NRAS mutation

The ferroptosis inducer erastin also inhibits melanoma growth. Combining the ATAD2 inhibitor BAY-850 with the MEK inhibitor trametinib potently suppresses melanoma growth. Our study identifies ATAD2 as a key driver of melanoma and provides a rationale for targeting ATAD2 in conjunction with the MAPK pathway to treat melanoma.

Clinically, one patient succumbed to disease one month and another patient experienced a recurrence at 43 months, whereas the remaining patients had no evidence of disease at 3-24 months of follow-up. MLA displays unique cytomorphologic features and accurate identification of MLA on cytology should prompt confirmatory tests to exclude potential morphologic mimics and ensure appropriate diagnosis.

Subsequently, multiple hepatic metastases and pelvic dissemination developed, and conventional chemotherapy including bevacizumab was ineffective...Switching to sorafenib led to further progression, but reintroduction of LVB reduced Tg levels...The patient has survived seven years since recurrence, including six years on LVB. The tumor behaved similarly to poorly differentiated thyroid carcinoma, with Tg levels reflecting disease activity and LVB demonstrating the potential for long-term tumor control.

Mucosal and vulvovaginal melanomas are biologically and clinically distinct from cutaneous melanoma and continue to have poor survival outcomes. Their rarity restricts high-quality evidence, highlighting the need for collaborative, innovative research to inform effective treatment strategies.

Here we show that the BET inhibitor PLX51107 potently suppresses the growth of NRAS -mutant AML cell lines, and that these activities are enhanced by co-treatment with the MEK inhibitor PD0325901. AMLs that relapsed after frontline chemotherapy showed similar transcriptional remodeling. These studies demonstrate transcriptional plasticity in primary AMLs that relapse following in vivo treatment with either targeted agents or chemotherapy, and support evaluating BET inhibition in leukemias with monocytic differentiation and RAS mutations.

MM arising within CGMN poses diagnostic and therapeutic challenges. While molecular and epigenomic profiling supports accurate classification and understanding of disease biology, the role of immunotherapy remains uncertain-marked by reduced efficacy and significant immune-related toxicity. A multidisciplinary approach is essential to guide management and improve outcomes in this rare pediatric malignancy.

Identification of clinical and genetic biomarkers for recurrence risk prediction in resected melanoma may aid in clinical decision-making for early disease monitoring and optimal design of therapeutic strategies.

Four clinical examples illustrated LB-guided therapies. This largest-to-date aSCC cohort reinforces molecular profiling-especially LB-as a key tool for guiding personalized therapy.

In the context of the imaging and molecular study results, a diagnosis of giant cellular blue nevus was made. This case highlights a rare presentation of giant CBN and the utility of integrating next-generation sequencing with histopathologic evaluation to distinguish the latter from melanoma and support clinical decision making.

We present a case of a man in his 70s with metastatic melanoma who experienced progression through sequential treatments including pembrolizumab in combination with the HDAC inhibitor entinostat, and ipilimumab. Transdifferentiation has been observed in a wide range of malignancies, but the molecular mechanisms of this phenomenon are poorly understood. This case provides the first molecularly validated example of melanoma to rhabdomyosarcoma transdifferentiation presenting as spatially segregated metastatic lesions with distinct, unmixed histologies and illustrates a mechanism of resistance to immunotherapy driven by phenotypic plasticity.