Colorectal cancer (CRC) represents a heterogeneous group of diseases that imposes a considerable global and national health burden. Although most CRC patients are diagnosed at an early stage and undergo potentially curative treatment, a significant proportion experience recurrence. Currently, adjuvant chemotherapy decisions are primarily based on clinicopathological characteristics, which have well-recognized limitations in accurately identifying patients harboring minimal residual disease (MRD), often resulting in unnecessary chemotherapy exposure. Circulating tumor DNA (ctDNA) has emerged as a promising surrogate marker for MRD, offering a more precise approach to identifying patients at risk of recurrence after curative-intent surgery and refining adjuvant chemotherapy decisions. Growing evidence from multiple studies has demonstrated that ctDNA outperforms traditional clinicopathological factors as a marker for MRD. This review synthesizes key studies supporting the role of ctDNA in MRD detection for CRC patients and evaluates clinical trials investigating the application of ctDNA in guiding adjuvant therapy decisions. This emerging strategy holds the potential to transform the adjuvant treatment paradigm in colorectal cancer by optimizing therapeutic precision and minimizing unnecessary treatment.

Autoimmune hemolytic anemia (AIHA) is a rare disease characterized by autoantibodies directed at red blood cells. Patients typically present with anemia and are diagnosed by positive direct antiglobulin (DAT) test. AIHA is subclassified into warm or cold based on antibodies involved and depending on their optimal temperature in which they react with RBC antigens. Warm AIHA can be either primary (idiopathic) or secondary depending on etiology. Secondary causes are associated with malignancy, connective tissue and inflammatory diseases, infections (typically viral infections), or drugs (e.g., antibiotics, chemotherapeutic agents). Epstein-Barr virus (EBV) is a herpes virus that is commonly associated with cold AIHA, with only one reported case of EBV-induced warm AIHA. It has been postulated that antibodies against EBV cross-react with antigens expressed on RBC membranes and activate the complement cascade similarly. This case report describes a case of a 32-year-old male who presented with warm AIHA secondary to EBV reinfection.

Infectious mononucleosis (IM) is an acute disease caused by Epstein-Barr virus (EBV) infection affecting adolescents and young adults. Clinically, IM presents with fever, lymphadenopathy, and tonsillar pharyngitis. Guillain-Barré syndrome (GBS) has been reported as a possible rare complication of IM. IM-induced GBS is known but rarely reported in the literature. Here, we describe the case of a 19-year-old male with no significant medical history who was diagnosed with GBS following EBV-associated IM. A 19-year-old Caucasian male presented from a referring facility after complaining of generalized weakness involving the upper and lower extremity for about five days. Symptoms began with a sensation of tingling and numbness in the fingertips and toes that progressed over five days to where he was no longer able to ambulate. Physical examination was significant for oropharyngeal exudates, posterior oropharyngeal erythema, tonsillar hypertrophy, cervical lymphadenopathy, flaccid paralysis with areflexia, and paresthesia. Diagnostic workup was consistent with IM and GBS based on cerebrospinal findings. He was subsequently admitted to the intensive care unit, where he received plasmapheresis and intravenous immunoglobulin with significant improvement. This is a rare case of EBV-associated IM GBS. IM is a self-limiting disease but can lead to GBS as one of the known but rare complications. Neurological events have been reported in approximately 2% of patients. Only a few cases of IM leading to GBS have been reported in the literature. Detailed history and physical examination can help identify patients with IM-induced GBS. Moreover, increased awareness can help physicians easily identify and manage GBS, enabling timely recognition and initiation of prompt supportive care to improve recovery time.

Background: Cisplatin, gemcitabine, and durvalumab combination is a standard first-line treatment for advanced biliary tract cancer. This study aimed to assess the impact of genetic alterations on outcomes in patients with advanced biliary tract cancer treated with cisplatin, gemcitabine, and durvalumab in real-world clinical practice. Methods: Patients with unresectable, locally advanced, or metastatic biliary tract cancer treated with cisplatin and gemcitabine plus durvalumab across 39 centers in 11 countries in Europe, the United States, and Asia were included in this analysis. Results: The cohort included 513 patients with advanced biliary tract cancer. The 5 most frequently altered genes were TP53 (22.1%), KRAS (13.7%), CDKN2A/B (13.6%), ARID1A (12.2%), and IDH1 (9.2%). In multivariate analysis, SMAD4 mutations were associated with improved progression-free survival (PFS) (hazard ratio [HR] = 0.49, P = .018) and overall survival (HR = 0.11, P = .023), while TP53 mutations were linked to worse PFS (HR = 1.62, P = .0047) and TERT mutations to worse overall survival (HR = 8.92, P = .0012). No other genomic alterations were statistically associated with outcomes. Subgroup analysis showed that TP53 mutations negatively affected PFS and overall survival in intrahepatic cholangiocarcinoma, while KRAS mutations were associated with poorer PFS in extrahepatic cholangiocarcinoma. No gene alterations were linked to outcomes in gallbladder cancer. Conclusions: This large-scale analysis, with comprehensive molecular profiling, supports the positive prognostic impact of SMAD4 mutations for PFS and overall survival and highlights the negative prognostic roles of TP53 (PFS) and TERT (overall survival) mutations, providing valuable insights for personalized treatment strategies in biliary tract cancer.

Paraneoplastic rheumatic disorder (RD) is a disorder that may present before, concurrent with, or after the diagnosis of malignancy. Paraneoplastic RDs are a clinical expression of occult cancer that is not directly related to a tumor or metastasis and manifests as rheumatoid symptoms. The RD is determined by the organ system affected by articular, muscular, cutaneous, vascular, or miscellaneous symptoms. Each case is challenging to diagnose because cancer may present with similar symptoms as a common rheumatic disorder. Of note, the majority of cases have minimal responsiveness or no responsiveness to standard rheumatoid treatment. Therefore, it is imperative to recognize and treat the underlying cancer accordingly. Herein, we present four different diagnostic dilemma cases of RD: case #1 - leukocytoclastic vasculitis and C3 glomerulopathy, case #2 - scleroderma, case #3 - Raynaud’s syndrome and possible lupus-like syndrome, and case #4 - inflammatory myositis. Institutional IRB approval was obtained for this case series. We will discuss and review the literature on each topic. In addition, we will mention a review of paraneoplastic rheumatoid arthritis. As rheumatic disease is associated with the use of immune checkpoint inhibitors (ICIs) for cancer treatment, we will briefly discuss some of the most common rheumatic presentations in the setting of these drugs. This case review aims to inform clinicians about the atypical presentation of paraneoplastic RD and to highlight the need for interdisciplinary management between rheumatologists, oncologists, and primary care practitioners.

Urothelial carcinoma (UC) is the most common malignancy of the urinary tract, with urothelial bladder cancer accounting for approximately 90% of cases. Metastatic UC (mUC) is a particularly aggressive subset that presents significant treatment challenges, especially in patients who are often older than 70 years and have multiple comorbidities. For several decades, cisplatin-based chemotherapy has been the standard first-line treatment for locally advanced (LA) mUC. However, its utility has been limited as many patients are ineligible owing to their health status, and overall survival rates remain suboptimal. Recent advancements, including antibody-drug conjugates and immunotherapies, have begun to reshape the treatment landscape for LA/mUC. The combination of enfortumab vedotin and pembrolizumab has shown promising clinical outcomes. The approval of multiple novel drugs and combination therapies not only provides new opportunities for patient care but also creates the need for physicians to adapt to this evolving therapeutic paradigm. This review explores the latest clinical data on the management of LA/mUC and offers insights into sequencing therapies for patients with LA/mUC.