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Cancer biology in diabetes.

Sen S, He Y, Koya D, Kanasaki K - J Diabetes Investig (2014)

Bottom Line: Recent evidence suggests that diabetes could contribute to the initiation and progression of certain cancers in addition to the classic diabetic complications.The recent discovery of the possible anticancer effects of metformin, a classic antidiabetic drug, has led physicians and scientists to reconsider the interaction between diabetes and cancer.In the present review, we analyze recent reports in this field, and explore possible mechanistic links between diabetes and cancer biology.

View Article: PubMed Central - PubMed

Affiliation: Division of Diabetes & Endocrinology Kanazawa Medical University Ishikawa Japan ; The Department of Vascular and Thyroid Surgery The Affiliated Hospital of Luzhou Medical College Luzhou China.

ABSTRACT
Diabetes is a serious metabolic disease that causes multiple organ dysfunctions. Recent evidence suggests that diabetes could contribute to the initiation and progression of certain cancers in addition to the classic diabetic complications. Furthermore, some of the drugs used clinically to treat patients with diabetes might affect cancer initiation, progression and mortality. The recent discovery of the possible anticancer effects of metformin, a classic antidiabetic drug, has led physicians and scientists to reconsider the interaction between diabetes and cancer. In the present review, we analyze recent reports in this field, and explore possible mechanistic links between diabetes and cancer biology.

No MeSH data available.


Related in: MedlinePlus

Glucogen‐like peptide‐1 and cancer. Mechanism of GLP‐1‐potentiated insulin secretion in β‐cells and a possible cancer pathway. AC, adenylatecyclase; ADP, adenosine diphosphate; ATP, adenosine triphosphate; IGF‐BP3, insulin‐like growth factor binding‐protein 3; cAMP, cyclic adenosine monophosphate; IGF, insulin‐like growth factor; PI3‐Akt; phosphatidyl‐inositol 3‐kinase‐Protein Kinase B; PKA, protein kinase A; PPARγ, peroxisome proliferator‐activated receptor‐γ; Ras‐ERK, renin–angiotensin system–extracellular regulated protein kinases.
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jdi12208-fig-0002: Glucogen‐like peptide‐1 and cancer. Mechanism of GLP‐1‐potentiated insulin secretion in β‐cells and a possible cancer pathway. AC, adenylatecyclase; ADP, adenosine diphosphate; ATP, adenosine triphosphate; IGF‐BP3, insulin‐like growth factor binding‐protein 3; cAMP, cyclic adenosine monophosphate; IGF, insulin‐like growth factor; PI3‐Akt; phosphatidyl‐inositol 3‐kinase‐Protein Kinase B; PKA, protein kinase A; PPARγ, peroxisome proliferator‐activated receptor‐γ; Ras‐ERK, renin–angiotensin system–extracellular regulated protein kinases.

Mentions: Some other studies have analyzed the possible mechanistic connection between GLP‐1 and cancer from duration, age, and some other factors148, and they found that the GLP‐1 receptor, and the phosphatidyl‐inositol 3 kinase‐protein kinase B renin–angiotensin system–extracellular regulated protein kinases pathways might play a role (Figure 2).


Cancer biology in diabetes.

Sen S, He Y, Koya D, Kanasaki K - J Diabetes Investig (2014)

Glucogen‐like peptide‐1 and cancer. Mechanism of GLP‐1‐potentiated insulin secretion in β‐cells and a possible cancer pathway. AC, adenylatecyclase; ADP, adenosine diphosphate; ATP, adenosine triphosphate; IGF‐BP3, insulin‐like growth factor binding‐protein 3; cAMP, cyclic adenosine monophosphate; IGF, insulin‐like growth factor; PI3‐Akt; phosphatidyl‐inositol 3‐kinase‐Protein Kinase B; PKA, protein kinase A; PPARγ, peroxisome proliferator‐activated receptor‐γ; Ras‐ERK, renin–angiotensin system–extracellular regulated protein kinases.
© Copyright Policy - creativeCommonsBy-nc-nd
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4020326&req=5

jdi12208-fig-0002: Glucogen‐like peptide‐1 and cancer. Mechanism of GLP‐1‐potentiated insulin secretion in β‐cells and a possible cancer pathway. AC, adenylatecyclase; ADP, adenosine diphosphate; ATP, adenosine triphosphate; IGF‐BP3, insulin‐like growth factor binding‐protein 3; cAMP, cyclic adenosine monophosphate; IGF, insulin‐like growth factor; PI3‐Akt; phosphatidyl‐inositol 3‐kinase‐Protein Kinase B; PKA, protein kinase A; PPARγ, peroxisome proliferator‐activated receptor‐γ; Ras‐ERK, renin–angiotensin system–extracellular regulated protein kinases.
Mentions: Some other studies have analyzed the possible mechanistic connection between GLP‐1 and cancer from duration, age, and some other factors148, and they found that the GLP‐1 receptor, and the phosphatidyl‐inositol 3 kinase‐protein kinase B renin–angiotensin system–extracellular regulated protein kinases pathways might play a role (Figure 2).

Bottom Line: Recent evidence suggests that diabetes could contribute to the initiation and progression of certain cancers in addition to the classic diabetic complications.The recent discovery of the possible anticancer effects of metformin, a classic antidiabetic drug, has led physicians and scientists to reconsider the interaction between diabetes and cancer.In the present review, we analyze recent reports in this field, and explore possible mechanistic links between diabetes and cancer biology.

View Article: PubMed Central - PubMed

Affiliation: Division of Diabetes & Endocrinology Kanazawa Medical University Ishikawa Japan ; The Department of Vascular and Thyroid Surgery The Affiliated Hospital of Luzhou Medical College Luzhou China.

ABSTRACT
Diabetes is a serious metabolic disease that causes multiple organ dysfunctions. Recent evidence suggests that diabetes could contribute to the initiation and progression of certain cancers in addition to the classic diabetic complications. Furthermore, some of the drugs used clinically to treat patients with diabetes might affect cancer initiation, progression and mortality. The recent discovery of the possible anticancer effects of metformin, a classic antidiabetic drug, has led physicians and scientists to reconsider the interaction between diabetes and cancer. In the present review, we analyze recent reports in this field, and explore possible mechanistic links between diabetes and cancer biology.

No MeSH data available.


Related in: MedlinePlus