I/D, −2578C/A and −460T/C polymorphisms are associated with risk to breast cancer in Punjab, North India.

The purpose of this study was to evaluate the association of seven VEGF promoter polymorphisms with breast cancer risk in Punjabi population from North West India. We screened DNA samples of 102 sporadic breast cancer patients and 102 unrelated healthy, gender, and age-matched individuals for seven VEGF promoter polymorphisms [-417 C/T (rs833062), -172 C/A (rs59260042), -165 C/T (rs79469752), -160 C/T, -152 G/A (rs13207351), -141 A/C (rs28357093) and -116 G/A (rs1570360)] by direct sequencing. The frequency of GG, GA, and AA genotype of -152 G/A polymorphism was 26.47 vs 38.34%, 46.08 vs 51.96%, and 27.45 vs 9.80%, in patients and controls, respectively. VEGF -152 AA genotype was significantly associated with increased risk for breast cancer (OR = 4.04, 95%CI, 1.69-9.68, p = 0.001; recessive model OR = 3.48, 95%CI, 1.59-7.63, p = 0.001). For VEGF -116 G/A polymorphism, G and A allele frequencies were 65.2 vs 76.47% and 34.8 vs 23.53% in patients and controls, respectively. Individuals having -116 AA genotype (OR = 3.40; 95%CI, 1.24-9.37; p = 0.014) and A allele (OR = 1.73; 95%CI, 1.12-2.67; p = 0.012) were associated with increased risk for breast cancer. VEGF -165 C/T and -141 A/C polymorphisms were associated with reduced risk for breast cancer. There was significantly decreased frequency of CT genotype (4.90 vs 18.63%; p = 0.002) and T allele (2.45 vs 9.31%; p = 0.003) of -165 C/T polymorphism among breast cancer patients as compared to controls. VEGF -141 A and C allele frequency were 96.57 vs 91.18% and 3.43 vs 8.82% in patients and controls, respectively. Significant reduced risk for breast cancer was observed with AC genotype (OR = 0.34, 95%CI, 0.14-0.86; p = 0.019) and C allele (OR = 0.37; 95%CI, 0.15-0.89; p = 0.023) of -141 A/C polymorphism. We did not observe association of VEGF -417 T/C, -172 C/A, -160 C/T polymorphisms with breast cancer risk in the studied subjects (p0.05). The VEGF -152 G/A and -116 G/A polymorphisms were found to be significantly associated with increased risk for breast cancer while -165 C/T and -141 A/C polymorphisms were found to be associated with decreased risk for breast cancer in Punjabi population from North West India.