ctDNA was detectable in the first post-operative pre-chemotherapy samples of 8 of 35 (22.9%) patients and was associated with inferior RFS (HR, 3.69; P = 0.033). ctDNA was detected in the first post-chemotherapy samples of 8 of 36 (22.2%) patients and was also associated with inferior RFS (HR, 8.76; P < 0.001). Postoperative and post-chemotherapy ctDNA is a promising prognostic marker for resected NSCLC. ctDNA analyses may define a subgroup that remains at high risk of relapse despite standard adjuvant chemotherapy, and may help to inform intensified therapeutic strategies.Postoperative and post-chemotherapy ctDNA is a promising prognostic marker for resected NSCLC. ctDNA analyses may define a subgroup that remains at high risk of relapse despite standard adjuvant chemotherapy, and may help to inform intensified therapeutic strategies. Globally, the incidence and mortality due to esophageal cancer are increasing, particularly in low- and middle-income countries. Cancer of the esophagus is the eighth in incidence and seventh in cancer mortality in Ethiopia. A few studies have shown an increasing burden, however, little is known about the survival pattern and its determinants among esophageal cancer patients in Ethiopia. Therefore, we assessed the survival pattern and its determinants among esophageal cancer patients. We conducted a retrospective cohort study among 349 esophageal cancer patients who were diagnosed at or referred to Tikur Anbessa Specialized Hospital, Ethiopia from January 2010 to May 2017. Using an abstraction form, nurses who were working at the oncology department extracted the data from patient charts. To estimate and compare the probability of survival among covariate categories, we performed a Kaplan-Meier survival analysis with the log-rank test. To identify the prognostic determinants of survival, we performed a muvery low one-, two- and three-year survival. Despite a very low overall survival, patients who received either chemotherapy, radiotherapy or surgery showed a better survival compared with those who did not receive any treatment. Hence, it is essential to improve the survival of patients with esophageal cancer through early detection and timely initiation of the available treatment options.Multiple myeloma (MM) is an incurable disease with a limited life expectancy of five years from diagnosis. Uncontrolled disease or infections are the main causes of mortality. Daratumumab, a monoclonal antibody against CD38, is approved to treat patients with MM. Its target, CD38, is expressed not only on MM cells but also on common lymphoid precursors and subsets of normal lymphocytes. Daratumumab-induced lymphopenia is common, but its clinical significance is understudied. In this study, we report the baseline characteristics, rates of severe lymphopenia, infections, and clinical trajectory of multiple myeloma patients (n = 100) treated with daratumumab-based regimens at the Ohio State University Comprehensive Cancer Center. We discover high rates of infections, hospital utilization, and severe lymphopenia and identify risks factors for severe lymphopenia, such as low pretreatment absolute lymphocyte count (ALC) values. DNA Repair modulator Severe lymphopenia persists in 23% of patients, resulting in worst survival outcomes. Our data underline the importance of monitoring ALC and consider future use of prophylactic measures or alternative regimens in subsets of MM patients. We performed this clinical trial to evaluate the efficacy and safety of apatinib and oral etoposide in patients with HER2-negative locally advanced or metastatic breast cancer (MBC). Patients with HER2-negative MBC previously treated with anthracycline and taxanes and failed ≥1 prior chemotherapy regimens were recruited. The starting dose of apatinib was 500 and 425 mg in patients with ECOG scores of 0-1 and 2, respectively. The etoposide capsules were given at 50 mg/m on days 1 to 10 for 21 days. The primary end point was objective response rate (ORR). Secondary end points included progression-free survival (PFS), disease control rate (DCR), overall survival (OS), and safety. Thirty-one eligible patients were enrolled. The median follow-up time was 11 months. The median PFS for all patients was 6.9 months [95% confidence interval (CI) 6.0-7.9], and 6.9 months (95% CI 5.3-8.6) and 6.6 months (95% CI 1.4-11.7) for patients with apatinib 425 and 500mg once daily, respectively. The ORR was 35.5% (11/31). The DCR was 87.1% (27/31). The median OS was 20.4 months (95% CI 11.4-29.3). The median PFS of patients who had hypertension and proteinuria was longer than that for those without hypertension and proteinuria. The most common grade 3/4 treatment-related AEs were hypertension (12/31, 38.7%), fatigue (3/31, 9.7%), thrombocytopenia (3/31, 9.7%). Apatinib combined with etoposide capsules is effective and tolerable in heavily pretreated, metastatic HER2-negative breast cancer patients. A lower apatinib dose provide equivalent efficacy and reduced toxicity. https//clinicaltrials.gov/, identifier NCT03535961.https//clinicaltrials.gov/, identifier NCT03535961.Phenytoin (diphenylhydantoin) is a widely used antiepileptic drug for controlling both generalized and partial seizures. Reversible cerebellar symptoms, including cerebellar ataxia, have been recognized as an adverse event of phenytoin use for many years. On the other hand, cerebellar degeneration has been reported with chronic use in an epileptic patient treated with this drug. We are reporting an interesting case of phenytoin induced acute pan-cerebellar syndrome with cerebellar atrophy on neuro-imaging that improved many years after discontinuation of the drug. Discontinuation of phenytoin may give a chance for the patient to recover slowly, months after stopping the drug. It is very important for the attending neurologist to educate the patients and their families on some common clinical manifestations suggestive of drug toxicity and perform a regular follow-up and clinical examination at regular intervals.Status epilepticus (SE) is rare in juvenile myoclonic epilepsy (JME). This report presents three patients with myoclonic status epilepticus (MSE). MSE is defined as prolonged period of myoclonic jerks that are correlated with epileptiform discharges on electroencephalogram. The precipitating factors among the three patients were introduction of carbamazepine in case1, missing the dose in case2, and introduction of oxcarbazepine in case3. Of the three patients, one patient was a misdiagnosed case of JME. In him the diagnosis of JME was established after 35 years when he developed MSE with the addition of oxcarbazepine to the antiseizure medication (ASM) which he was taking. Detailed review of the history revealed that he used to get occasional myoclonic jerks with deprived sleep and stress. This patient illustrates that the diagnosis of JME can be missed or delayed if history of myoclonic jerks is not elicited, particularly in patents with pubertal onset epilepsy. The other lesson is that possibility of JME should be considered in patients with drug resistant epilepsy (pseudo-drug resistance).