Etiology of Pancreatic Cancer
Pancreatic cancer has emerged as the most lethal human cancers. In fact, the World Health Organization (WHO) has termed it an unresolved health problem of the 21st century. The disease presently causes about 30,000 deaths in the U.S. per year (Yarbro et al. 2015). Despite past efforts, conventional interventions like radiation, surgery, chemotherapy and combination of these had minimal success in the course of this aggressive disease. It is imperative to develop an in-depth understanding of the molecular biology of pancreatic cancer to help us effectively diagnose, prevent and treat the disease. Nearly all pancreatic cancer patients experience metastases and die due to the frustrating metabolic effects of their unrestrained growth (Shrikhande et al. 2010). Hence, a crucial requirement for progress is the establishment of effective systemic interventions, can reverse the aggressive biology of the disease.
According to the WHO, pancreatic cancer is the fifth most common form of cancer in the United States (Reber, 2010). For this reason, such a vital disease must be understood. Throughout this essay, there will be various discussions relating to the disease, in an attempt to offer better insight into it. First, the essay begins with the causes of pancreatic cancer followed by pathophysiology and the clinical manifestations. The study also covers sections on signs and symptoms resulting from altered pathophysiology. Some diagnosis options and current intervention strategies for tackling the disease are also identified.
Causes of Pancreatic Cancer
Pancreatic cancer is argued to result from damage to the DNA. Often, this damage is commonly known as mutations. These mutations could either be inherited from parents or acquired, as a person grows old (Reber, 2010). A good number of people with genetic pancreatic cancer tend to inherit one mutant copy and one intact copy of a cancer-related gene. As the people with genetically acquired cancer syndrome age, some will experience damages to the good copy of the gene in one of their pancreatic cells. The cell will have two damaged copies of the gene: an inherited and an acquired gene. Consequently, this pancreatic cell will start to develop abnormally and will eventually form cancer (Neoptolemos, 2010). This means that not all people with an inherited predisposition are likely to develop cancer. On the contrary, because persons with a hereditary cancer syndrome tend to have only one good copy of the cancer-related gene, they are highly prone to acquire cancer. For those with a genetic subjection to pancreatic cancer, it means, if something wrong happens to the only good gene, then, they will be in trouble.
Sometimes, the DNA can be damaged accidentally. Probably, the WHO believes that this is the least fulfilling explanation. However, it is true. Each of the human body cells contains two copies of the 23 chromosomes, and the resulting 46 chromosomes carry billions of DNA base pairs (Neoptolemos, 2010). As the cell divides, it must copy the entire DNA. The cell machinery used to copy the DNA might not be perfect. At times, it makes errors when copying the DNA (Yarbro et al. 2015). It is good from the angle of a species or population because such faults permit evolution to take place. However, since one of such chance errors in DNA, copying damages key cancer-related genes in one of the pancreatic cells, then this cell would develop into cancer (Hoff, Evans, & Hruban, 2015)..
The final way our DNA can be damaged is through our behaviors. For instance, a cigarette contains carcinogens (cancer causing substances, which can damage our DNA. Given that the carcinogens damage primary cancer-related gene within the pancreatic cell, then this cell would grow into cancer. In simple words, smoking can cause pancreatic cancer (Reber, 2010).
As a malignant disease, pancreatic cancer results from the accumulation of acquired gene mutations. The multigenic nature of pancreatic cancer is reflected in the abnormalities in three categories of genes namely tumor-suppressor genes, oncogenes and genomic maintenance genes. It is believed that mutations that accumulate in such genes happen in a predictable time course. Often, the biology of pancreatic cancer is associated with inactivation and mutations of tumor suppressor and oncogenes, coupled with abnormalities in developmental variables. They tend to affect the downstream signal transduction pathways engaged in the control of differentiation and growth. Such perturbations tend to confer immense growth and survival advantage to pancreatic cancer cells (Yarbro et al. 2015). Obviously, this is manifested by the growth of metastatic and invasive phenotypes, which appear to be resistant to almost all conventional interventions. For instance, studies in the U.S. have established that pancreatic cancer in human beings over-expresses various developmental variables and their receptors, among them vascular endothelial growth factor, the epidermal growth factor family...
The disruption of inhibitory growth variables and the abundance of growth-fostering variables trigger sufficiency in growth signals, the evasion of programmed cell death and metastasis (Hoff, Evans, & Hruban, 2015).
The human retroperitoneum houses the pancreas. At the onset, the growth of cancer seems to be silent in this area (Jeruc, 2012). The symptoms are normally an indication of advanced disease. Clinical manifestation relies on the stage of the disease as well as the location of the primary tumor. It could be located in the body or tail, neck process, the pancreatic head or multifocal disease (Shrikhande et al. 2010). A bulk of these tumors emerges in the pancreatic head. Thus signs and symptoms could entail epigastric pain, right -- upper quadrant, jaundice, diarrhea, vomiting or nausea secondary to obstruction of the gastric outlet and steatorrhea because of pancreatic insufficiency. Worsening or new onset of previously stable illnesses, mostly not because of cancer, might alert the doctor to the potential of pancreatic cancer. Moreover, worsening or new back pain could be an indication of cancer in the pancreatic tail or body. Still, systemic manifestations entail rapid and profound weight loss, thromboembolic disease or anorexia (Shen & Pompe-Kirn, 2010).
Often, abdominal ultrasounds are utilized as the initial diagnosis test for patients presenting with nonspecific abdominal pains. The specificity and sensitivity of ultrasound in the diagnosis of pancreatic tumors is roughly 95% and 90% respectively. However, it worsens as the disease advances. Ultrasound is restricted by its inability and operator dependency to distinguish autoimmune or chronic pancreatitis from cancer. Therefore, ultrasound stands as a bridge to CT imaging. The stage and putative diagnosis of pancreatic cancer are normally conducted with triphasic contrast-enhanced CT that serves to furnish orientation of the tumor with surrounding organs and vessels. While MRI is argued to be similar to CT imaging, its limited availability tends to restrict its utility to patients with contraindications to CT, among them nephropathy and pregnancy, or in cases where resectability remains unclear even after CT (Hoff, Evans, & Hruban, 2015).
The accuracy of these imaging modalities regarding diagnosis obviates the importance of preoperative tissue diagnosis in tumors that are surgically resectable. CT-guided biopsy, commonly known as Endoscopic ultrasound is warranted in situations where imaging is uncertain; chronic or autoimmune pancreatitis (Katlic et al. 2011). It is also used in unresectable illnesses before initiating chemoradiation therapy. It is necessary to deploy regular preoperative biliary drainage based on endoscopic retrograde cholangiopancreatography. Nonetheless, brushings could be useful during therapeutic stenting in clients with cholangitis, patients unable to undergo immediate surgery or an unknown pancreatic head mass.
The symptoms of tumors situated in the body and head of the pancreas are normally triggered by the compression of surrounding structures (Shrikhande et al. 2010). They include the duodenum, the pancreatic duct, coeliac nerves and the bile duct. Eventually, these events bring patients to medical attention, and the doctor can easily make the diagnosis of pancreatic cancer. In cases where the pancreatic head tumor is small, the only sign could be painless jaundice. However, a majority of patients report an antecedent period of back or abdominal pain, followed by the growth of obstructive jaundice. Other signs include the growth of malabsorption and diabetes mellitus (Shen & Pompe-Kirn, 2010). Pancreatitis is the least common symptom, which might occur when there is less significant obstruction of the pancreatic duct. When dealing with patients with an unknown pancreatitis risk factor, the physician should consider a pancreatic neoplasm as a potential underlying cause. In patients, initial signs could be linked to the primary tumor, with pain in the left upper quadrant or abdomen. However, these patients tend to present with symptoms relatable to metastatic illness (Hoff, Evans, & Hruban, 2015).
From the, inherited (genetic) cancer syndromes heightens the risk of pancreatic cancer. Common syndromes include the familial atypical multiple mole melanoma syndromes (FAMMM), the Peutz-Jeghers syndrome and non-polyposis colorectal cancer syndrome.
Cigarette smoking is argued to double the risk of pancreatic cancer. Today, scientists estimate that one out of four cases of pancreatic cancer result from smoking cigarettes. Besides, smoking is related to early age at diagnosis. In fact, the risk of pancreatic cancer drops to normal in individuals who stop smoking. This means that smoking is the major preventable causes of pancreatic cancer (Jeruc, 2012).
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