Clinical Oncology: Case Reports

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Commentary, Clin Oncol Case Rep Vol: 5 Issue: 10

Pancreatic Cancer Causes and Epidemiology

Alice John*

Editorial Office, Clinical Oncology: Case Reports, United Kingdom

*Corresponding Author: Alice John
Editorial Office, Clinical Oncology: Case Reports, United Kingdom
E-mail: [email protected]

Received: October 04, 2022; Manuscript No: COCR-22-79478;
Editor Assigned: October 06, 2022; PreQC Id: COCR-22-79478 (PQ);
Reviewed: October 20, 2022; QC No: COCR-22-79478 (Q);
Revised: October 22, 2022; Manuscript No: COCR-22-79478 (R);
Published: October 29, 2022; DOI: 10.4172/cocr.5(10).256

Citation: John A (2022) Pancreatic Cancer Causes and Epidemiology. Clin Oncol Case Rep 5:10


Our understanding of the biology of pancreatic cancer has significantly advanced, and improvements in patient management have also occurred. There is growing evidence that identifying non-invasive antecedents of this malignant disease can be accomplished by screening first-degree relatives of those with several family members who have been diagnosed with pancreatic cancer. Despite a decline in the incidence and mortality of other prevalent malignancies, the number of fatalities from pancreatic tumors has been steadily increasing. Only approximately 4% of people with pancreatic cancer will survive 5 years following diagnosis, despite advancements in its detection and treatment. Because surgical excision is currently the only treatment option for malignant illness localized to the pancreas, survival is higher. Unfortunately, 80% to 85% of patients have advanced incurable disease when they first arrive. Additionally, the majority of chemotherapeutic drugs do not effectively treat pancreatic cancer. We must thus comprehend the basic processes that underlie the emergence and growth of pancreatic tumors. Pancreatic ductal adenocarcinoma, the most prevalent and lethal type of pancreatic cancer, will be covered in this seminar.

Keywords: Pancreatic Cancer; Treatment; Diagnosis; Malignant disease; Adenocarcinoma


An estimated 227 000 deaths from pancreatic cancer occur each year globally and are the fourth highest cause of cancer death in the United States. Smoking, ageing, male sex, diabetes mellitus, obesity, non-O blood group, occupational exposures, African-American ethnicity, high-fat diets, diets high in meat and poor in vegetables and folate, and probably Helicobacter pylori infection and periodontal disease are risk factors for this cancer. According to preliminary research, metformin may offer protection against the onset of pancreatic cancer. Consuming coffee is not thought to increase your risk of getting sick. Cigarette smoking and family history are the main contributors to pancreatic cancer, despite the fact that the cause is complicated and multivariate. Smoking causes about 20% of pancreatic tumors, and malignancies from smokers have more genetic abnormalities than cancers from non-smokers.

About 7% to 10% of those with pancreatic cancer have a family history, which is a significant risk factor for the disease. Most studies classify families with a pair of first-degree relatives who have been diagnosed with pancreatic tumors as having familial pancreatic cancer. According to a prospective study of families affected by this malignancy, first-degree relatives of people with familial pancreatic cancer have a nine fold higher risk of developing the disease than people in general. In families with three or more first-degree relatives who have pancreatic cancer, the risk increases 32-fold. Additionally, research suggests that first-degree relatives of individuals with sporadic pancreatic cancer have a slightly greater chance of developing the disease compared to the general population. Patients with familial pancreatic cancer also have more precancerous lesions than those with sporadic pancreatic tumors and have an increased risk of developing extra-pancreatic cancers. The risk is highest in kindred’s with familial pancreatic cancer who have a case of young-onset pancreatic cancer (age 50 years) in the family compared to those without a young-onset case.

Family members can receive genetic testing, cancer screening, and chemoprevention if necessary if a person's gene for developing cancer has been identified. The underutilization of germline genetic testing in pancreatic cancer patients is likely due in large part to a failure to recognize the likelihood of a familial cancer syndrome from the family history. Many doctors fail to adequately document a patient's family history of cancer. Kindred’s with altered susceptibility genes for pancreatic cancer typically do not exhibit a high penetrance of the disease. Consensus recommendations for genetic testing for hereditary susceptibility to pancreatic cancer have not been created due to this and the fact that a large portion of the inherited sensitivity to the disease is yet unknown. Patients of Jewish ancestry, those with a strong family history of breast cancer, or those with numerous first-degree relatives who have pancreatic cancer should consider BRCA2 gene testing after receiving appropriate genetic counselling; germline CDKN2A testing should be done if there is a family history of familial atypical multiple-mole melanoma. A thorough family history of cancer can be used to predict clinical risk even without genetic testing, and mendelian risk-prediction tools have been tested for use in people with familial pancreatic cancer.

The most common stromal cell type, cancer-associated fibroblasts, may interact with cancerous cells to cause tumor development, growth, and metastasis. The potential benefits of blocking T regulatory lymphocytes-cells that inhibit antitumor immune responses-or using vaccines that contain irradiated genetically modified pancreatic cancer cells or immune-stimulatory pancreatic cancer antigens like overexpressed (like mesohaline) or mutated proteins have been the focus of research on the immune system's role in the progression of pancreatic cancer. Additionally, research has been done on how cancer cells and cancer-associated fibroblasts evade the immune system. It is debatable what function tumor-initiating cells-also known as cancer stem cells-play in the emergence of pancreatic cancer. It is challenging to reconcile the idea of tumour-initiating cells with the clonal selection offered to neoplastic cells by tumourigenic mutations acquired during carcinogenesis, despite the fact that putative cells have been discovered. According to one theory, cancer stem-cell markers can be used to identify the cells that are most likely to withstand a specific cellular stress at any given time, such as the capacity to develop in naked mice or withstand chemotherapy drugs.

Early-stage pancreatic cancer is typically clinically silent, and symptoms normally don't show up until the tumor has spread to nearby tissues or distant organs. When pancreatic cancer symptoms are present, the majority of patients already have advanced illness. Patients with pancreatic cancer whose abdominal CT scans were performed for another reason prior to their diagnosis are frequently noted in retrospect to have had subtle abnormalities suspect for pancreatic cancer up to a year before the onset of symptoms, suggesting a missed opportunity for early detection. Weight loss, obstructive jaundice, and abdominal or mid-back pain are common pancreatic cancer presentation symptoms. Anorexia, malnutrition due to pancreatic ductal blockage, and cachexia can all cause weight loss. Attacks of pancreatitis may occasionally be brought on by pancreatic-duct blockage. Deep and superficial venous thrombosis is common and may be the first sign of a cancerous condition. With more advanced disease, it's possible to experience nausea and vomiting as well as gastric-outlet obstruction. Depression and panniculitis are less frequent symptoms. At the time of diagnosis, about 25% of pancreatic cancer patients had diabetes mellitus, and another 40% had poor glucose tolerance.

Uncertain factors may contribute to the diabetogenic state; however pancreatic cancer resection can occasionally reverse diabetes. Researchers are looking into whether older people with newly diagnosed diabetes could be identified with early-stage pancreatic cancer. However, the majority of persons with newly diagnosed diabetes do not also have pancreatic cancer. There aren't many clinical indicators that point to pancreatic cancer in people with newly diagnosed diabetes, except from weight loss. Therefore, additional screening procedures would be required for elderly people with newly diagnosed diabetes.


A multidisciplinary team composed of oncologists, surgeons, radiologists, gastroenterologists, radiation oncologists, pathologists, pain management specialists, social workers, dieticians, and (when necessary) palliative care specialists is the best option for treating patients with pancreatic cancer. At the molecular, pathological, and clinical levels, pancreatic cancer is a diverse condition. The biology of a patient's malignancy, their performance status, and their pattern of disease development are just a few of the variables that affect how well they respond to treatment and how their case turns out.

At the majority of specialized centers, surgical mortality from pancreatic resection is low. According to the results of multiple studies, pancreaticoduodenectomy mortality is significantly lower in high-volume centers than it is in low-volume ones. Consensus committees advise that pancreaticoduodenectomy procedures be performed at facilities where at least 15 to 20 of these operations are performed annually. In addition, a lot of candidates for curative resection forego surgery. Pancreatic anastomotic leakage and delayed gastric emptying are examples of postoperative problems following resection. The best surgical techniques to reduce pancreaticoduodenectomy postoperative problems have been determined through a number of randomized trials. The results of these studies did not clearly demonstrate one technique's superiority over another. When it allows for a R0 resection and can be performed without leading to increased operational morbidity, portal or superior mesenteric vein resection and reconstruction are appropriate. For certain pancreatic-tail resections, laparoscopic resection is a practical method. Before laparoscopic resection, tiny lesions can be localized with endoscopic tattooing. Patients with cholangitis, those who have related liver dysfunction, and those who are symptomatic must undergo preoperative biliary drainage (such as with severe pruritus). Otherwise, standard preoperative biliary drainage may not be required because, according to the results of the study, routine preoperative drainage had worse outcomes than surgical resection alone for people with obstructive jaundice caused by pancreatic cancer. On the other hand, obstructive jaundice in the neoadjuvant situation must be treated before chemotherapy and radiation begin. Additionally, biliary drainage will reduce non-specific CA19-9 concentrations, enabling a more accurate assessment of disease burden.

The success of targeted therapies in the treatment of various malignancies emphasizes the need for more research to find fresh targets and more accurate indicators of therapeutic response. Clinical studies for a number of targeted drugs are being conducted for pancreatic cancer. Poly (ADP-ribose) polymerase (PARP) inhibitor sensitivity is associated with BRCA2-PALB2-Fanconi DNA repair pathway abnormalities in pancreatic cancer cells. To enable DNA repair, PARP enzymes add long, branching chains of poly (ADP-ribose) to nicked DNA, causing histones to separate from the DNA. Olaparib showed response rates for recurrent breast and ovarian cancer of roughly 40% in phase 1 and 2 clinical trials of patients with a germline BRCA2 gene mutation. For people with pancreatic cancer, clinical studies with PARP inhibitors are currently being conducted. Patients with metastatic pancreatic adenocarcinoma are being studied in a phase 2 clinical trial using the hedgehog pathway inhibitor GDC-0449 (company, town, country), in conjunction with gemcitabine and the nanoparticle version of paclitaxel (NCT01088815). Sorafenib, a multikinase inhibitor, as well as drugs that target dasatinib, g secretase, MTOR, TNFSF10 (also known as TRAIL), and IGF1 are some of the other therapeutics under investigation. Pancreatic cancer endoscopic therapies, such as cryotherapy, photodynamic therapy, radiofrequency ablation, and chemotherapy, are being researched, although there is no proof that they are more effective than normal therapy.

When testing new drugs, clinical trial design is always crucial, but pancreatic cancer stands out because of its high death rate and often small therapeutic results. Many pancreatic cancer clinical trials face challenges like patient enrollment issues (patients with varying outcomes due to poor performance status or various patterns of advanced disease), trial design challenges (underpowered trials), and the lack of predictive markers (and sufficient tumor tissue) to identify subgroups that will respond to treatment.


An essential part of treatment is pain management. Effective therapy can be guided by determining the source of the pain. Endoscopic ultrasonography or CT-guided ablation of the plexus is effective treatments for the pain caused by celiac plexus invasion. When a disease is locally advanced, radiation can ease the pain. Biliary stenting is beneficial for most individuals with pancreatic-head tumors who experience obstructive jaundice. Plastic stents lose their patent more quickly than do metal ones. 147 20% of people experience gastric-outlet obstruction, which can be treated with duodenal wall stents or Percutaneous Endoscopic Gastrostomy (PEG) insertion. Surgery to treat obstructive jaundice and gastric-outlet obstruction is typically not essential because of the success of endoscopic wall stents, while it might be beneficial for those with a long life expectancy. Prophylaxis is advised because patients with pancreatic cancer frequently experience venous thromboembolism. The results of multiple randomized trials show that low-molecular-weight heparin offers superior prophylaxis than warfarin due to the characteristics of the hypercoagulable state. When the pancreatic ducts are blocked or the pancreatic gland tissue is scant, pancreatic enzyme therapy may be necessary. Patients and their families can find vital information and support on the Johns Hopkins Pancreatic Cancer website and from organizations like the Pancreatic Cancer Action Network and Pancreatic Cancer UK.

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