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Friday, November 4, 2011

breast cancer

Breast cancer is a cancer of the breast tissue. This is the most common type of cancer suffered by women. Men can also develop breast cancer, although less likely than 1 in 1000 [citation needed]. The most common treatment is with surgery and if necessary followed by chemotherapy or radiation.
Devinitions 
Cancer is a condition where the cells have lost normal control mechanisms, so that experienced abnormal growth, rapid and uncontrolled. [1]

table of contents


    
In addition, breast cancer (mammary carcinoma) is defined as a disease of malignant neoplasm derived from the parenchyma. The disease is by the Word Health Organization (WHO) is inserted into the International Classification of Diseases (ICD) with code number 17. [2]
  
Patofisiologi  
Some types of breast cancers often show dysregulation of hormones HGF and Met oncogenes, and excess expression of enzymes TOD-6. [3]
  
Transformasi  
Cancer cells are formed from normal cells in a complicated process called transformation, which consists of initiation and promotion stages.

Phase initiationAt the initiation stage occurs a change in the genetic material of cells that provoke cell becomes malignant. Changes in the genetic material of cells is caused by an agency called carcinogens, which could be chemicals, viruses, radiation (radiation) or sunlight. But not all cells have the same sensitivity to a carcinogen. Genetic abnormalities in cells or other substances, called promoters, causing the cells more susceptible to a carcinogen. Even the physical disturbance menahunpun can make cells more sensitive to experience a malignancy.
Progesterone, a hormone that induces ductal side-branching in the mammary gland and breast epithelial cells lobualveologenesis the estimated trajectory acts as an activator in breast cell tumorigenesis induced by carcinogens. Progestin will induce transcription of cell cycle regulators cyclin D1 to secreted epithelial cell. Secretion can be increased approximately 5 to 7-fold by estrogen stimulation, [4] because estrogen is a hormone that activates the expression of progesterone on perceiving epithelial cells. [5] In addition, progesterone also induces calcitonin secretion gland morphogenesis and luminal cells. [6 ]
 

Phase promotionsAt the stage of promotion, a cell that has undergone initiation to become malignant. Cells that have not passed the stage of initiation is not affected by the promotion. Because it takes several factors to the occurrence of malignancies (combination of sensitive cells and a carcinogen). 

Phase metastasisMetastasis to the bone is that often occurs in breast cancer, some of which are accompanied by other complications such as simtoma hypercalcaemia, pathological fractures or spinal cord compression. [7] so are osteolytic metastases, which means that osteoclast induction of cancer cells is a mediator osteolysis and influence differentiation and activity of osteoblasts and osteoclasts others to increase bone resorption.
Bone is made of a unique tissue matrix protein with calcium-containing crystals hydroxyappatite so that the mechanism used by cancer cells to make space on the extracellular matrix with the use of matrix metalloproteinase enzymes are not effective. Therefore, allowing the invasion of bone resorption occurs as a result of interaction between neoplastic breast cancer cells with endothelial cells is mediated by VEGF expression. [7] VEGF is an angiogenic mitogen that react positively with endothelial cells. Without the negative angiogenic factors such as angiostatin, endothelial cells that interact with cancer cells through the perceiving VEGF VEGFR-1 and VEGFR-2, will shed the extracellular matrix, migrate and form tubules

ClassificationThere are several types of cancer cells that can terkultur in breast cancer, namely MCF-7 cells, T-47D cells, cells MDA-MB-231 cells, MDA-MB-468 cells, BT-20 and BT-549 cells. 

HistopathologyBased on the WHO histological classification of breast tumors, breast cancers are classified as follows:

   
1. Non-invasive carcinoma
          
* Non-invasive ductal carcinoma
          
* Lobular carcinoma in situ
   
2. Invasive carcinoma
          
* Invasive ductal carcinoma
                
o Papilobular carcinoma
                
o Solid-tubular carcinoma
                
o Scirrhous carcinoma
                
Special types o
                
o Mucinous carcinoma
                
o Medulare carcinoma
          
* Invasive lobular carcinoma
                
o adenoid cystic carcinoma
                
o squamos cell carcinoma
                
o The spindle cell carcinoma
                
o Apocrin carcinoma
                
o Carcinoma with metaplasia of cartilage or osseous metaplasia
                
o Tubular carcinoma
                
o secretory carcinoma
                
o Other
   
3. Paget's Disease
StadiumStaging of cancer is a condition of appraisal physicians when diagnosing a disease suffered by cancer patients, which have so far is a good rate of spread of cancer into surrounding organs or tissues or spread elsewhere. Stadium is only known to a malignant tumor or cancer and in benign tumors do not exist. To determine the stage, must be supported by clinical examination and other investigations of histopathology or PA, x-rays, ultrasound, and if possible with a CT scan, scintigrafi, etc.. Lots of ways to determine the stage, but the most widely adopted today is the stage of cancer based on TNM classification system recommended by the UICC (International Union Against Cancer of the World Health Organization) / AJCC (American Joint Committee On Cancer, sponsored by the American Cancer Society and American College of Surgeons). 

TNM SystemTNM is an abbreviation of "T" is the tumor size or the size of the tumor, "N" is the node or regional lymph nodes and "M" that is distant metastasis or spread. These three factors T, N, and M assessed both clinically prior to surgery, even after surgery and histopathologic examination (PA). In breast cancer, TNM assessment as follows:

    
* T (tumor size), tumor size:
          
o T 0: can not find a primary tumor
          
o Q 1: The size of the tumor diameter of 2 cm or less
          
o T 2: the size of the tumor diameter of 2-5 cm
          
o Q 3: The size of the tumor diameter> 5 cm
          
o Q 4: tumor size whatever, but there have been spread to the skin or chest wall or on both, may be ulcers, edema or swelling, redness of breast skin or a small lump on the skin outside the main tumor
    
* N (node), regional lymph nodes (KGB):
          
o N 0: no metastases in regional lymph nodes in the armpit / axilla
          
N o 1: there is metastasis to the axilla lymph nodes that can still be driven
          
o N 2: there is metastasis to the axilla are difficult KGB driven
          
N o 3: no metastasis to lymph nodes above the collarbone (supraclavicula) or the internal mammary lymph nodes in the bone near the sternum
    
* M (metastasis), distant spread:
          
o M x: distant metastasis can not be assessed
          
o M 0: no distant metastasis
          
o M 1: there are distant metastases
After each factor of T, N, and M obtained, three factors are then combined and stage of cancer will be obtained as follows:

    
* Stage 0: T0 N0 M0
    
* Stage 1: T1 N0 M0
    
* Stage IIA: T0 N1 N1 M0/T1 M0/T2 N0 M0
    
* Stage II B: T2 N1 M0 / T3 N0 M0
    
* Stage IIIA: T0 M0/T1 N2 N2 N2 M0/T2 M0/T3 M0/T2 N1 N2 M0
    
* Stage III B: T4 N0 M0 M0/T4 N1 N2 M0/T4
    
* Stage III C: Any T N3 M0
    
* Stage IV: Any T, Any N, M1
GeneticDNA micro-arrayDNA micro-array is a method that begins by comparing normal cells with cancer cells and see the differences that occur in genetic expression between the two cell types. Although differences in genetic expression are not necessarily indicate the hallmark of cancer cells oncogenes, but some researchers consider that the group some of the group / cluster of genes have a tendency to leave genetic traces occur in other cells to the same genetic expression, called a genetic profile. Thus, the dynamics of functional genes and genomes can be observed as the process of transcription of mRNA, identification of binding domains of protein nucleic acid, single-nucleotide polymorphism analysis. [8]
A number of genetic profiles have been proposed by various parties, some of which are:

    
* Genetic Profile of the American Society of Clinical Oncology which offers a classification based on CA 15.3, CA 27.29, CEA, perceiving estrogen, progesterone perceiving, perceiving the epidermal growth factor-2, urokinase plasminogen activator, plasminogen activator inhibitor 1. [9] The use of the following categories as basic diagnostics are also considered not enough; DNA / ploiditas with the use of flow cytometry, p53, cathepsin D, cyclin E, certain multiparameter assays, detection of micro-metastases in the bone marrow and the levels of tumor cells in blood circulation.
    
* Profile of genetic-called normal breast-like, basal, luminal A, luminal B, and ERBB2 +. [10]
    
* Subtypes based on the profile ESR1/ERBB2 ESR1 + / ERBB2-, ESR1-/ERBB2-, and ERBB2 +. [10]
Profile intrinsic Perou-SørlieFrom the standpoint of histology, breast tumor cells is a complex network consisting of various cell types in addition to cancer cells. [11] To obtain a genetic profile of a tumor, note the typical genetic expression of each cell that is the result of transcription of certain gene clusters, and then sought similarity clusters in other cells of different types.
On the intrinsic profile, found eight genetic clusters which is a variation of certain cells found in the tumor.

   
1. Endothelial cells. A cluster of genes is a hallmark of the genetic expression of endothelial cells, such as CD34, CD31, von Willebrand factor, both endothelial cells from cultured HUVEC and HMVEC.
   
2. Stromal cells. Protein expression of stromal cell is the genetic clusters identified in advance and include several isomers of collagen
   
3. Normal breast cells and adipose-rich with genetic clusters include fatty-acid binding protein 4 and PPAR
   
4. B cells, leaving a trail of such genetic form of the protein immunoglobulin gene expression during infiltration and provide variation in genetic clusters as in the expression of cell culture RPMI-8226 multiple myeloma.
   
5. T cells also left a genetic imprint that be an indication of infiltration activity. A geneteik clusters include cluster of differentiation and 2 subunits CD3 T cells found in the perceiving MOLT-4 cells from the culture of childhood leukemia.
   
6. Makrofaga. A genetic clusters that appeared to be the hallmark of makrofaga / monocytes are the expression of CD68, acid phosphatase 5, chitinase and lysozyme.
There are two types of epithelial cells in these glands, namely basal cell or cell mioepitelial, and luminal epithelial cells. Many genes are only owned by one of these cell types and are rarely found genes that are owned by the two cells. Genetic clusters include basal cell keratin-5, keratin-17, integrin-4 and laminin. While the luminal cell genetic clusters include transcription factors associated with perceiving the estrogen-binding protein such as GATA-3, X-box binding protein-1 and hepatocyte nuclear factor-3. 

Panorama of oncogenicClassification according to the oncogenic trajectory is divided into 4 subtypes are called

    
* Luminal A expression accompanied perceiving hormones, either estrogen, progesterone, or both, and without expression of HER-2 (English: human epidermal growth factor receptor 2). At the luminal A subtype, occurring over-expression of proteins that play a role in the trajectory of fatty acid metabolism and cellular signal transduction path using steroids, in particular through perceiving the expression of estrogen. [12]
    
* Luminal B by the perceiving hormone +, HER-2 +.
    
* Triple negative with perceiving hormone -, HER-2 -.
    
* HER-2 over-expressing the pengecerap hormone -, HER-2 +.
Based on this classification, the sampling results from 2544 cases in the U.S., 73% was found to suffer from the luminal subtype A, 12% of patients with luminal B, 11% were triple negative cancers and 4% is the kind of HER-2 over-expressing. [13]
Several other experts added subtypes such as;

    
* Basal-like system with excess expression of proteins that play a role in cell proliferation and differentiation, p21 trajectory and signal transduction in the cell cycle checkpoint between G1 phase and S phase [12]
    
* Basal trajectory A with ETS and the BRCA1 gene. [14]
    
* Basal B with trajectories mesenchymal cells and / or stem cells / progenitor cells
Clinical PresentationClinical symptoms of breast cancer may include: 

Lumps in the breastGenerally a lump that is not pain in the breast. The lump was initially small, the longer it will be even greater, and then attached to the skin or cause changes in the skin of the breast or the nipple.

Erosion or nipple eczemaSkin or nipple had become interested in (retracted), pink or brownish edema until it becomes to look like an orange peel skin (peau d'orange), contract, or arising out ulcers (ulcers) in the breast. Borok the longer it will be even greater and deeper so that it can destroy the entire breast, often malodorous, and bleed easily. Other features include:

    
* Bleeding on the nipple.
    
* Pain or aches in general only emerged when the tumor was large, had ulcers arise, or when it appears metastases to the bones.
    
* Then there enlarged lymph nodes in the armpit, swelling (edema) on the arm, and the spread of cancer throughout the body (Handoyo, 1990).
Advanced breast cancer is very easily recognizable by knowing operbilitas Heagensen criteria as follows:

    
* There is extensive edema of the breast skin (over 1 / 3 area of ​​breast skin);
    
* Presence of satellite nodules on the skin of the breast;
    
* Type of breast cancer karsinimatosa mastitis;
    
* There parasternal model;
    
* There is a supraclavicular nodule;
    
* Presence of arm edema;
    
* Presence of distant metastases;
    
* And there are two of the signs of locally advanced, namely skin ulceration, skin edema, skin fixed to the wall of the thorax, axillary lymph node 2.5 cm in diameter, and axillary lymph nodes attached to each other.
The exit of the fluid (Nipple discharge)Nipple discharge is a discharge from the nipple spontaneously and not normal. The liquid that comes out is called normal if it occurs in women who are pregnant, nursing, and contraceptive pill users. A woman should be wary if the nipple discharge of bloody watery liquid with red or brown, out on his own without having to massage the nipple, continues, only in one breast (unilateral), and liquids other than breast milk. 

The factors causing 

Risk factorsAccording Moningkey and Kodim, the specific causes of breast cancer is still unknown, but there are many factors that are estimated to have an influence on the occurrence of breast cancer include:

   
1. Reproductive factors: reproductive characteristics associated with risk of breast cancer is nuliparitas, menarche at a young age, menopause at an older age, and first pregnancy at older age. The main risk of breast cancer is increasing age. It is estimated, the period between the first occurrence of menstruation by age at first pregnancy is a window of initiation of breast cancer progression. Anatomically and functionally, will experience breast atrophy with age. Less than 25% of breast cancers occur in the period before the onset of menopause so that the tumor is estimated to occur well before the occurrence of clinical change.
   
2. The use of hormones: estrogen hormone associated with the occurrence of breast cancer. Reports from the Harvard School of Public Health states that there is a significant increase in breast cancer in users of estrogen replacement therapy. A meta-analysis stated that although there is no risk of breast cancer in users of oral contraceptives, women taking this drug for a long time have a high risk to develop breast cancer before menopause. The cells are sensitive to hormonal stimulation may experience changes in benign or become malignant degeneration [15].
   
3. Fibrocystic Disease: In women with adenosis, fibroadenoma, and fibrosis, there is no increased risk of breast cancer. In hiperplasis and papilloma, slightly increased risk of 1.5 to 2 times. While in atypical hyperplasia, the risk increases to 5 times.
   
4. Obesity: There is a positive relationship between body weight and body shape with breast cancer in postmenopausal women. Variation of the frequency of this cancer in Western countries and not the West as well as the frequency changes after migration indicates that there is the influence of diet on the occurrence of this malignancy.
   
5. Consumption of fat: fat consumption is estimated as a risk factor for breast cancer. Willett et al. conduct during the 8-year prospective study of consumption of fat and fiber in relation to risk of breast cancer in women aged 34 to 59 years.
   
6. Radiation: Exposure to ionizing radiation during or after puberty increases the risk of breast cancer. Of the few studies conducted concluded that radiation-related cancer risk linearly with dose and time of exposure age.
   
7. Family history and genetic factors: Family history is an important component in the history of the patient to be carried out screening for breast cancer. There is an increased risk of malignancy in women whose family had breast cancer. In genetic studies found that breast cancer associated with specific genes. If there is BRCA 1, which is a breast cancer susceptibility gene, the probability of occurring breast cancer by 60% at age 50 years and by 85% at age 70 years. Age factors are very influential -> about 60% of breast cancers occur in the age of 60 years. The greatest risk of age 75 years [16]
Genetic Factorscancer can occur because of some genetic factors are inherited from parent to child. Genetic factors in question is the presence of mutations in several genes that play an important role in the formation of breast cancer gene in question is some of the genes are oncogenes and tumor suppression genes that nature.
Pensupresi tumor gene plays an important role in the formation of breast cancer include BRCA1 and BRCA2 genes. 

Treatment of cancerThere are several breast cancer treatment whose application depends a lot on the stage of clinical disease (Tjindarbumi, 1994), namely: 

MastectomyMastectomy is the surgical removal of the breast. There are three types of mastectomy (Hirshaut & Pressman, 1992):

    
* Modified Radical Mastectomy, ie surgical removal of the entire breast, breast tissue in the sternum, collarbone and ribs, as well as lump around the armpit.
    
* Total (Simple) Mastectomy, which is surgical removal of the entire breast, but not the glands in the armpit.
    
* Radical Mastectomy, ie surgical removal of part of the breast. Usually called a lumpectomy, which is removal of only the tissue containing cancer cells, not the whole breast. This operation is always followed by the provision of radiotherapy. Lumpectomy is usually recommended in patients with large tumors less than 2 cm and located at the edge of the breast. 

RadiationRadiation / radiation is the process of irradiation to the affected area of ​​cancer using X-rays and gamma rays are aimed at killing cancer cells remaining in the breast after surgery (Denton, 1996). The effect of this treatment the body becomes weak, poor appetite, the color of the skin around the breast to black, as well as hemoglobin and leukocytes tended to decline as a result of radiation. 

ChemotherapyChemotherapy is the process of anti-cancer drugs or sitokina in pill or capsule or liquid through an IV that aims to kill cancer cells through the mechanism of chemotaxis. Not only in breast cancer cells, but also throughout the body (Denton, 1996). The effect of chemotherapy is that patients experience nausea and vomiting and hair loss due to the influence of drugs given during chemotherapy. 

Paths of metabolismAcid is a bisphosphonate compound inhibiting osteoclast activity and bone resorption are often used to fight osteoporosis induced by ovarian suppression, hypercalcemia, and abnormalities of bone metabolism, demonstrated effectiveness to reduce breast cancer cell metastasis to bone. [17] Although bisphosphonates are generally well tolerated acid intake body, long-term use can cause side effects such as osteonecrosis and declining renal function. [18]
CT can induce breast cancer cells to produce cAMP and inhibit cancer cell growth. [19] The molecule cAMP is formed from the expression that connects the perceiving CT adenylate cyclase by at least one fruit guanine nucleotide-binding protein. CAMP response to CT can be decreased when the cells terinkubasi mitogenic compounds in the form of 17beta-estradiol and EGF, and increased as the incubation period of growth inhibitory compounds such as tamoxifen and 1,25 (OH) 2D3; as well as oligonucleotides and proto-oncogene c-myc. However, the use of tamoxifen increases the risk of endometrial polyps, hyperplasia and cancer, through the mechanism of adrenomedullin. [20]
The response of cAMP production is strong, not found in compounds other than CT. Adenylate cyclase effector compounds such as forskolin and compound beta-adrenergic receptor agonist such as isoproterenol produces only a little cAMP production.
In cells MDA-MB-231, CT would induce phosphorylation of c-Raf at Serina position 259 through the trajectory of protein kinase A and causes the inhibition of phosphorylation of ERK1 / 2 is required for cell viability of MDA-MB-231, [21] and inhibits the expression the necessary UPA mRNA cells MDA-MB-231 for the invasion and metastasis. [22] Nevertheless calcitonin had no effect signifan to inhibit proliferation of MCF-7 cells. Apoptotic cells MDA-MB-231 also induced by lipoic acid which inhibits phosphorylation of AKT and AKT mRNA, the activity of Bcl-2 and Bax protein, MMP-9 and MMP-2, [23] and increased activity of caspase-3. [24] 

Strategy of preventionIn principle, prevention strategies are grouped into three major groups, namely the prevention of the environment, the host, and milestones. Almost every epidemiologist agreed that the most effective prevention for the incidence of non communicable diseases are health promotion and early detection. Similarly, in breast cancer, prevention is carried out such as: 

Primary PreventionPrimary prevention of breast cancer is one form of health promotion because it is done in people who are "healthy" through efforts to avoid exposure to various risk factors and implement a healthy lifestyle. Pencagahan this primer can also be a breast self examination (breast self-examination) is done regularly so that it can reduce breast cancer risk factors. [25] 

Prevention of secondarySecondary prevention conducted on individuals who are at risk for developing breast cancer. Every normal woman and have a normal menstrual cycle is the population at risk of breast cancer. Secondary prevention was done by early detection. Several methods of early detection continues to experience growth. Screening by mammography is claimed to have accuracy of 90% of all breast cancer patients, but continuous exposure to mammography in healthy women is one risk factor for breast cancer. Therefore, screening with mammography can still be carried out by several considerations, among others:

    
* Women who have reached the age of 40 years are encouraged to do the cancer risk assessement survey.
    
* In women with risk factors received a referral for a mammogram done every year.
    
* Women normally get a referral mammography every 2 years until they reach the age of 50 years.
Foster and Constanta found that breast cancer mortality by less in women who perform BSE (Breast Self-Examination) than those without. Although the sensitivity of BSE to detect breast cancer only 26%, when combined with mammography is early detection sensitivity to 75% 

Prevention of tertiaryTertiary prevention is usually directed at individuals who have positive breast cancer. Proper treatment of breast cancer patients according to the stage is going to be able to reduce kecatatan and prolong survival. Tertiary prevention is essential to improve the quality of life of patients and prevent complications of the disease and continue treatment. Measures of treatment may include surgery, although no effect on patient survival. If the cancer has distant metastatic disease, chemotherapy with sitostatika action. At a certain stage, the treatment provided was only for symptomatic and are encouraged to seek alternative treatment.

footnotes

  1. ^ (http://www.mediasehat.com/utama07.php)
  2. ^ (http://www.tempo.co.id/medika/arsip/082002/pus-3.htm)
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  4. ^ (Inggris)"Progesterone, in addition to estrogen, induces cyclin D1 expression in the murine mammary epithelial cell, in vivo.". Department of Cell Biology, Baylor College of Medicine; Said TK, Conneely OM, Medina D, O'Malley BW, Lydon JP.. http://www.ncbi.nlm.nih.gov/pubmed/9275084. Diakses pada 23 Juli 2011. 
  5. ^ (Inggris)"Progesterone action in normal mouse mammary gland.". Physiology Department, Michigan State University; Wang S, Counterman LJ, Haslam SZ.. http://www.ncbi.nlm.nih.gov/pubmed/2226309. Diakses pada 23 Juli 2011. 
  6. ^ (Inggris)"Progesterone induction of calcitonin expression in the murine mammary gland.". Department of Molecular and Cellular Biology, Baylor College of Medicine; Ismail PM, DeMayo FJ, Amato P, Lydon JP.. http://www.ncbi.nlm.nih.gov/pubmed/14765981. Diakses pada 23 Juli 2011. 
  7. ^ a b (Inggris) "Vascular endothelial growth factor acts as an osteolytic factor in breast cancer metastases to bone". The School of Surgical Sciences, The Medical School, Framlington Place, University of Newcastle; S E Aldridge, T W J Lennard, J R Williams, dan M A Birch. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362001. Diakses pada 16 Juli 2011. 
  8. ^ (Inggris) "Expression genomics in breast cancer research: microarrays at the crossroads of biology and medicine". Genome Institute of Singapore; Lance D Miller dan Edison T Liu. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1868923. Diakses pada 21 Juli 2011. 
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  12. ^ a b (Inggris) "Distinct molecular mechanisms underlying clinically relevant subtypes of breast cancer: gene expression analyses across three different platforms.". Department of Genetics, Institute for Cancer Research, Rikshospitalet-Radiumhospitalet Medical Center; Sørlie T, Wang Y, Xiao C, Johnsen H, Naume B, Samaha RR, Børresen-Dale AL.. http://www.ncbi.nlm.nih.gov/pubmed/16729877. Diakses pada 21 Juli 2011. 
  13. ^ (Inggris) "Breast Cancer Risk Factors Vary by Tumor Subtype". BREASTCANCER.ORG. http://www.breastcancer.org/risk/new_research/20090522.jsp. Diakses pada 21 Juli 2011. 
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  20. ^ (Inggris) "Adrenomedullin and tumour angiogenesis". Nuffield Department of Obstetrics and Gynaecology, Nuffield Department of Clinical Laboratory Sciences, Molecular Angiogenesis Laboratory, Cancer Research UK, Weatherall Institute of Molecular Medicine, The University of Oxford, John Radcliffe Hospital, Institute for Biomedical Research, Birmingham University Medical School; L L Nikitenko, S B Fox, S Kehoe, M C P Rees, dan R Bicknell. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361077. Diakses pada 17 Juli 2011. "The increased risk of endometrial polyps, hyperplasia and cancer in women receiving tamoxifen treatment for breast cancer prompted our group to look for genes induced in endometrial isolates by tamoxifen, but not oestrogen. PCR differential display identified the vasoactive peptide adrenomedullin (AM) as one such gene." 
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  25. ^ [3]

1 comment:

  1. All thanks to this great herbal doctor who cured me from (LUPUS DISEASE) his name is dr imoloa.  I suffered lupus disease for over 8 years with pains like: joints, Skin rash,  Pain in the chest,  swollen joints and many more.  The anti-inflammatory drugs couldn’t cure me, until I read about his recommendation. 2 months ago, I contacted him through his email address. drimolaherbalmademedicine@gmail.com . and he sent me the herbal treatment through DHL courier service and he instructed me on how to drink it for good two weeks. after then,  And I was confirmed cured and free at the hospital after taken his powerful herbal medications You too can be cured with it if interested, he also uses his powerful herbal healing medicine to cure disease like:parkison disease, vaginal cancer, epilepsy,  Anxiety Disorders, Autoimmune Disease,  Back Pain,  Back Sprain,   Bipolar Disorder,  Brain Tumour,  Malignant,  Bruxism, Bulimia,  Cervical Disk Disease, cardiovascular disease, Neoplasms,  chronic respiratory disease,  mental and behavioural disorder,  Cystic  Fibrosis,  Hypertension, Diabetes, asthma,  Inflammatory autoimmune-mediated arthritis.  chronic kidney disease, inflammatory joint disease, back pain,  impotence,  feta  alcohol spectrum,  Dysthymic Disorder,   Eczema, skin cancer,  tuberculosis,  Chronic Fatigue Syndrome, constipation, inflammatory bowel  disease, bone cancer, lungs cancer,  mouth ulcer,  mouth cancer, body pain, fever, hepatitis A.B.C.,   syphilis,  diarrhea,  HIV/AIDS,  Huntington's Disease,  back acne,  Chronic renal failure,   addison disease,  Chronic Pain,   Crohn's  Disease,   Cystic Fibrosis,  Fibromyalgia,   Inflammatory Bowel Disease,  fungal  nail disease, Lyme Disease, Celia disease, Lymphoma, Major  Depression,  Malignant Melanoma,   Mania,  Melorheostosis,   Meniere's  Disease,  Mucopolysaccharidosis , Multiple Sclerosis,  Muscular  Dystrophy,  Rheumatoid Arthritis, Alzheimer's Disease      Contacts him today  and get permanently cure. contact him via... email- drimolaherbalmademedicine@gmail.com  /whatssapp-+2347081986098.

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