Triple Negative Breast Cancer The Role Of Metabolic Pathways-Books Pdf

Triple negative breast cancer the role of metabolic pathways
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Malaysian J Pathol December 2014, growth factor receptor 2 HER2 positive disease as expression arrays are becoming more. and will improve survival particularly in those commonplace in defining breast cancer types. that present at an early stage However there The different molecular subtypes of breast. remains approximately 15 percent of breast cancer reflect the expression of distinct gene. cancers that do not overexpress oestrogen patterns The luminal subtypes of breast cancer. receptors OR progesterone receptors PR tend to express hormone receptors and have. or HER2 and therefore do not respond to these properties of luminal epithelial cells such as. targeted therapies Due to their lack of expression expression of low molecular weight cytokeratins. of these three markers they have been termed ERBB2 breast cancer over express HER2 and. triple negative TN breast cancers and are the the normal breast cancer type were found to. subject of this review express genes associated with adipose tissue. and non epithelial cells such as lipoprotein, Triple negative breast cancer lipase and integrin 7 12 13 Basal like breast. cancer BLBC is so named due to expression of,The incidence of TN breast cancer cases in. genes typical of basal myoepithelial cells such,Malaysia is around 17 a rate similar to that. as high molecular weight cytokeratins 12 14 The,found in Western studies 4 Triple negative TN.
consensus is that these types of breast cancer,breast cancers tend to be of a higher grade and. originate from the myoepithelial or basal layer,stage than other breast cancers 5 they also tend. of cells within the duct Cytokeratins CKs are,to have poorer survival and are more likely. intermediate filament proteins that help comprise,to metastasize to distant sites 6 8 Compared to. the mammalian cell cytoskeleton The expression,other breast cancers TN breast cancers occur.
of particular CKs reflects the type differentiation. in a younger age group for example a median,state and function of the epithelial cell The. age of diagnosis of 48 years was reported by,expression of CKs can aid the classification. one group whilst another found that TN breast,of breast cancer 12 13 15 17 For example luminal. cancer was more common in those under the,epithelial cells and therefore breast cancers of. age of 40 8 9,luminal type typically express higher levels.
TN breast cancers are less likely to be,of CKs such as CK7 CK8 CK18 and CK19. diagnosed by screening methods such as,whilst myoepithelial or basal cells tend to. mammography or ultrasound the reasons for,express CK5 6 CK14 and CK17 14 15 However. this could be due to the rapid growth rate of TN,there is a debate as to whether BLBC actually. tumours or differences in tumour density of TN,originate from the myoepithelial basal cells or.
breast cancers compared to other breast cancer,just share a similar phenotype 18 Since molecular. types making their detection more difficult by,profiling is not currently cost efficient and. imaging techniques 10 Currently patients with, feasible to carry out on a large scale in particular. these highly aggressive tumours have a poor,on routine surgical specimens IHC staining of. prognosis with no specific therapy available,the basal CKs such as CK5 6 CK14 and CK17.
for their treatment unlike hormone receptor and,has been found to be an effective alternative to. HER2 positive breast cancer 11 To define TN,identify BLBC 11 16 19 From molecular profiling. breast cancers by markers they do not express,and IHC studies there is an overlap between TN. is an unsatisfactory way of classifying and,and BLBC 56 84 of TN cases express basal. studying these important tumours Fortuitously,markers however not all BLBCs are TN 11 14 20.
expression profiling has identified a group,BLBC like TN breast cancers also tend to be. of breast carcinomas that are to some extent,associated with poorer survival Rakha et al 17. synonymous with triple negative breast cancer,reported similar findings BLBC was associated. in that the majority of them are negative for OR, with the poorest survival rates in both lymph node. PR and HER2,negative and positive cases The development.
of BLBC has been associated with certain,Basal like breast cancer. risk factors for example early menopause, Breast cancers have been traditionally defined by multi parity and not breast feeding following. their histological features i e their appearance childbirth as with TN breast cancer breast. under the microscope when stained with cancer at a younger age was also more likely. haematoxylyin and eosin or by the markers to be BLBC 21. they express with immunohistochemistry,IHC Molecular profiling techniques such. TRIPLE NEGATIVE BREAST CANCER, The role of metabolic pathways in breast cancer syndrome is more common in patients with TN. breast cancers than other breast cancers but it,Obesity is on the increase worldwide particularly.
is yet to be determined whether the metabolic, in western countries and it is estimated that it will. syndrome increases the risk of TN disease 32,increase healthcare costs by around 2 billion. by 2030 in the UK due to the increased risk,of developing diseases such as diabetes heart. Breast cancers with BRCA1 abnormalities tend,disease and cancer 22 Postmenopausal women. to be of the TN basal like phenotype In addition,with a body mass index BMI of over 30 have.
to its tumour suppressor gene function operating,a 31 increased risk of developing breast cancer. through cell cycle controls BRCA1 has also,compared to postmenopausal women with a BMI. been shown to be involved in the regulation,below 25 obese women who develop breast. of fatty acid synthesis through interaction with,cancer also tend to have poorer overall survival. acetyl coA carboxylase ACC 33 BRCA1 binds,and increased breast cancer progression and.
to the phosphorylated or inactive form of ACC,metastasis than women of a healthy weight 23 28. the rate limiting enzyme in fatty acid synthesis,One study reviewed the evidence for the. and stabilises it If BRCA1 is mutated or present,association between obesity and breast cancer and. in low levels ACC is more abundant in its active,proposed the involvement of several pathways. form thus converting acetyl coA to malonylcoA,Increased fat levels or adiposity can increase.
to increase fatty acid synthesis by fatty acid,circulating levels of insulin and insulin like. synthase It has been suggested that women,growth factor I IGF I tumour necrosis factor. with BRCA1 mutations could be treated with,TNF and adipokines such as leptin 28 TNF. diabetic drugs such as metformin or through,is an inflammatory cytokine that is secreted by. calorie deprivation and exercise as this would,adipocytes that can lead to increased expression.
increase AMP activated protein kinase AMPK,of aromatase thus activating hormonal dependent. levels that would in turn inhibit ACC 34 Fatty,tumorigenic pathways Leptin is also secreted by. acid synthase FAS is up regulated in many,adipocytes and regulates food intake by acting. cancers including those of the breast prostate,on the hypothalamus Leptin can act as a growth. and colon 35 FAS expression is associated with,factor in breast cancer cell lines resulting in.
an increased risk of breast cancer reoccurrence36,a more aggressive phenotype 29 30 Lorincz and. and up regulation of FAS confers chemo,Sukumar 2006 used the evidence to propose. resistance down regulation of FAS causing,the mechanisms by which obesity is linked to. breast cancer cell lines to become more sensitive,breast cancer 28 However as the majority of. to chemotherapy drugs 37 38 Insulin like growth,these mechanisms occur through the oestrogen.
factor IGF I has been shown to up regulate,receptor this does not take into account the link. FAS in malignant breast cancer cells and when,between obesity and breast cancers that do not. FAS was suppressed IGF I mediated cell growth,express oestrogen receptors such as TN breast. was inhibited 38,cancers and many HER2 positive tumours. The Warburg effect,Type 2 diabetes,The Warburg effect describes the phenomenon by.
Type 2 diabetes is associated with an increased,which cancer cells rely on aerobic glycolysis for. breast cancer risk insulin resistance leads to,energy rather than oxidative phosphorylation 39. increased levels of circulating insulin that can,The Reverse Warburg effect is based on the. activate signalling pathways such as RAS and,observation that the benign tissue to include. PI3K through the insulin receptor and cause,stromal fibroblasts surrounding cancer cells also.
increased proliferation and decreased apoptosis 31. uses aerobic glycolysis for energy It is postulated. There is some evidence linking other aspects of,that epithelial cancer cells stimulate the. metabolism and TN breast cancer For instance,fibroblasts to undertake aerobic glycolysis and. the metabolic syndrome is a combination of,thus secrete the products lactase and pyruvate. medical disorders such as central obesity,These metabolites would effectively feed the. raised triglyceride levels in the blood and high, cancer cells resulting in increased proliferation 40.
blood pressure which substantially increase an,One study found that human breast cancer. individual s risk of developing heart problems,stromal tissue had features of the Reverse. or diabetes Studies have investigated the,Warburg effect such as inflammation and markers. association of breast cancer with the metabolic,of aerobic glycolysis It suggested that loss of. syndrome and its associated diseases metabolic,Malaysian J Pathol December 2014.
Cav 1 may be a useful biomarker of oxidative breast cancer study using IHC concluded that. stress in the tumour microenvironment 41 Others FABP7 was associated with improved survival. have found that markers associated with the probability 45 another concluded that FABP7 was. Reverse Warburg effect predict a poor outcome associated with poor survival 46 Such differences. in breast cancer patients 42 It has been suggested could be a reflection of the cohorts being selected. that an increase in reactive oxygen species may and differing in size and also in how the. cause mutations in mitochondrial DNA and thus results are interpreted 45 46 In vitro studies have. dysfunctional metabolism at the cellular level 43 shown that FABP7 inhibits cancer cell growth. In addition a recent article highlighted a link overexpressing FABP7 in the MDA MB 231. between glucose metabolism reactive oxygen breast cancer cell line significantly inhibited. species production and Epithelial Mesenchymal cell growth and promoted differentiation 47 This. Transition EMT a feature often associated with effect was synergised with supplementation of. basal like breast cancer 44 the fatty acid docosahexaenoic acid DHA 48. In contrast a study on FABP7 in melanoma, Fatty acid binding proteins cell lines found that down regulating FABP7. expression decreased cell proliferation and,Fatty acids in tissues are frequently bound to. invasion and increased when FABP7 was over,binding proteins which are thought to play a. expressed 49 When tested by IHC in patients,role in their solubilisation transport storage. and metabolism There are 9 fatty acid binding with melanoma the expression of FABP7 was. proteins FABPs all around 15kDa in size with associated with poorer survival and relapse. a barrel tertiary structure that forms a cavity although FABP7 expression was lost when. where FAs bind additionally FABPs have a patients progressed from primary to metastatic. helix loop helix motif which is thought to be disease 50 Loss of heterozygosity of the FABP7. the point of entry for the FAs gene in metastatic melanomas may be responsible. for the loss of FABP7 expression and thus, Fatty acid binding protein 7 improved prognosis 50 In neural glioblastomas.
Fatty acid binding protein 7 FABP7 is also FABP7 is also associated with a poor prognosis. known as brain lipid binding protein BLBP and in animal models dietary supplementation of. FABP B as it was first discovered in the DHA has been found to increase FABP7 mRNA. brain Gene expression analysis shows Fatty in the brain of rats 51 52. acid binding protein 7 FABP7 is frequently FABP3 also called mammary derived growth. overexpressed in BLBC 13 There is conflicting inhibitor MDGI has high sequence homology. with FABP7 and has been shown to be down,evidence as to whether FABP7 expression Fig 1. regulated by IGF I in mutant mice Furthermore,is associated with poor or good prognosis one. FIG 1 A triple negative invasive ductal carcinoma IDC showing strong cytoplasmic and nuclear staining for. FABP7 in the invasive tumour compartment,TRIPLE NEGATIVE BREAST CANCER. it was found that insulin like growth factor II women 59 It is interesting to note that traditionally. IGF II a ligand of the IGF axis expression was the consumption of dairy products has been. inversely correlated with FABP3 expression 53 significantly less in Malaysia than in Western. FABP3 similarly to FABP7 is also thought countries. by some to inhibit cancer cell growth and Low serum IGFBP 3 levels have been. Triple negative breast cancer The role of metabolic pathways Sarah JR DEAN and Anthony RHODES Faculty of Health amp Life Sciences University of the West of England Bristol UK and Department of Pathology University of Malaya Kuala Lumpur Malaysia Abstract The incidence of breast cancer in Malaysia and other Asian countries is on the increase reflecting lifestyle changes some of

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