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Summary of Gastric Cancer

Epidemiology & Etiology: Aspirin and other nonsteroidal anti-inflammatory agent use has been associated with a lower risk for cancer of the gastroesophageal junction and other gastrointestinal tumors.41 Cigarette smoking, H. pylori infection, Epstein-Barr virus, radiation exposure, and prior gastric surgery for benign ulcer disease also have been implicated as risk factors. Diagnosis: Staging includes chest x-ray, chest CT scans, and abdominal imaging to rule out metastasis and to determine surgical resectability. PET scans are not (yet) recommended as standard diagnostic procedure in view of limited sensitivity, but can be helpful to determine the resectability of gastric cancers in select cases.48 The role of EUS is less clear in gastric cancer than in esophageal and gastroesophageal junction cancers. Treatment: D2 lymphadenectomy was associated with lower locoregional recurrence (12% vs. 22%) and gastric cancer–related death rates (37% vs.

Summary of Esophageal cancer treatment

Epidemiology & Etiology: Approximately 60% of cases of distal esophageal or gastroesophageal adenocarcinomas have evidence of Barrett’s esophagus. High-grade dysplasia is an indication for more aggressive management, including surgical resection. Tumor markers, such as TP53, may be predictors of potential progression to malignant disease. There is an inverse association between Helicobacter pylori (H. pylori) infection and adenocarcinomas of the lower esophagus, presumably a result of the reduced acidity associated with atrophic gastritis.9   Infection with human papillomavirus (HPV) has been correlated with an increased incidence of squamous cell cancers of the upper esophagus.10 Diagnosis: endoscopic ultrasound (EUS), have become more important in the evaluation and staging of esophageal cancer.11 EUS, in the hands of a skillful sonographer, can accurately assess the depth of penetration in as many as 90% of tumors and determine involvement o

Summary of treatment of pancreatic cancer

Epidemiology & Etiology: Data regarding coffee and excess alcohol consumptions are conflicting; therefore, they cannot be considered true etiologic factors. There is an association between pancreatic cancer and diabetes; however, it is more likely that diabetes is an early manifestation of cancer and not necessarily a predisposing factor. Selective mutations of BRCA2, and, to a lesser degree, BRCA1 have been associated with familial pancreatic cancer. Approximately 10% to 20% of patients are thought to have a familial predisposition. Pancreatic adenocarcinomas arise from ductal epithelial cells. Pancreas cancer has the highest lethality of all the gastrointestinal malignancies. Diagnosis: Diagnostic tests used for pancreas cancer are CT scan, MRI, EUS, and endoscopic retrograde cholangiopancreatography. Diagnostic tests, such as PET and EUS, may play a role in distinguishing cancer from other abnormalities and most importantly are used to adequate

Treatment of hot flushes 2ry to Tamoxifen

A clinical trial looked at the efficacy of gabapentin compared with venlafaxine, utilizing patient preference as its primary endpoint.  Patients were randomly assigned to receive venlafaxine compared with gabapentin in relatively standard doses recommended by previous placebo-controlled clinical hot flash trials.  Patients were treated for 4 weeks and then had a 2-week washout period, before being crossed-over to the alternative treatment.  Although both agents appeared to reduce hot flashes to similar extents (approximately a 65% (reduction) and had similar amounts of toxicities, 68% of patients preferred venlafaxine compared with 32% who preferred gabapentin (p = 0.01).  The authors concluded that venlafaxine should be recommended as an initial treatment but that some patients did better with gabapentin, supporting a trial of this medication if venlafaxine was not efficacious enough.  In 2013, paroxetine was FDA-approved for the treatment of hot flashes. However, this drug

Paclitaxel acute pain syndrome

Paclitaxel produces a disabling syndrome of subacute aches and pains in a majority of patients, which had been commonly referred to as arthralgias and myalgias.  These symptoms generally begin 1 to 3 days after administration and are self-limited, usually resolving within a week.  Symptoms have been described in large axial muscular and joint regions and generally are not accompanied by objective musculoskeletal or neurologic examination changes. The symptom location, temporal relationship, and self-limited nature of the syndrome make paclitaxel-induced acute pain syndrome (APS) distinct from paclitaxel-associated peripheral neuropathy.  In the more distant past, the exact characterization of paclitaxel-induced APS had not been well defined. There had been very little known about how exactly patients characterize these symptoms or how these symptoms compare or contrast to symptoms of neuropathy. Given that paclitaxel, administered to rats, causes dorsal root ganglion injury by 24 h

Quick summary of glioblastoma multiforme (GBM) treatment

Surgical resection followed by involved-field RT plus concurrent temozolomide followed by up to six cycles of adjuvant temozolomide.  Adjuvant temozolomide alone may be considered in elderly patients with poor performance status, especially for O6-methylguanine-DNA-methyltransferase (MGMT) promoter methylated tumors.  Adjuvant radiation therapy alone may be considered in elderly patients with MGMT promoter UNmethylated tumors Bevacizumab is FDA approved for the treatment of recurrent glioblastoma. It's addition in the adjuvant setting didn't improve survival.

3 important Mutations and syndromes in oncology

-  RET germline mutation is found in Multiple Endocrine Neoplasia Type II. - TP53 mutation is found in Li-Fraumeni syndrome. -  MLH1 mutation is found in Lynch syndrome.