Pancreatic cancer has the worst survival of any solid tumor. Overall, pancreatic cancer accounts for about 3% of all cancers in the US and about 7% of all cancer deaths. The American Cancer Society's estimates that 57,600 people (30,400 men and 27,200 women) will be diagnosed with pancreatic cancer in the United States for 2020 and approximately 47,050 people (24,640 men and 22,410 women) will die of this disease. FOLFIRINOX, or the combination of gemcitabine with nab-paclitaxel remain to be the major treatment options for these patients for both local and metastatic disease. This slow progress is a result of partly the complex pathogenesis of this disease, and partly the fact that window of opportunity to treat these patients is short as majority of them are diagnosed at an advanced stage. This is a real challenge but also provides an opportunity for new ideas and novel approaches. In this paper, we will present few interesting studies presented at the American Society of Clinical Oncology (ASCO) 2020 virtual Annual Meeting.

Pancreatic cancer is a very aggressive disease and survival remains dismal even with treatment. Currently, management of patients with pancreatic cancer has been complicated by the ongoing COVID-19 pandemic. Medical oncologists face the dilemma of whether to treat or to not treat these patients who are at high-risk of complications and even death from COVID-19. No current guidelines are available and our limited experience at this time makes it more difficult to manage these patients. Although we have general strategies available from experience in Italy, we need more treatment specific strategies to help mitigate risks of complications and toxicities from chemotherapy in order to protect our patients from COVID-19 as much as possible.

Chronic hepatitis C virus (HCV) infection increases the risk for several types of cancer, including hepatocellular carcinoma (HCC) and B-cell non-Hodgkin lymphoma, as primary and second primary malignancies. HCV-infected patients with cancer, particularly those undergoing anticancer therapy, are at risk for development of enhanced HCV replication, which can lead to hepatitis flare and progression of liver fibrosis or cirrhosis. Risk factors for HCV infection include injection drug use, blood transfusion, or solid organ transplantation before 1992, receipt of clotting factor concentrates before 1987, long-term hemodialysis, chronic liver disease, HIV positivity, and occupational exposure. Widely available direct-acting antivirals are highly effective against HCV and well tolerated. Identification of HCV-infected individuals is the essential first step in treatment and eradication of the infection. One-time screening is recommended for persons born from 1945 to 1965; screening is also recommended for persons with risk factors. Recently, a public health recommendation has been drafted to screen all adults age 18 to 79 years. Two oncology organizations recommend screening all patients with hematologic malignancies and hematopoietic cell transplant recipients, and a recently published multicenter prospective study supports universal HCV screening for all patients with cancer. HCV screening entails testing for anti-HCV antibodies in serum and, when results are positive, HCV RNA quantitation to confirm infection. Direct-acting antiviral therapy eradicates HCV in almost all cases. Virologic cure of HCV prevents chronic hepatitis and progression to liver fibrosis or cirrhosis. HCV eradication also decreases the risk of developing HCV-associated primary and second primary malignancies, and it may allow HCV-infected patients access to important cancer clinical trials. Patients with HCV-related cirrhosis require lifelong surveillance for HCC, even after viral eradication.

Cancer and atrial fibrillation (AF) are common conditions, but for patients affected with both, there is a lack of data about management of anticoagulation and cerebrovascular outcomes. In the first section of this review, we summarize the most relevant studies on stroke risk and management of AF in patients with active cancer, attempting to answer questions of whether to anticoagulate, whom to anticoagulate, and what agents to use. In the second section of the review, we suggest a decision algorithm on the basis of the available evidence and provide practical recommendations for each of the anticoagulant options. In the third section, we discuss the limitations of the available evidence. On the basis of low-quality evidence, we find that patients with cancer and AF have a risk of stroke similar to that of the general population but a substantially higher risk of bleeding regardless of the anticoagulant agent used; this makes anticoagulation-related decisions complex and evidence from the general population not immediately applicable. In general, we suggest stopping anticoagulation in patients with high risk of bleeding and in those with a moderate bleeding risk without a high thromboembolic risk and recommend anticoagulation as in the general population for patients at a low risk for bleeding. However, regardless of initial therapy, we recommend reassessing whether anticoagulation should be given at each point in the clinical course of the disease. High-quality evidence to guide anticoagulation for AF in patients with cancer is needed.

Pancreatic enzyme replacement therapy is safe and effective at treating pancreatic exocrine insufficiency. There are multiple causes of pancreatic exocrine insufficiency including chronic pancreatitis, cystic fibrosis and pancreatic cancer. Testing fecal elastase-1 level is useful for the diagnosis of pancreatic exocrine insufficiency. Starting doses of pancreatic enzyme replacement therapy should be at least 30-40,000 IU with each meal and 15-20,000 IU with snacks. pancreatic enzyme replacement therapy should be taken in divided doses throughout meals. Patients who do not respond to initial dosages should be evaluated for alternative etiologies and pancreatic enzyme replacement therapy optimized. Despite ease of use and benefit of pancreatic enzyme replacement therapy, challenges still remain clinically and this review hopes to provide a concise guide for clinicians.

Lung cancer is the leading cause of cancer-related death in the United States. Approximately 20% of these patients present with brain metastases (BMs). Surgical resection, stereotactic radiosurgery, and whole-brain radiation therapy have historically been the primary treatment modalities for patients with non-small-cell lung cancer (NSCLC) and BMs. The treatments for BMs have become complex with the discovery of targetable molecular drivers and the development of an astonishing number of tyrosine kinase inhibitors. Many of these tyrosine kinase inhibitors have robust and durable efficacy against CNS metastases. In many circumstances, these drugs can defer local therapy and even reduce the risk of CNS progression. More recently, immune checkpoint inhibitors have changed the treatment landscape for many patients with NSCLC; however, the role of immunotherapy in patients with BMs is the subject of ongoing investigations. This article will review the current data and our approach to patients with NSCLC and BMs.