Colonic Hyperplasia and Hyperproliferation Induced by a Nutritional Stress Diet With Four Components of Western-Style Diet

Newmark, Harold L.; Lipkin, Martin; Maheshwari, N

doi:10.1093/jnci/82.6.491

Cited by 113 publications

(72 citation statements)

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“…Our results indicated that ionized calcium cannot be used as a prognostic factor. These results agreed with Brada el al [46] and disagreed with Kristensen et al [47] as survival was found to be inversely associated with serum ionized calcium levels. It was found that elevated levels of phosphorus were necessary for adequate growth of some types of cancers [6], [7].…”

Section: Discussionsupporting

confidence: 75%

“…This rise in phosphorus is due to heightened requirements of protein synthesis needed during accelerated cell growth [8]. Furthermore, a high phosphate diet has been reported to promote colonic cell hyperplasia and hyperproliferation in mice, indicating a role of Pi in carcinogenesis [47]. Elevated Pi has been suggested to promote development of cancer via amplifying Akt (also known as protein kinase B) signaling activities and enhancing cap-dependent translation, eventually resulting in increased cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

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The role of serum 25-hydroxyvitamin D, ionized calcium and phosphorus in breast cancer females: A case-control study

Moneim¹,

Hewala

Rashad³

et al. 2015

IJBAS

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Aim: To evaluate the diagnostic and prognostic value of serum 25-hydroxyvitamin D (25(OH) D), ionized calcium and phosphorus in comparison with serum CA15.3 as the most commonly used breast cancer marker. Participants and methods: This study was conducted on 45 breast cancer female patients with recently detected breast cancer before surgery and 45 apparently healthy female controls of matched age, menstrual and socioeconomic status as breast cancer patients group. Serum 25(OH) D, ionized calcium, phosphorus and CA15.3 were measured using readyfor-use commercially available kits. Results: Serum levels of 25(OH) D and ionized calcium in the breast cancer patients group were significantly lower than those of the control group, while serum levels of phosphorus and CA15.3 in breast cancer patients group were significantly higher than those of the control group. The area under the ROC curve for serum ionized calcium (81.7%) was significantly greater than that of 25(OH) D (75.3%), CA 15.3 (70.1%) and phosphorus (62.8%). The odd's ratio of vitamin D was 0.0937 (95% CI=0.0311-0.2823), of ionized calcium was 0.0464 (95% CI=0.015-0.141) and of phosphorus was 2.6801(95% CI=1.1269-6.3742) in breast cancer patients group. Serum phosphorus was significantly correlated with age and menopausal status of breast cancer patients. Conclusion: Our results suggest that serum ionized calcium and 25(OH) D were superior to serum CA15.3 and phosphorus for prediction of breast cancer. In addition, our results indicate that 25 (OH) D and calcium may decrease the risk for breast cancer incidence, while phosphorus may increase this risk. None of the assayed biomarkers has a prognostic role in breast cancer.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

The role of serum 25-hydroxyvitamin D, ionized calcium and phosphorus in breast cancer females: A case-control study

Moneim¹,

Hewala

Rashad³

et al. 2015

IJBAS

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“…In particular, there is a clear association between abdominal obesity, as reflected by a higher waist circumference, and colon cancer and advanced adenoma risk in both men and women (28), findings confirmed in studies where visceral fat-measured by CT scanning-was strongly associated with colorectal adenoma detection and inversely associated with circulating adiponectin levels (29). Accumulating evidence in experimental animals support these data and indicate that normal colonic epithelial cells as well as CRC cells proliferate more rapidly in obese animals and in mice fed a hypercaloric diet (30,31). Moreover, tumor development and size is increased after subcutaneous injection of CRC cells in obese compared to non-obese mice (32).…”

Section: Obesity and Colorectal Cancer Riskmentioning

confidence: 62%

Translational approaches to addressing complex genetic pathways in colorectal cancer

Early

Fontana

Davidson

2008

Translational Research

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Colorectal cancer (CRC) is among the most prevalent cancers worldwide and represents a major public health challenge in the developed world. From the perspective of translational investigation, scientists have enormous opportunity to elucidate the molecular genetic mechanisms contributing to CRC pathogenesis since the majority of cancers arise from adenomatous precursor lesions. The process of adenoma growth and transformation is accompanied by cumulative mutations in dominant genetic pathways that confer a growth advantage. While this developmental process permits interrogation of informative pathways prior to the development of cancer, only a minority of adenomas progress to CRC. Accordingly, a major challenge for clinical translational investigators is to identify the molecular signatures that indicate increased likelihood for adenoma progression. By corollary, these molecular signatures include mutations in high penetrance alleles, including the Adenomatous Polyposis Coli (APC) gene as well as other alleles in the Wnt/β-catenin signaling pathway that specify increased genetic susceptibility to CRC. Interactions between these high penetrance alleles and other modifier genes as well as with environmental factors are of particular importance in understanding the complex network of events leading to CRC. This brief review will highlight three areas where important questions concerning genetic and environmental risk factors have fueled translational investigation into possible pathways leading to CRC.There have been substantial advances in the last two decades in our understanding of the molecular pathways that lead to colorectal cancer (CRC), the results of research that demonstrated the role of mutational activation of oncogenes coupled with loss of function of tumor suppressor genes in a model that advanced the concept of finite, but cumulative mutational events (summarized in (1)). These studies in preclinical, animal models as well as cell-based models, clinical observational and randomized studies in humans have led to a more complete understanding of the role of both environmental and genetic factors in CRC pathogenesis.One tangible result of this expanded scientific foundation is an emerging consensus that familial or inherited factors play an increasingly relevant role in our approach to patients with CRC(2). Examples of dominant genetic pathways include those governed by Adenomatous Polyposis Coli (APC) tumor suppressor gene, and also the microsatellite instability pathway 4 To whom communication should be directed

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“…First, it allows the accumulation of proliferating cells in the colonic crypts, it being well known that hyperproliferation coupled with hyperplasia are early morphogenetic events leading to the development of microadenomas (33,34). Under this condition, the homeostatic balance between mitotic activity and apoptosis is lost, even if the apoptotic level is higher than in normal mucosa (35).…”

Section: Discussionmentioning

confidence: 99%

Germline APC Mutation on the β-Catenin Binding Site Is Associated with a Decreased Apoptotic Level in Colorectal Adenomas

et al. 2003

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Germline mutations in APC tumor suppressor gene are responsible for familial adenomatous polyposis (FAP). A major role of these genetic changes is the constitutive activation of ␤-catenin-Tcf-4 mediated transcription of nuclear target genes, but other cellular functions can be misregulated. To assess how different APC mutations can drive the early steps of colonic tumorigenesis, we studied the effect of 10 different germline-truncating alterations on the phenotype of the corresponding adenomas. A significant reduction of apoptosis, uncoupled with an increased c-myc and cyclin-D1 expression, was seen with a frameshift mutation on codon 1383, in the 20-aa repeats of the ␤-catenin degradation domain, independent of a somatic alteration on the wildtype allele. The decreased apoptotic level was associated with a higher incidence of cancerization. No other APC mutation was linked with a similar effect, even in presence of a somatic allelic loss. These findings suggest that mutations in critical sites of the ␤-catenin degradation domain of APC gene can convey a selective advantage to the colonic neoplastic clones by altering the apoptotic surveillance rather than enhancing the ␤-catenin-Tcf-4 transcription of growth-promoting genes.

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Colonic Hyperplasia and Hyperproliferation Induced by a Nutritional Stress Diet With Four Components of Western-Style Diet

Cited by 113 publications

References 0 publications

The role of serum 25-hydroxyvitamin D, ionized calcium and phosphorus in breast cancer females: A case-control study

The role of serum 25-hydroxyvitamin D, ionized calcium and phosphorus in breast cancer females: A case-control study

Translational approaches to addressing complex genetic pathways in colorectal cancer

Germline APC Mutation on the β-Catenin Binding Site Is Associated with a Decreased Apoptotic Level in Colorectal Adenomas

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