Breast cancer, the most common cancer in women, is the leading cause of death in women ages 40 to 44 years old

and the second most common killer after lung cancer of women of all ages. Risk factors and possible causes of breast cancer can be classified as reproductive, hormonal, environmental and familial. Although high-risk populations can be identified, the majority of breast cancers occur in women whose only risk are gender and age.

Precipitating factors are those that can be modified. For breast cancer, one of the precipitating factors is reproductive history. Having no children (nullparity) or the first full-term pregnancy after age 30 places a woman at increased risk. The relative risk is higher for the woman who delays childbirth than for the nullparitous woman. Another is radiation exposure. A greater than expected incidence of breast cancer has seen in women exposed to ionizing radiation to the chest. This will result in DNA and RNS structure destruction. The third precipitating factor is alcohol consumption. Several studies have shown an increased risk of breast cancer associated with alcohol consumption of 2 or more drinks per day. The age at which drinking begins, amount and type of alcohol consumed, and duration of consumption and how recent it was appear to be important variables in fully understanding the risk than can be attributed to alcohol. Alcohol appears to increase levels of circulating estrogens and androgens. Heavy alcohol consumption may also be associated with poor nutrition or other environmental factors that may affect general health, access to care, and stage at diagnosis. The last precipitating factors are obesity and dietary fat. The incidence of breast cancer is increased in industrialized countries with a high socioeconomic status and increased consumption of dietary fat, suggesting a relationship. Obesity is associated with an increased risk of breast cancer in postmenopausal women. Most circulating estrogen in postmenopausal women is produced in fat tissue. Dietary fat intake during childhood and adolescence may influence breast cancer risk.

Meanwhile, predisposing factors are those that cannot be modified. One of which is gender. Women are more likely than men to develop breast cancer. In the United States, breast cancer accounts for 32% of all invasive cancers in women and less than 1% of the cancers in men. The second predisposing factor is race or ethnicity. Caucasians are at a higher risk of developing breast cancer. Ethnicity also is associated with risk, with nonwhite women being at lower risk of developing breast cancer but a greater risk of dying from the disease. Age is also another factor that is influential to the occurrence of breast cancer. The incidence of breast cancer increases with age. Most breast cancer cases are diagnosed in women over 40 years old and older, but the majority of cases occur in women over age 50. Family history of cancer or genetics can also predispose one of developing cancer. Women with a family history of breast cancer in one firstdegree relatives have had breast cancer, and is increased further if these diagnoses were at a younger age. In some families, the clustering breast cancer may be accounted for only by chance or possibly from interactions among shared environmental and lifestyle factors not yet understood. Another is if a person has a personal history of cancer. A previous diagnosis of breast cancer increases a womans lifetime risk for developing a second breast cancer in the opposite (contralateral) breast. Estimates are that the relative risk if 4.0 or greater. A previous history of primary ovarian, endometrial, or colon cancer has been associated with an increased risk of breast cancer (relative risk 1.1 to 2.0). The last predisposing factor is menstrual history or hormonal factors. Early onset of menarche (before age 120, late menopause (at 55 or above), and greater total duration of years of regular menses are associated with an increased risk of breast cancer. This increased risk is thought to be due to the total lifetime exposure of the breast to estrogen and progesterone, with fluctuations in cell growth and change in the breast tissues with each ovulatory cycle.

Due to the influences of the precipitating and predisposing factors, chemical carcinogens are inside the system. Endocrine metabolism, although it considered a normal occurrence in the

body, can also influence the occurrence of breast cancer. Normally, endocrine metabolism will lead to the synthesis, distribution and metabolism of the hormone estrogen. Parts of the body will utilize it and the excess will either be eliminated or it can also be used for protection. However, if that does not occur, metabolites will be the result. Said metabolites will lead to the DNA adduct. DNA adduct is a piece of DNA covalently bonded to a cancer-causing chemical. This process could be the start of carcinogenesis. There will also be oxidative damage and lipid peroxidation which could affect the DNA of the cells. There will also be redox imbalance. It is an alteration in the homeostasis which is contributory to carcinogenesis. Altered transcription in the DNA also occurs. Although, research and studies have only hypothesized about it.

The metabolites also lead to estrogen receptor ligand pathway. Estrogen mediates its effects by binding to its receptors, estrogen receptor (ER)-alpha and ER-beta. Because ER- was the first receptor subtype to be identified in the breast, most studies have focused on the biological role of ER- in the mammary gland. It has recently been shown that ER- is also expressed in breast cancer, but its function remains elusive. Classically, ER- is thought to function as a ligandactivated transcription factor. By interacting with estrogen-response elements contained in the promoter region of specific genes, modulation of gene expression ultimately results in the biological effects of estrogen. Extracellular signals can also stimulate ER--mediated transcription in the absence of estrogen. In recent years, emerging evidence has revealed that a role for ER- is to affect gene expression in the absence of direct DNA binding. For example, liganded ER- can influence gene expression by associating with other transcription factors without binding directly to DNA. Despite the clear understanding of the genomic mechanism of estrogen action, it is also postulated that estradiol can exert nongenomic effects on cell biology by interacting with other proteins, including a putative membrane estrogen receptor, growth factor receptors, and intermediate cell signaling molecules.

This will lead to the presence of signal transduction. These pathways mediate the ability of cells to respond to hormonal and environmental stimuli. Diverse and rapid cellular responses to external stimuli may involve proliferation, differentiation, migration or programmed cell death. In the normal cell a tightly regulated cross-talk network between multiple independent and convergent pathways maintains the cell in a specific developmental and functional pathway. Aberrations in these signal transduction pathways can result in cellular transformation cell proliferation and differentiation. Furthermore, experimental evidence suggests that pathway cross-talk augments the tumorigenic and metastatic potential of transformed cells. Additionally, cross-talk between diverse signal transduction pathways appears to play a critical role in the progression and therapeutic resistance of breast cancer.

These occurrence lead to cumulative and epigenetic alterations. These alterations are recognized as significant factors in the development of breast cancers. Epigenetic mechanisms coordinate biological processes such as X-chromosome inactivation, position effect variegation, genomic imprinting, RNA interference, and reprogramming of the genome during differentiation and development leading to gene silencing . Defects in any of these functions may cause human disorders including breast cancer. Epigenetic malfunctions are manifested through aberrant methylation and acetylation of genes and histones involved in normal tissue development to activate or silence gene expression. Consequently, abnormal tissue differentiation and growth may result from the loss of crucial cell adhesion proteins and overexcitation of estrogen receptor pathways. Additionally, migration of abnormal cells is increased. Angiogenesis which nourishes tumor growth and important intracellular signal transduction networks such as those for apoptosis, DNA repair, and detoxification are involved. Thus, numerous molecular processes could go awry because of epigenetic malfunctions. Epigenetic mechanisms are strongly

influenced by environmental factors such as the chemicals in foods. The occurrences of such epigenetic processes, therefore, suggest that individuals should ingest a balanced diet that includes foods which are known to be protective and supportive while avoiding or limiting exposures to the known risk factors for breast cancers.

Because of the two alterations, proto-oncogenes are altered and activated. The tumor suppressor cells, p53, which are supposed to protect the body, are inactivated. Thus, there will be alterations in cell-signaling pathways and loss of apoptosis. With the factors and the alterations that have occurred, there will be overgrowth of cells that line the breast cells. This is called as atypical ductal hyperplasia. The proliferating atypical cells have enlarged, irregular, hyperchromatic nuclei and small nuclei. The said cells will be then mixed with the normal secretory or myoepithelial cells without reaching to a c homogenous population of atypical cells. This includes a continuum of changes ranging from an insignificant increase in cellularity to features characteristics of ductal carcinoma in situ. This is now what can be called as stage 0 of breast cancer. Meaning the tumor is in place, there is no regional lymph node metastasis nor is there distant metastasis.

If stage 0 is not diagnosed, the carcinoma breaks the boundary of the milk ducts of the breast. The cancer cells then spread into other parts of the breast and become invasive. From stage 0, the disease has progressed to invasive ductal carcinoma. This is stage 1 of cancer. In stage 1 cancer, the tumor is 2 centimeters or less in greater dimension. Theres no regional lymph node metastasis nor is there distant metastasis. Stage 1 is divided into two subcategories. The first of which is Stage 1A which is described as invasive breast cancer in which the tumor measures up to 2 centimeters and the cancer has not spread outside the breast; no lymph nodes are involved. The other is stage 1B which is describes as invasive breast cancer in which there is no tumor in the breast; instead small groups of cancer cells larger than 0.2 millimeter but not larger than 2 millimeters are found in the lymph nodes or there is a tumor in the breast that is no larger than 2 centimeters, and there are small groups of cancer cells larger than 0.2 millimeter but not larger than 2 millimeters in the lymph nodes. If stage 1 is diagnosed and treated with either surgery, radiation therapy, chemotherapy, hormone therapy, biological therapy and clinical trials, the prognosis will be good. However, if this stage is not diagnosed nor treated, it will proceed to stage 2 breast cancer. Stage 2 breast cancer is divided into two subcategories. The first of which is stage 2A. It can be described as invasive breast cancer in which no tumor can be found in the breast, but cancer cells are found in the lymph nodes in the axillary area or the tumor mreasure up to 2 centimeters or smallers and has spread to the axillary lymph nodes. It can also bre described as cancer in which the tumore is larger than 2 centimeters but not larger than 5 centimeters and has no spread to the axillary lymph nodes. The other subcategory is Stage 2B in which the tumor is larger than 2 centimeters but no larger than 5 centimeters and has spread to the axillary lymph nodes. Or it could also be that the tumor is larger than 5 centimeters but has not spread to the axillary lymph nodes. In this stage, overall, the cancer cells has spread into the axillary lymph nodes. If stage 2 cancer can be diagnosed and treated with surgery, radiation therapy, chemotherapy, hormone therapy, biological therapy and clinical trials, the prognosis is good. However, if not, the disease will progress into stage 3 cancer. Stage 3 cancer has 3 subcategories. The first of which is Stage 3A in which either no tumor is found, but cancer is found in axillary lymph nodes, which are clumped together or sticking to other structures, or cancer may have spread to lymph nodes near the breastbone or the cancer is any size and has spread to axillary lymph nodes, which are clumped together or sticking to other structures. Stage 3B on the other hand is described as invasive cancer in which the cancer may be any size

and has spread to the chest wall and/or skin of the breast AND may have spread to axillary lymph nodes, which are clumped together or sticking to other structures, or cancer may have spread to lymph nodes near the breastbone. The last subcategory is stage 3C wherein there may be no sign of cancer in the breast or, if there is a tumor, it may be any size and may have spread to the chest wall and/or the skin of the breast AND the cancer has spread to lymph nodes above or below the collarbone AND the cancer may have spread to axillary lymph nodes or to lymph nodes near the breastbone. In stage 3, cancer cells have spread to the axillary lymph nodes and are clumped together or sticking to other structures. The said cells will also spread to the chest wall, breast bone and below the collar bone. If this can be diagnosed and be treated with radiation and chemotherapy, the prognosis is fair. If not, the disease will progress to the last stage of breast cancer, stage 4. Stage IV describes invasive breast cancer that has spread beyond the breast and nearby lymph nodes to other organs of the body, such as the lungs, distant lymph nodes, skin, bones, liver, or brain. With this stage, metastasis occur to the nearest organs. Since axillary lymph nodes have been involved, the cancer cells will now metastasize to the spine. When the spine is already in the said organ, the cancer cells will stimulate the production of osteoclasts in the spine. Osteoclasts are cells that nibble and break down bone and are responsible for bone resorption. This will lead to bone breakdown. Since there is now a break in the bone, growth factors within the bone is released. There will now be interaction between the breast cancer cells and bone caignite a vicious cycle of increased bone destruction. Due to the release of growth factors in the bone, the tumor will have a conducive environment for tumor growth. Because of the growing tumor, the spine will experience stress. Soon, there will be spinal fracture. The tumor will still continue to grow because it has sufficient nutrition. The growing tumor will now place increased pressure on the spinal cord resulting to cord compression. Due to cord compression, the nerves at the lower extremities are affected. Specifically those that control motor, bowel and bladder function. This will lead to hemiplegia. Together with the paralysis of the lower extremities, bladder distention and loss of rectal sphincter tone will occur. This will predispose the client into developing AUTONOMIC DSYREFLEXIA. The most common cause of autonomic dysreflexia (hyperreflexia) is a distended bladder or rectum. But, any sensory stimulation can elicit this condition. There will be stimulation of sensory receptor below the level of the cord injury. The intact peripheral sensory nerves transmit impulses that ascend in the spinothalamic and posterior columns. Sympathetic neurons located in the intermediolateral gray matter of the spinal cord is stimulated. The inhibitory outflow above the injury from the cerebral vasomotor centers is then increased thereafter. But unfortunately, it will be unable to pass below the block of spinal injury. This large sympathetic outflow causes release of various neurotransmitters. This will result into piloerection, skin pallor and severe vasoconstriction in arterial vasculature. The intact autonomic nervous system then reflexively responds with an arterial spasm. There will be elevation in blood pressure and vasodilation above the level of injury. Due to vasodilation of pain-sensitive intracranial vessels, the client with autonomic dysreflexia will have headacge. The vasomotor brainstem reflexes attempt to lower blood pressure by increasing parasympathetic stimulation to the heart through the vagus nerve. The heart rate then decreases (BRADYCARDIA). However, the visceral and peripheral vessels do not dilate because the efferent impulses cannot pass through the cord. If the condition is treated with decompression and surgical fixation of the spine, corticosteroids, 21-aminosteroid tiriliad, opiate antagonist naloxone, Ca channel blockers, glutamate receptor blockers, growth-promoting and growth-inhibiting factors, nutrition, lung function, skin integrity and bladder and bowel management, rehabilitation and elevation of the head of the bed, the prognosis could either be good or fair. However if it cannot be treated, there will be complications that shall worsen the clients condition. These are cerebrovascular accident, severe peripheral hypertension, retinal or cerebral hemorrhage, myocardial infarction and seizures. If not managed well, it will end with death.