Wspolczesna Onkologia-Contemporary Oncology最新文献

Actinic keratosis (AK) is a common precancerous skin lesion with the potential to progress into cutaneous squamous cell carcinoma (cSCC). Understanding molecular markers involved in AK pathogenesis can aid in assessing disease severity, monitoring treatment response, and identifying patients at risk of malignant transformation. This review examines key biomarkers, including Ki-67, p53, matrix metalloproteinases (MMPs), cyclooxy-genase-2 (COX-2), and minichromosome maintenance protein 2 (MCM2), focusing on their role in AK progression and response to photodynamic therapy. Ki-67, a proliferation marker, declines following successful AK treatment, making it a useful therapeutic indicator. p53 mutations, common in AK, are linked to disease progression, but post-treatment persistence of mutant cells suggests the need for multiple therapy sessions. MMP-1 and MMP-2 contribute to extracellular matrix remodeling and may serve as markers of treatment efficacy. COX-2, associated with inflammation, is upregulated in AK, but its prognostic significance remains uncertain. MCM2 expression correlates with AK severity and proliferation, yet its role in cSCC progression requires further investigation. These findings highlight the importance of molecular biomarkers in AK diagnosis and treatment monitoring, suggesting that while Ki-67 and MMPs may be valuable therapeutic markers, additional research is needed to fully integrate these biomarkers into clinical practice.

Introduction: In 2020 in Poland a total of 3 589 people had pancreatic cancer (PC). Only 20% of patients were diagnosed with surgical disease. New therapeutic options that demonstrate statistically significant improvements in overall survival (OS) and progression-free survival (PFS) are still being sought. However, the assessment of treatment efficacy and safety in non-selected patients in a real-life setting may provide useful information to support decision-making processes in routine practice.

Material and methods: The aim of the clinical study was a retrospective analysis of the medical history of 182 patients with the diagnosis of metastatic pancreatic cancer (mPC), who were treated with combination treatment of nab-paclitaxel with gemcitabine (GEM-NAB) between February 2017 and September 2023. Our study also aimed to identify important population-based predictors for survival in patients diagnosed with mPC.

Results: The median age was 66 years (range 37-84 years). Median OS was 9.2 months (95% CI: 8.3-10.03), and median PFS was 5.47 months (95% CI: 4.83-6.1); 26 patients achieved either a partial or complete response (overall response rate 14%). GEM-NAB was well tolerated. The most common adverse events were alopecia, fatigue, neutropenia, anemia, and peripheral neuropathy. This study identified specific clinical and laboratory parameters (neutrophil to lymphocyte ratio, antigen Ca 19.9, mechanical jaundice, peripheral neuropathy and 2^nd and 3^rd lines of treatment) as independent prognostic factors.

Conclusions: Our results confirm the efficacy and tolerability of GEM-NAB as standard first-line treatment in patients with mPC. Among the factors having the greatest impact on OS was the 3^rd line of treatment, and for PFS the presence of peripheral neuropathy.

Microglandular adenosis (MGA) is a rare benign breast condition characterized by disorganized small glands composed of epithelial cells without myoepithelial components. Microglandular adenosis can coexist with invasive breast cancer (IBC), particularly the triple-negative (TN) subtype. Emerging evidence suggests MGA may be a precursor to IBC, supported by shared morphological and molecular features. We present the case of a 66-year-old woman with a palpable mass in the left breast. Initial mammography and biopsy suggested malignancy. The patient underwent breast-conserving surgery with resection of the sentinel lymph node. Histopathological analysis confirmed triple-negative, basal-like invasive breast carcinoma with focal salivary gland-type carcinoma differentiation, likely arising from an MGA-like component. The patient subsequently received adjuvant chemotherapy, and no recurrence was observed after a 30-month follow-up. This case underscores the importance of recognizing MGA as a potential precursor to invasive breast carcinoma, particularly the TN subtype. Increased awareness and the use of comprehensive diagnostic methods are essential for improving patient outcomes and managing the risks associated with MGA, especially in cases that may progress to more aggressive forms of cancer.

Introduction: Accelerated chronic lymphocytic leukemia (A-CLL) is a rare histological variant of CLL, which is associated with an aggressive clinical presentation and worse prognosis. The aim was to study the characteristics and treatment outcomes of A-CLL patients.

Material and methods: The retrospective analysis included 106 A-CLL patients treated in Poland between 2013 and 2023.

Results: Median overall survival (OS) for treatment-naive A-CLL was 6.05 years (95% CI: 4.7-NA) and median progression-free survival (PFS) was 5.66 years (95% CI: 4.05-6.34). Factors associated with worse PFS were: Eastern Cooperative Oncology Group > 2 (p < 0.0001) and del17p (p = 0.002). In the whole group, fludarabine-based regimens improved OS (p = 0.002) and PFS (p = 0.002). This therapy proved superior to R-CHOP-like protocols for both OS (p = 0.002) and PFS (p = 0.004). The difference in survival between fludarabine-based regimens and targeted therapy was not significant. However, the group of patients treated with new therapies was very heterogeneous. Fludarabine (p = 0.004) or targeted therapy (p = 0.02) in any line of treatment during acceleration was associated with a reduced risk of death.

Conclusions: This study represents one of the largest datasets of A-CLL patients and shows its poorer prognosis compared to typical CLL. Chronic lymphocytic leukemia directed therapy should be considered as a treatment modality of choice for A-CLL. R-CHOP protocols are less effective.

Glioblastoma (GBM) is the most aggressive and lethal primary brain tumor, characterized by rapid progression, treatment resistance, and poor prognosis, with a survival rate of less than five years despite advances in medical interventions. A hallmark of GBM is metabolic reprogramming, which supports tumor growth and progression. Mitochondrial dysfunction plays a critical role in this metabolic shift by altering energy production and disrupting key cellular pathways. However, the precise molecular mecha-nisms underlying these alterations remain inadequately understood. This review highlights the fundamental contributions of mitochondrial oxidative phosphorylation (OXPHOS) and the electron transport chain (ETC) to GBM pathology. Notably, deficiencies in mitochondrial DNA and its associat-ed molecular components have been identified as key factors contributing to impaired mitochondrial function. Additionally, an imbalance in reactive oxygen species production within the ETC has been implicated in driving cellular and metabolic changes that promote tumor progression. Given the central role of mitochondrial metabolism in GBM, targeting OXPHOS and ETC components presents a promi-sing therapeutic approach. This review also discusses current pharmacolo-gical strategies aimed at modulating mitochondrial respiration, with a focus on drugs and compounds that selectively inhibit OXPHOS complexes. Understanding the intricate relationship between mitochondrial dysfunction and GBM progression may provide valuable insights for developing novel therapeutic interventions, ultimately improving clinical outcomes for patients with this devastating disease.

Introduction: Malnutrition is highly prevalent in cancer patients, significantly influencing their clinical outcomes and prognosis. The study was conducted to investigate the association between inflammatory biomarkers, nutritional status and progression of the disease across various types of cancers.

Material and methods: Retrospective data from 200 consecutive Caucasian cancer patients admitted to a major oncology hospital for cancer treatment were analyzed according to age, sex, cancer type, nutritional status (percentage body weight loss - %BWL), body mass index (BMI), percentage of dietary intake from the calculated requirement for nutrients (%DI)), and laboratory results (albumin levels, total protein concentration, C-reactive protein - CRP). Inflammatory biomarkers such as prognostic nutritional index (PNI), neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) were assessed.

Results: Prognostic nutritional index (ρ = -0.464, p < 0.001), PLR (ρ = 0.293, p = 0.019), albumin level (ρ = -0.490, p < 0.001), platelet count (ρ = 0.114, p = 0.370), neutrophil count (ρ = 0.273, p = 0.030), CRP (ρ = 0.293, p = 0.019) and lymphocyte count (ρ = -0.288, p = 0.021) were significantly associated with %BWL. No significant association was found with NLR. Cancer dissemination was significantly associated with PNI (OR: 0.93, 95% CI: 0.88-0.98), PLR (OR: 1.00, 95% CI: 1.00-1.01), albumin (OR: 0.86, 95% CI: 0.80-0.93), platelet count (OR: 1.01, 95% CI: 1.00-1.01), %BWL (OR: 1.06, 95% CI: 1.02-1.10) and %DI (OR: 0.97, 95% CI: 0.96-0.99) but not with NLR, total protein level, total lymphocyte count, or BMI. For patients with albumin levels below 35 g/l, the likelihood of disseminated cancer was more than five times higher (OR: 5.45, 95% CI: 2.05-14.48).

Conclusions: The intensity of inflammation may be responsible for the severity of malnutrition and cancer prognosis.

Rosai-Dorfman disease (RDD), or sinus histiocytosis with massive lymphadenopathy, is a rare histiocytic disorder that often mimics malignancies and immune-mediated conditions such as IgG4-related disease (IgG4-RD). We report a 73-year-old male with a 2-year history of systemic symptoms, including fever, significant weight loss, and generalised lymphadenopathy, accompanied by strikingly elevated IgG4 levels. Advanced imaging revealed metabolically active lesions in lymph nodes, paranasal sinuses, and bones, complicating the differential diagnosis and raising concerns for malignancy or IgG4-RD. Histopathological examination revealed hallmark features of RDD, including S-100 positivity highlighting emperipolesis and negative CD1a staining, leading to the final diagnosis. The patient initially improved with glucocorticosteroids but achieved sustained symptom resolution with methotrexate, underscoring the potential of antimetabolites for systemic RDD. This case exemplifies the diagnostic and therapeutic challenges of RDD, emphasizing the importance of a multidisciplinary approach and further investigation of targeted therapies for complex and systemic presentations.

Renal cancer accounts for approximately 4.4% of all malignant tumors worldwide. In the case of tumors limited to the kidney, the primary method of treatment is surgery. For advanced renal cell carcinoma (RCC), one of the treatment methods is targeted therapy aimed at molecular targets via tyrosine kinase inhibitors (TKIs). These drugs are administered orally, significantly improving the comfort of patients. However, for a drug administered in oral form to produce the intended effect in the body, it must undergo many transformations during which it interacts with various chemical compounds. These include other medications taken by the patient and those derived from food. As a result of these interactions, at each stage of the drug's transformation, there may be interactions between that drug and these substances. Information about possible drug-drug interactions is widely available. In contrast, knowledge about drug-food interactions is a relatively new area of medical research. It has been demonstrated that these interactions can affect not only the increased toxicity of the therapy but also its effectiveness. This study reviews the possible interactions of popular food products with TKIs used in RCC treatment, at different stages of drug metabolism, and the possible mechanisms of these interactions.

Introduction: It is widely accepted that anaplastic lymphoma kinase (ALK) fusion gene-positive non-small cell lung cancer (NSCLC) patients are more likely to be in their 50s, female, and non-smoking. This seems to be due to the background of patients involved in clinical trials of ALK-tyrosine kinase inhibitors. However, in daily clinical practice, it is not uncommon to encounter elderly ALK-positive NSCLC patients with a smoking history. In light of this background, we conducted a survey to clarify the clinical backgrounds of ALK-positive patients with NSCLC, particularly regarding age and smoking.

Material and methods: A retrospective medical chart survey of patients with ALK-positive NSCLC diagnosed in 2012 to 2024 in our six institutes was conducted.

Results: During the study period, 140 pa-- tients were diagnosed with ALK-positive NSCLC, of which 90 (64.3%) were women. The median age of all 140 pa-- tients was 63 years (range, 26-84 years). Among these 140 patients, 38.6% had a history of smoking. There was a significant difference in the distribution of smokers by sex and age.

Conclusions: Even among NSCLC patients who are elderly or have a history of smoking, there may be some who miss out on the best possible treatment by exclusion from ALK testing. Discussions considering the efficiency and cost of testing are needed, and it is essential to collect and reanalyse as much information as possible about the clinical characteristics of ALK-positive NSCLC patients.

Introduction: Despite the introduction of new therapies for the treatment of advanced melanoma, treatment is ineffective for a certain number of patients. The efficacy of chemotherapy after failure of anti-programmed death receptor (PD-1) immunotherapy alone or combined with anti-cytotoxic T-lymphocyte-associated antigen (CTLA) is not fully understood. It is believed that due to the immunomodulatory effect of cytostatic agents, its efficacy may be greater when applied after the failure of immunotherapy. The aim of this study was to evaluate the efficacy of different chemotherapy regimens after failure of immunotherapy.

Material and methods: Patients with advanced melanoma after failure of immunotherapy (anti-PD1+/- anti-CTLA-4) and BRAF mutation-targeted therapy with a BRAF/MEK inhibitor were included in a multicenter, retrospective analysis. Patients were treated with one of four chemotherapy regimens: dacarbazine (DTIC); paclitaxel with carboplatin; cisplatin, vinblastine and dacarbazine (CVD) or bleomycin, DTIC, lomustine, vincristine. The objective response rate (ORR), disease control rate (DCR), median progression-free survival (PFS) and overall survival (OS) were compared in study patients.

Results: One hundred twenty-four patients were included in the study. Objective response rate was 16.88%, DCR was 38.96%, while median PFS and OS were 2.75 [95% CI: 2.25-3.5] and 6 months [95% CI: 4.75-40], respectively. There were no statistically significant differences in ORR, DCR, median PFS, and OS rates between the patients receiving different chemotherapy regimens.

Conclusions: In advanced melanoma patients after failure of immune-checkpoint inhibitors with or without BRAF/MEK inhibitors, the choice of chemotherapy regimen remains dependent on the patient's general condition, comorbidities, the need for rapid reduction of tumor masses, and physician and patient preference.