Cervical cancer is a public health problem diagnosed in advanced stages, and its main risk factor is persistent high-risk human papillomavirus infection. Today, it is necessary to study new treatment strategies, such as immunotherapy, that use different targets of the tumor microenvironment. In this study, the K14E7E2 mouse was used as a cervical cancer model to evaluate the inhibition of indolamine-2,3-dioxygenase 1 (IDO-1) and C-X-C chemokine receptor type 2 (CXCR-2) as potential anti-tumor targets. DL-1MT and SB225002 were administered for 30 days in two regimens (R1 and R2) based on combination and single therapy approaches to inhibit IDO-1 and CXCR-2, respectively. Subsequently, the reproductive tracts were resected and analyzed to determine the tumor areas, and IHCs were performed to assess proliferation, apoptosis, and CD8 cellular infiltration. Our results revealed that combined inhibition of IDO-1 and CXCR-2 significantly reduces the areas of cervical tumors (from 196.0 mm² to 58.24 mm² in R1 and 149.6 mm² to 52.65 mm² in R2), accompanied by regions of moderate dysplasia, decreased papillae, and reduced inflammation. Furthermore, the proliferation diminished, and apoptosis and intra-tumoral CD8 T cells increased. In conclusion, the combined inhibition of IDO-1 and CXCR-2 is helpful in the antitumor response against preclinical cervical cancer.

Background/Objectives: B-cell acute lymphoblastic leukemia (B-ALL) remains the most common pediatric malignancy. This study aimed to evaluate clinical outcomes in pediatric B-ALL in Southern Mexico and determine how socioeconomic vulnerabilities—specifically indigenous status and treatment non-adherence—independently drive relapse and compromise survival in a resource-limited setting. Methods: A retrospective cohort study was conducted, including 146 patients (0–17 years) treated between 2010 and 2024 using modified Total XIII and XV protocols. Survival was estimated via Kaplan–Meier. Independent prognostic factors for overall survival (OS) and relapse were identified using multivariable Cox proportional hazards models. Results: The 5-year OS was 50%, and event-free survival (EFS) was 37.6%. Survival varied significantly by clinical risk: 88% for low-risk, 77% for standard-risk, and 31% for high-risk patients. Relapse occurred in 45.8% of patients. Beyond established biological predictors like hyperleukocytosis and high-risk cytogenetics, socioeconomic vulnerabilities profoundly impacted outcomes. Documented treatment non-adherence significantly reduced 5-year OS (23.4% vs. 56.1%, p = 0.001) and disproportionately affected indigenous patients (55.5% vs. 10.1% in non-indigenous). Multivariable analysis identified indigenous status as an independent predictor of increased relapse hazard (HR = 1.89, p = 0.049), alongside male sex and high leukocyte count. Conclusions: Survival outcomes in this cohort are markedly lower than in high-income countries. The high incidence of relapse is deeply intertwined with local structural inequities. Improving survival requires complementing biological risk stratification with targeted strategies to overcome socioeconomic barriers and prevent treatment non-adherence.