Archive of Oncology
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Archive of Oncology covers resources on the mechanism, cause, and treatment of cancer including environmental and genetic risk factors, and cellular and molecular carcinogenesisOncology Institute of Vojvodina, Sremska Kamenica, Serbia, Faculty of Medicine, University of Novi Sad, Serbiaen-USArchive of Oncology0354-7310Impressum
https://aseestant.ceon.rs/index.php/aoo/article/view/62349
Archive of Oncology
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2025-10-232025-10-23312Intro with Editorial Board
https://aseestant.ceon.rs/index.php/aoo/article/view/62350
Archive of Oncology
Copyright (c) 2025 Archive of Oncology
2025-10-232025-10-23312Comparation of animal models of acute toxicity of doxorubicin
https://aseestant.ceon.rs/index.php/aoo/article/view/57014
<p class="MDPI17abstract" style="margin: 0cm; margin-bottom: .0001pt; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">Background</span></strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">: Animal models are essential for research in biomedicine. The cardiotoxicity of doxorubicin is the most common and severe side effect of this potent chemotherapeutic agent, and in order to investigate its prevention, a large number of studies have been performed on animal models. Unfortunately, the models are not uniform and the applied doses as well as the effectiveness vary significantly, often with great animal suffering.</span></p> <p class="MDPI17abstract" style="margin: 0cm; margin-bottom: .0001pt; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">Methods</span></strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">: Male Wistar rats were divided into three groups of 10 animals each and treated with saline solution intraperitoneally (group C), or with doxorubicin intraperitoneally in a single dose of 15 mg/kg (group G15) or 20 mg/kg (group G20). Body weight, mortality, the condition of animals, intensity of lipid peroxidation, activity of antioxidant enzymes and myocardial tissue damage (using doxorubicin damage score, DDS) were analyzed.</span></p> <p class="MDPI17abstract" style="margin: 0cm; margin-bottom: .0001pt; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">Results</span></strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">: Group 20, in comparison with groups G15 and C, exhibited the worse general condition, higher mortality and significantly higher intensity of lipid peroxidation. Both doses of doxorubicin induced a statistically significant decrease of </span><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; letter-spacing: -.1pt; mso-bidi-font-weight: bold;">superoxide dismutase (SOD), </span><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif';">glutathione peroxidase (GSH-Px), and glutathione-S-transferase (GST) </span><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">activity compared to the control group<span style="letter-spacing: -.15pt; background: white; mso-bidi-font-style: italic;">.</span> Among the doxorubicin-treated groups, GR is significantly more reduced in G15. GST is significantly more reduced in G20 while SOD and GSH-Px do not differ. The DDS score indicates myocardial tissue injury in both G15 and G20. </span></p> <p class="MDPI17abstract" style="margin: 0cm; margin-bottom: .0001pt; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">Conclusions</span></strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: windowtext;">: Both applied doses induce animal models of acute doxorubicin induced oxidative stress and cardiotoxicity</span><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif';">. A higher dose is more suitable for studies of oxidative stress, but should be applied with caution due to higher mortality. A lower dose is more suitable for studies focused on tissue morphology. </span></p>Milana BosanacBojana Andrejić VišnjićGolub SamardžijaJelena AmidžićNemanja MartićMaja Stefanović
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2025-10-232025-10-233123810.2298/AOO250224008BTranscriptome changes and deregulated biological pathways associated with NF1-mutated pheochromocytoma
https://aseestant.ceon.rs/index.php/aoo/article/view/59261
<p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: 200%;"><strong style="mso-bidi-font-weight: normal;"><span lang="EN-US" style="font-size: 12.0pt; line-height: 200%; font-family: 'Times New Roman',serif; mso-ansi-language: EN-US;">Background:</span></strong><span lang="EN-US" style="font-size: 12.0pt; line-height: 200%; font-family: 'Times New Roman',serif; mso-ansi-language: EN-US;"> Pheochromocytoma (PHEO) is a rare tumor of intraadrenal sympathetic origin. At least of 25-30% of PHEOs have been found to be linked to germline or somatic mutations in the <em style="mso-bidi-font-style: normal;">NF1</em> gene, which functions as a tumor suppressor. Despite the high frequency of NF1 mutations in PHEOs, the exact mechanism underlying the pathogenesis of these tumors has not yet been fully elucidated. </span></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: 200%;"><strong style="mso-bidi-font-weight: normal;"><span lang="EN-US" style="font-size: 12.0pt; line-height: 200%; font-family: 'Times New Roman',serif; mso-ansi-language: EN-US;">Methods:</span></strong><span lang="EN-US" style="font-size: 12.0pt; line-height: 200%; font-family: 'Times New Roman',serif; mso-ansi-language: EN-US;"> A large-scale analysis of transcriptomic profiles and biological pathways associated with <em style="mso-bidi-font-style: normal;">NF1</em>-related PHEOs was conducted utilizing RNA-Seq and miRNA-Seq data from the The Cancer Genome Atlas (TCGA) project.</span></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: 200%;"><strong style="mso-bidi-font-weight: normal;"><span lang="EN-US" style="font-size: 12.0pt; line-height: 200%; font-family: 'Times New Roman',serif; mso-ansi-language: EN-US;">Results:</span></strong><span lang="EN-US" style="font-size: 12.0pt; line-height: 200%; font-family: 'Times New Roman',serif; mso-ansi-language: EN-US;"> A total of 21 differentially expressed transcripts (14 genes, 3 long noncoding RNAs, and one microRNA) were identified in association with germline and somatic mutations in the <em style="mso-bidi-font-style: normal;">NF1</em> gene. The present study detected a decrease in the mRNA levels of <em style="mso-bidi-font-style: normal;">NF1</em>, as well as of its interacting partners, <em style="mso-bidi-font-style: normal;">SPRED3</em> and <em style="mso-bidi-font-style: normal;">EZR</em>. Decreased expression of oncogenic microRNA miR-423-3p was also observed. Seven differentially expressed genes (<em style="mso-bidi-font-style: normal;">SHC3</em>, <em style="mso-bidi-font-style: normal;">SHC1</em>, <em style="mso-bidi-font-style: normal;">STAT3</em>, <em style="mso-bidi-font-style: normal;">NF1</em>, <em style="mso-bidi-font-style: normal;">KSR1</em>, <em style="mso-bidi-font-style: normal;">NOS2</em>, and <em style="mso-bidi-font-style: normal;">ALDOC</em>) were found to be overrepresented in a number of distinct biological pathways, including those associated with RAS and HIF-1 signaling, pathway linked to resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, and the growth hormone-associated pathway. These findings suggest deregulation of these pathways in <em style="mso-bidi-font-style: normal;">NF1</em>-mutated PHEOs.</span></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: 200%;"><strong style="mso-bidi-font-weight: normal;"><span lang="EN-US" style="font-size: 12.0pt; line-height: 200%; font-family: 'Times New Roman',serif; mso-ansi-language: EN-US;">Conclusion:</span></strong><span lang="EN-US" style="font-size: 12.0pt; line-height: 200%; font-family: 'Times New Roman',serif; mso-ansi-language: EN-US;"> The results obtained demonstrate the consequences of <em style="mso-bidi-font-style: normal;">NF1</em> mutations at the level of the transcriptome. Furthermore, they confirm a change in RAS signaling pathways in <em style="mso-bidi-font-style: normal;">NF1</em>-related PHEOs.</span></p>Anastasiya SnezhkinaAnastasiya KobelyatskayaMaria FedorovaDmitry KalininVladislav PavlovAnna Kudryavtseva
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2025-10-232025-10-2331291510.2298/AOO250602010SThe efficacy of durvalumab in locally advanced lung carcinoma
https://aseestant.ceon.rs/index.php/aoo/article/view/59313
<p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman',serif; mso-fareast-font-family: 'Times New Roman';"> </span></strong><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';">Background:</span></strong><span style="font-size: 12pt; font-family: 'Times New Roman', 'serif';"> The integration of durvalumab, an immune checkpoint inhibitor, as consolidation therapy following platinum-based chemoradiotherapy has redefined the standard of care for patients with stage III, unresectable non-small cell lung cancer (NSCLC) who have not experienced disease progression. Although clinical trials, particularly the PACIFIC study, demonstrated significant improvements in survival outcomes, real-world data are still needed to validate these findings in routine clinical settings. This retrospective study aimed to evaluate the real-world efficacy of durvalumab in patients treated at the Institute for Pulmonary Diseases of Vojvodina, focusing on key clinical endpoints, progression-free survival (PFS), duration of clinical benefit (DoCB), and overall response rate (ORR), while exploring the influence of demographic and tumor-related factors.</span></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';">Methods:</span></strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';"> The study included 25 patients with stage III NSCLC, ECOG 0–1, and PDL-1 expression ≥1%, who received durvalumab after chemoradiotherapy. The treatment responses were evaluated using iRECIST criteria. The Kaplan-Meier analysis was used for survival metrics, and univariate Cox regression assessed the impact of histology, smoking status, PDL-1 expression, gender, and ECOG status.</span></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';">Results:</span></strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';"> A partial response was achieved in 36% of the patients, stable disease in 40%, and progression in 24%, with an ORR of 36%. The mean PFS was 19.8 months, and DoCB 25 months. Although the adenocarcinoma subtype, female gender, lower pack-year index, and higher PDL-1 expression suggested more favorable outcomes, no statistically significant differences were found.</span></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';">Conclusion:</span></strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';"> These findings confirm the clinical benefit of durvalumab consolidation in real-world practice, with outcomes comparable to pivotal trials. Despite the small sample size, the observed trends highlight potentially relevant prognostic markers. Expanding the patient cohort and extending the follow-up will further clarify these associations and support the evidence-based personalization of the NSCLC treatment.</span></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';"> </span></strong></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: normal;"><strong><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; mso-fareast-font-family: 'Times New Roman';"> </span></strong></p> <p class="MsoNormal" style="margin-bottom: .0001pt; text-align: justify; line-height: normal;"> </p> <p class="MsoNormal" style="line-height: normal;"><span style="font-size: 12.0pt; font-family: 'Times New Roman','serif';"> </span></p> <p class="MsoNoSpacing" style="text-align: justify; line-height: 150%;"> </p>Isidora Knežević
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2025-10-232025-10-23312162210.2298/AOO250604007KCoexistence of chronic lymphocytic leukaemia and polycythemia vera
https://aseestant.ceon.rs/index.php/aoo/article/view/57279
<p class="MsoNormal" style="text-align: justify; line-height: normal;"><span lang="TR" style="font-size: 12.0pt; font-family: 'Times New Roman','serif'; color: black; background: white;">We report a rare case of coexistence of chronic lymphocytic leukaemia (CLL) and polycythemia vera (PV) in a patient initially diagnosed and treated for CLL. A 61-year-old man presented with fatigue and night sweats, with laboratory tests showing elevated haemoglobin, hematocrit (HCT), leukocyte count and splenomegaly. Peripheral blood smear revealed lymphocytosis with basket cells, and flow cytometry confirmed CLL (RAI stage II). FISH analysis was negative for del13q, del11q, trisomy 12, del 17p and del6q. Chemotherapy was started because of B symptoms. Persistent splenomegaly and elevated HCT at follow-up prompted further evaluation, which revealed a JAK2 V617F mutation and an erythropoietin (EPO) level <1 mIU/mL, confirming PV. The patient achieved remission for CLL, but required hydroxyurea and acetylsalicylic acid for PV. The coexistence of CLL and PV is rare and the underlying mechanisms are not well understood, although a common clonal haematopoietic stem cell origin or germline mutations are possible explanations. Although chemotherapeutic agents are known to induce PV, the elevated HCT at the time of CLL diagnosis suggests a pre-existing relationship between the two diseases. Therefore, elevated HCT in CLL patients should prompt consideration of PV.</span></p>Ozlem BeylerCengiz Demir
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2025-10-232025-10-23312232510.2298/AOO250305009BInstructions for Authors
https://aseestant.ceon.rs/index.php/aoo/article/view/62351
Archive of Oncology
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