Insulin resistance (IR) is a prevalent metabolic condition characterized by reduced cellular responsiveness to insulin and consequent hyperinsulinemia, and it is a key component of type 2 diabetes and metabolic syndrome. A growing body of evidence suggests IR is a critical accomplice in the pathogenesis of various cancers. This review synthesizes evidence on underlying molecular mechanisms, including the integrated roles of the insulin/IGF system, chronic inflammation, metabolic reprogramming, and mitochondrial dysfunction. This review proposes that metabolic dysregulation should be viewed as a modifiable oncogenic force. This perspective illuminates new pathways for understanding cancer development and offers promising avenues for prevention and therapeutic intervention.

Colorectal cancer (CRC) develops through both conventional adenoma–carcinoma and serrated neoplasia pathways, yet noninvasive screening still under-detects the advanced precursor lesions that enable true cancer prevention. Stool-based screening reduces CRC mortality, but its preventive impact remains constrained by limited detection of advanced precancerous lesions (APLs), including advanced adenomas and sessile serrated lesions. Next-generation multitarget stool DNA assays (mt-sDNA; e.g., Cologuard Plus) have established high sensitivity for CRC and specificity approaching 94%, leaving improved APL detection as the principal opportunity for innovation. This review presents a consensus framework for a multi-omic stool screening paradigm that integrates host epigenetic markers (DNA methylation) with gut microbiome features using artificial intelligence (AI). Multi-omics capture complementary layers of early tumor biology: epithelial shedding and field effects reflected in host methylation signals together with luminal ecological and inflammatory changes represented by microbial features. Evidence from cross-cohort microbiome studies indicates that microbial signatures provide an additive—rather than standalone—axis of information for CRC and its precursor lesions. Because microbiome-based models are highly susceptible to batch effects arising from collection devices, extraction chemistry, sequencing platforms, and bioinformatic pipelines, practical mitigation strategies are outlined, including harmonized pre-analytics, batch-aware study design, leakage-resistant validation, and computational harmonization. A translational roadmap linking analytical validity, locked-model development, and prospective colonoscopy-verified clinical validation is proposed, aligned with TRIPOD + AI, STARD, PROBAST-AI, SPIRIT-AI, CONSORT-AI, and DECIDE-AI reporting standards. Scenario modeling using BLUE-C prevalence estimates suggests that improving APL sensitivity from approximately 43% to 55–65% at ~94% specificity could translate to detecting roughly 13–23 additional advanced precancerous lesions per 1000 individuals screened, highlighting the potential prevention impact of a multi-omic approach. This framework aims to guide developers and clinical investigators toward next-generation stool tests capable of materially improving precursor-lesion detection while maintaining clinically acceptable specificity.

Gastroenteropancreatic neuroendocrine tumors (GEP-NETs) are a heterogeneous group of malignancies characterized by varying degrees of aggressiveness and clinical behavior. Despite advancements in treatment, including targeted therapies such as sunitinib and everolimus, peptide receptor radionuclide therapy with [177Lu]Lu-DOTATATE, and chemotherapy regimens like capecitabine plus temozolomide, the advanced GEP-NETs remain largely incurable. The limited efficacy of current treatments highlights the urgent need for novel therapeutic strategies. Recent years have seen a rise in several landmark clinical trials aimed at exploring new agents and combinations to improve patient outcomes in GEP-NETs. This literature review focuses on the ongoing clinical trials that hold promise for advancing the treatment landscape of GEP-NETs. We include some industry- and cooperative group-sponsored, phase II-III, randomized, and comparative trials in our review. We analyze the design, rationale, objectives, and preliminary findings of these trials, with a particular emphasis on those with pending results that may offer new insights into potential therapeutic targets. By examining these trials, we aim to provide a comprehensive overview of the evolving strategies in the management of GEP-NETs and underscore the importance of continued research innovation in addressing the challenges posed by the heterogeneity of GEP-NETs and in the pursuit of more effective and potentially curative treatment options.

This case report presents the first known instance of pembrolizumab-induced autoimmune encephalitis in a 41-year-old female patient with stage IIIc triple-negative breast cancer. The patient developed expressive aphasia three days after starting pembrolizumab in combination with chemotherapy, prompting comprehensive evaluations that ruled out infectious or metastatic causes. A diagnosis of pembrolizumab-associated autoimmune encephalitis was established following a lumbar puncture and MRI. After discontinuing the immune checkpoint inhibitors (ICI) and initiating high-dose corticosteroids (methylprednisolone), the patient's symptoms significantly improved within days. This case highlights the importance of recognizing and managing neurological immune-related adverse events (irAEs) associated with ICIs, as their incidence can be variable but potentially severe. Clinicians must maintain a high index of suspicion for neurological irAEs, especially with new neurological symptoms, as early diagnosis and intervention are crucial for optimizing patient outcomes while balancing effective cancer treatment. Ongoing research is essential to elucidate the mechanisms and management strategies for ICI-related autoimmune encephalitis.

Cardiovascular diseases are a leading cause of mortality in the United States. The increasing number of cancer patients experiencing cardiovascular side effects from chemotherapeutic drugs is a cause for concern. Trastuzumab is a highly effective targeted therapy for HER2-positive cancers but its use is limited globally due to its cardiotoxic effects. The most severe adverse effect is cardiomyopathy, which is characterized by contractile dysfunction and reduced left ventricular systolic function. The electrophysiological side effects of trastuzumab are still not fully understood. Due to these life-threatening side effects, trastuzumab is routinely discontinued. This review aims to provide a comprehensive overview of trastuzumab-induced cardiomyopathy, including the mechanisms by which trastuzumab exerts its cardiotoxic effects, the clinical manifestations, diagnostic strategies, and potential interventions to protect the heart. By shedding light on the various aspects of this condition, we hope to emphasize the importance of early detection and effective management, as well as the urgent need for further research to optimize the balance between successful cancer treatment and cardiovascular well-being. Cardiologists, oncologists, and researchers are at the forefront of this critical intersection between oncology and cardiology, working collaboratively to enhance patient outcomes in the era of trastuzumab therapy.