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can igf 1 cause cancer
- Thread starter clay4444
- Start date
justinjones1963
New member
It will not cause cancer but I believe that there are studies that have confirmed that if one has cancer, it will drastically spread the cancer.
Tatyana
Elite Mentor
Hot off the presses, a notification of a new publication
Study protocol: Insulin and its role in cancer
BMC Endocrine Disorders 2007,
7:10 doi:10.1186/1472-6823-7-10
K Harish ([email protected])
M Dharmalingam ([email protected])
M Himanshu ([email protected])
ISSN 1472-6823
Article type Study protocol
Submission date 16 July 2007
Acceptance date 22 October 2007
Publication date 22 October 2007
Article URL http://www.biomedcentral.com/1472-
Abstract
Background: Studies have shown that metabolic syndrome and its consequent
biochemical derangements in the various phases of diabetes may contribute to
carcinogenesis. A part of this carcinogenic effect could be attributed to
hyperinsulinism. High levels of insulin decrease the production of IGF-1 binding
proteins and hence increase levels of free IGF-1.
It is well established that bioactivity of free insulin growth factor 1 (IGF-1) increases tumor turnover rate.
The objective is to investigate the role of insulin resistance/sensitivity in carcinogenesis by studying the relation between insulin resistance/sensitivity and IGF-1 levels in cancer patients. We postulate that hyperinsulinaemia which prevails during initial phases of insulin resistance (condition prior to overt diabetes) increases bioactivity of free IGF-1, which may contribute to process of carcinogenesis.
Methods / Design: Based on our pilot study results and power analysis of the same, we have designed a two group case-control study. 800 proven untreated cancer patients (solid epithelial cell tumors) under age of 50 shall be recruited with 200 healthy subjects serving as controls. Insulin resistance/sensitivity and free IGF-1 levels shall be determined in all subjects. Association between the two parameters shall be tested using suitable statistical methods.
Discussion: Well controlled studies in humans are essential to study the link
between insulin resistance, hyperinsulinaemia, IGF-1 and carcinogenesis. This study could provide insights to the role of insulin, insulin resistance, IGF-1 in
carcinogenesis although a precise role and the extent of influence cannot be determined. In future, cancer prevention and treatment strategies could revolve around insulin and insulin resistance.
Background
The association of diabetes mellitus and cancer has been reported more than 100 years ago [1]. Population studies have shown increased evidence of this
association.
Diabetes has been recognized as a risk factor for development of
breast, endometrial, colorectal and pancreatic carcinomas [2]. Breast, endometrial, colorectal and pancreatic carcinomas are best studied with regard to their association with diabetes/insulin resistance. Population studies have shown that the effects of diabetes mellitus on colorectal cancer may be mediated through mechanisms ranging from increased colonic transit time to hyperinsulinaemia.
In relation to the latter, at least in the early phase of development, type 2 diabetes mellitus is associated with increased circulating insulin concentrations [3, 4]. A large cohort study concluded that diabetes is associated with a modestly increased risk for endometrial cancer among women [5]. Future research, particularly prospective studies with biological samples, could be very helpful in answering questions aimed at clarifying these mechanisms [5]. Data suggest that type 2 diabetes might be associated with up to 10–20% excess risk for breast cancer and that it could also have detrimental effects on the natural history, diagnosis, and treatment of breast cancer [1, 6].
In the past few years both laboratory investigations and population studies have provided some circumstantial evidence that insulin growth factor biochemical derangements may contribute to carcinogenesis.
Several studies implicate hyperinsulinism, a condition that prevails prior to the onset of diabetes (part of metabolic syndrome) as candidate mediator in carcinogenesis [10].
Studies have revealed that high levels of circulating insulin decreases levels of insulin like growth factor binding protein 1 and 3 (IGFBP 1,3). Thus free IGF-1 levels increase in circulation [11, 12].
Another aspect of IGF physiology is the IGF signaling. In this signaling process, IGF-1 receptor is a predominant factor and is crucial for tumor
transformation and survival of malignant cell. It has comparatively less role in normal cell growth [13].
Thus role of IGF-1 in promoting carcinogenesis and its prognosis is
well established. Over the recent years, IGF-1 physiology has been widely studied.
The IGF system, comprises of insulin-like IGF-I, IGF-II, and IGFBPs. IGF-1 as a
growth factor plays a dominant role over IGF-2 and hence is widely studied.
Until recently, growth hormone was the only known stimulant of IGF-1 production.
Different lines of evidence suggest that the IGF/IGFBP system may be regulated by factors other than growth hormones. States of nutritional deprivation, such as starvation and protein caloric under-nutrition and type 1 diabetes mellitus, in animal models have long been known to influence the production of IGFs [14-16].
Various studies have shown that resistance to insulin action, as found in diabetic patients, has been associated with an increase IGFBP-3 protease activity, there by reducing IGFBP-3 levels [17]. Also, Insulin increases IGF-I bioavailability through IGFBP-1 suppression [14, 18, 19]. Thus there is ample evidence to suggest that insulin resistant states increase free IGF-1 levels.
Medical literature suggests that well controlled biochemical and genetic studies are required to establish the link between insulin, IGF-1, diabetes and cancer. We propose to investigate the role of hyperinsulinemia in carcinogenesis.
The primary objective of the study is to investigate the role of insulin resistance or sensitivity in carcinogenesis.
This is done by studying the relation between insulin resistance/sensitivity and IGF-1 levels in cancer patients. The secondary objective is to study the above mentioned association with organ specific cancers if possible.
Carcinogenesis is multi-factorial.
The metabolic and genetic derangements that take place during carcinogenesis may be induced by carcinogens and inherited genetic
factors. The role of either could be variable in a given case. We hypothesize that people with insulin resistance are at risk of developing cancer due to high levels of circulating IGF-1.
Such a risk would increase if other such factors are prevalent / acquired. A person with high levels of IGF-1 may be predisposed to cancer and his/her risk of developing cancer would increase with the presence of other such factors. Cancer being a non-communicable disease, with multiple risk factors,
modifiable risk factors are very few.
Controlling hyperinsulinaemia would modify one major risk factor. IGF-1 levels in body change with age. In addition, risk IGF-1 has high bioactivity on epithelial cells. Thus their role in carcinomas is of significance rather than other types of malignancies. Hence we limit our study to carcinomas of breast, GIT, liver, prostate, uterus, cervix and ovaries.
Study protocol: Insulin and its role in cancer
BMC Endocrine Disorders 2007,
7:10 doi:10.1186/1472-6823-7-10
K Harish ([email protected])
M Dharmalingam ([email protected])
M Himanshu ([email protected])
ISSN 1472-6823
Article type Study protocol
Submission date 16 July 2007
Acceptance date 22 October 2007
Publication date 22 October 2007
Article URL http://www.biomedcentral.com/1472-
Abstract
Background: Studies have shown that metabolic syndrome and its consequent
biochemical derangements in the various phases of diabetes may contribute to
carcinogenesis. A part of this carcinogenic effect could be attributed to
hyperinsulinism. High levels of insulin decrease the production of IGF-1 binding
proteins and hence increase levels of free IGF-1.
It is well established that bioactivity of free insulin growth factor 1 (IGF-1) increases tumor turnover rate.
The objective is to investigate the role of insulin resistance/sensitivity in carcinogenesis by studying the relation between insulin resistance/sensitivity and IGF-1 levels in cancer patients. We postulate that hyperinsulinaemia which prevails during initial phases of insulin resistance (condition prior to overt diabetes) increases bioactivity of free IGF-1, which may contribute to process of carcinogenesis.
Methods / Design: Based on our pilot study results and power analysis of the same, we have designed a two group case-control study. 800 proven untreated cancer patients (solid epithelial cell tumors) under age of 50 shall be recruited with 200 healthy subjects serving as controls. Insulin resistance/sensitivity and free IGF-1 levels shall be determined in all subjects. Association between the two parameters shall be tested using suitable statistical methods.
Discussion: Well controlled studies in humans are essential to study the link
between insulin resistance, hyperinsulinaemia, IGF-1 and carcinogenesis. This study could provide insights to the role of insulin, insulin resistance, IGF-1 in
carcinogenesis although a precise role and the extent of influence cannot be determined. In future, cancer prevention and treatment strategies could revolve around insulin and insulin resistance.
Background
The association of diabetes mellitus and cancer has been reported more than 100 years ago [1]. Population studies have shown increased evidence of this
association.
Diabetes has been recognized as a risk factor for development of
breast, endometrial, colorectal and pancreatic carcinomas [2]. Breast, endometrial, colorectal and pancreatic carcinomas are best studied with regard to their association with diabetes/insulin resistance. Population studies have shown that the effects of diabetes mellitus on colorectal cancer may be mediated through mechanisms ranging from increased colonic transit time to hyperinsulinaemia.
In relation to the latter, at least in the early phase of development, type 2 diabetes mellitus is associated with increased circulating insulin concentrations [3, 4]. A large cohort study concluded that diabetes is associated with a modestly increased risk for endometrial cancer among women [5]. Future research, particularly prospective studies with biological samples, could be very helpful in answering questions aimed at clarifying these mechanisms [5]. Data suggest that type 2 diabetes might be associated with up to 10–20% excess risk for breast cancer and that it could also have detrimental effects on the natural history, diagnosis, and treatment of breast cancer [1, 6].
In the past few years both laboratory investigations and population studies have provided some circumstantial evidence that insulin growth factor biochemical derangements may contribute to carcinogenesis.
Several studies implicate hyperinsulinism, a condition that prevails prior to the onset of diabetes (part of metabolic syndrome) as candidate mediator in carcinogenesis [10].
Studies have revealed that high levels of circulating insulin decreases levels of insulin like growth factor binding protein 1 and 3 (IGFBP 1,3). Thus free IGF-1 levels increase in circulation [11, 12].
Another aspect of IGF physiology is the IGF signaling. In this signaling process, IGF-1 receptor is a predominant factor and is crucial for tumor
transformation and survival of malignant cell. It has comparatively less role in normal cell growth [13].
Thus role of IGF-1 in promoting carcinogenesis and its prognosis is
well established. Over the recent years, IGF-1 physiology has been widely studied.
The IGF system, comprises of insulin-like IGF-I, IGF-II, and IGFBPs. IGF-1 as a
growth factor plays a dominant role over IGF-2 and hence is widely studied.
Until recently, growth hormone was the only known stimulant of IGF-1 production.
Different lines of evidence suggest that the IGF/IGFBP system may be regulated by factors other than growth hormones. States of nutritional deprivation, such as starvation and protein caloric under-nutrition and type 1 diabetes mellitus, in animal models have long been known to influence the production of IGFs [14-16].
Various studies have shown that resistance to insulin action, as found in diabetic patients, has been associated with an increase IGFBP-3 protease activity, there by reducing IGFBP-3 levels [17]. Also, Insulin increases IGF-I bioavailability through IGFBP-1 suppression [14, 18, 19]. Thus there is ample evidence to suggest that insulin resistant states increase free IGF-1 levels.
Medical literature suggests that well controlled biochemical and genetic studies are required to establish the link between insulin, IGF-1, diabetes and cancer. We propose to investigate the role of hyperinsulinemia in carcinogenesis.
The primary objective of the study is to investigate the role of insulin resistance or sensitivity in carcinogenesis.
This is done by studying the relation between insulin resistance/sensitivity and IGF-1 levels in cancer patients. The secondary objective is to study the above mentioned association with organ specific cancers if possible.
Carcinogenesis is multi-factorial.
The metabolic and genetic derangements that take place during carcinogenesis may be induced by carcinogens and inherited genetic
factors. The role of either could be variable in a given case. We hypothesize that people with insulin resistance are at risk of developing cancer due to high levels of circulating IGF-1.
Such a risk would increase if other such factors are prevalent / acquired. A person with high levels of IGF-1 may be predisposed to cancer and his/her risk of developing cancer would increase with the presence of other such factors. Cancer being a non-communicable disease, with multiple risk factors,
modifiable risk factors are very few.
Controlling hyperinsulinaemia would modify one major risk factor. IGF-1 levels in body change with age. In addition, risk IGF-1 has high bioactivity on epithelial cells. Thus their role in carcinomas is of significance rather than other types of malignancies. Hence we limit our study to carcinomas of breast, GIT, liver, prostate, uterus, cervix and ovaries.
Last edited:
OldWiseMan
New member
Re: Hot off the presses, a notification of a new publication
WOW! That makes me want to to go grab some IGF. Ha
Do you think thee same can be said for HGH? I would think so..
WOW! That makes me want to to go grab some IGF. Ha
Do you think thee same can be said for HGH? I would think so..
Recombinant human insulin-like growth factor I (IGF-I): risks and benefits of normalizing blood IGF-I concentrations.Clark RG.
Tercica, Inc., San Francisco, CA 94080-7111, USA. [email protected]
Recombinant human (rh) insulin-like growth factor I (IGF-I) is being developed as a therapy for short stature caused by IGF deficiency (IGFD) and also for diabetes mellitus. To complement the human efficacy and safety data, a large amount of information is available regarding the pharmacology and toxicology of rhIGF-I in animals. This review summarizes the risks and benefits of normalizing blood IGF-I concentrations in IGFD, especially with regard to carcinogenicity, and compares and contrasts safety data for rhIGF-I, recombinant human growth hormone (rhGH), and insulin. A major difference between rhIGF-I and rhGH is that rhIGF-I (like insulin) has hypoglycaemic activity, whereas rhGH opposes insulin action and is diabetogenic. In most of their actions, gh - growth hormone (somatropin) - and IGF-I are similar. IGF-I mediates most of the actions of GH, so the safety of rhGH and that of rhIGF-I also share many common features. In animals, the transgenic expression of human growth hormone - somatropin - has been shown to act directly, by activating the prolactin receptor, to increase the incidence of mammary and prostate tumours. In comparison, the over-expression of IGF-I in animals or the administration of rhIGF-I does not have a carcinogenic effect. In formal toxicology and carcinogenicity studies, rhIGF-I has similar effects to insulin in that it can increase food intake, body size, and the growth rate of existing tumours. In animals and humans, IGFD has many long-term detrimental effects besides short stature: it increases the risk of diabetes, cardiovascular disease, and low bone mineral density. Therefore, a case can be made for replacement therapy with rhIGF-I to normalize blood IGF-I levels and reverse the detrimental effects of IGFD. Copyright 2004 S. Karger AG, Basel.
Tercica, Inc., San Francisco, CA 94080-7111, USA. [email protected]
Recombinant human (rh) insulin-like growth factor I (IGF-I) is being developed as a therapy for short stature caused by IGF deficiency (IGFD) and also for diabetes mellitus. To complement the human efficacy and safety data, a large amount of information is available regarding the pharmacology and toxicology of rhIGF-I in animals. This review summarizes the risks and benefits of normalizing blood IGF-I concentrations in IGFD, especially with regard to carcinogenicity, and compares and contrasts safety data for rhIGF-I, recombinant human growth hormone (rhGH), and insulin. A major difference between rhIGF-I and rhGH is that rhIGF-I (like insulin) has hypoglycaemic activity, whereas rhGH opposes insulin action and is diabetogenic. In most of their actions, gh - growth hormone (somatropin) - and IGF-I are similar. IGF-I mediates most of the actions of GH, so the safety of rhGH and that of rhIGF-I also share many common features. In animals, the transgenic expression of human growth hormone - somatropin - has been shown to act directly, by activating the prolactin receptor, to increase the incidence of mammary and prostate tumours. In comparison, the over-expression of IGF-I in animals or the administration of rhIGF-I does not have a carcinogenic effect. In formal toxicology and carcinogenicity studies, rhIGF-I has similar effects to insulin in that it can increase food intake, body size, and the growth rate of existing tumours. In animals and humans, IGFD has many long-term detrimental effects besides short stature: it increases the risk of diabetes, cardiovascular disease, and low bone mineral density. Therefore, a case can be made for replacement therapy with rhIGF-I to normalize blood IGF-I levels and reverse the detrimental effects of IGFD. Copyright 2004 S. Karger AG, Basel.
Recombinant rat and mouse growth hormones: risk assessment of carcinogenic potential in 2-year bioassays in rats and mice.
Farris GM, Miller GK, Wollenberg GK, Molon-Noblot S, Chan C, Prahalada S.
Department of Safety Assessment, Merck Research Laboratories, West Point, PA 19486, USA. [email protected]
Recombinant rat growth hormone (rrGH) and recombinant mouse growth hormone (rmGH) were developed to evaluate the potential carcinogenicity of each biologically active growth hormone (gh - growth hormone (somatropin) - ) as assessed in the respective species. Biological activities of rrGH and rmGH were demonstrated by showing an increase in body weight gain and serum levels of insulin-like growth factor-1 (IGF-1) in hypophysectomized rats receiving daily sc injections for 6 days. With the exception of pharmacologically mediated weight gain, rrGH and rmGH had no adverse effects in 5-week oral toxicity studies and no production of anti-recombinant GH antibodies. The high doses selected for the carcinogenicity studies provided systemic exposures of GH up to approximately 10-fold over basal levels. In the 105-week mouse carcinogenicity study, daily sc injections of rmGH at 0.1, 0.2, or 0.5 mg/kg/day were well tolerated and had no effects on survival or incidence of tumors. In the 106-week rat carcinogenicity study, daily sc injections of rrGH at 0.2, 0.4, or 0.8 mg/kg/day had a favorable effect on longevity in female rats administered 0.4 or 0.8 mg/kg/day, an increased weight gain in females and males, and no increase in the incidence of tumors. The absence of carcinogenic effects of recombinant GH administered daily for 2 years to rodents was consistent with publications of clinical experience, indicating a lack of convincing evidence for an increased risk of cancer in children receiving human recombinant GH replacement therapy.
Farris GM, Miller GK, Wollenberg GK, Molon-Noblot S, Chan C, Prahalada S.
Department of Safety Assessment, Merck Research Laboratories, West Point, PA 19486, USA. [email protected]
Recombinant rat growth hormone (rrGH) and recombinant mouse growth hormone (rmGH) were developed to evaluate the potential carcinogenicity of each biologically active growth hormone (gh - growth hormone (somatropin) - ) as assessed in the respective species. Biological activities of rrGH and rmGH were demonstrated by showing an increase in body weight gain and serum levels of insulin-like growth factor-1 (IGF-1) in hypophysectomized rats receiving daily sc injections for 6 days. With the exception of pharmacologically mediated weight gain, rrGH and rmGH had no adverse effects in 5-week oral toxicity studies and no production of anti-recombinant GH antibodies. The high doses selected for the carcinogenicity studies provided systemic exposures of GH up to approximately 10-fold over basal levels. In the 105-week mouse carcinogenicity study, daily sc injections of rmGH at 0.1, 0.2, or 0.5 mg/kg/day were well tolerated and had no effects on survival or incidence of tumors. In the 106-week rat carcinogenicity study, daily sc injections of rrGH at 0.2, 0.4, or 0.8 mg/kg/day had a favorable effect on longevity in female rats administered 0.4 or 0.8 mg/kg/day, an increased weight gain in females and males, and no increase in the incidence of tumors. The absence of carcinogenic effects of recombinant GH administered daily for 2 years to rodents was consistent with publications of clinical experience, indicating a lack of convincing evidence for an increased risk of cancer in children receiving human recombinant GH replacement therapy.
If you want to use something like G H or IGF I would choose IGF. It basically achives what G H would in the end but a lot quicker.
Can these drugs cause cancer? Sure they do, it promotes growth so cancer grows too along with muscle.
However, you need to have cancer already or have it in somewhat dormit stage to be activated. I G F does not cause cancer by itself however along with genetic predisposition and environment it can.
Can these drugs cause cancer? Sure they do, it promotes growth so cancer grows too along with muscle.
However, you need to have cancer already or have it in somewhat dormit stage to be activated. I G F does not cause cancer by itself however along with genetic predisposition and environment it can.
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