Colorectal cancer (CRC) is one of the most common malignant neoplasms, characterized by high mortality and ranking among the leading causes of cancer-related deaths. It remains a major focus of gastroenterologists and oncologists. However, modern clinical practice increasingly promotes multidisciplinary teams, improving early diagnosis and treatment outcomes. Despite advances in oncologic diagnostics, cooperation with neurologists remains insufficient, although their role is crucial in detecting and managing post-treatment complications and paraneoplastic neurological syndromes (PNS). The prevalence of PNS is estimated at ~0.01% in the oncologic population, though likely underestimated due to limited neurological evaluation. Neurological symptoms may precede CRC diagnosis, yet their nonspecific nature often leads to misinterpretation and diagnostic delay. This article reviews studies on paraneoplastic neurological syndromes in colorectal cancer, emphasizing the neurologist’s role in oncologic diagnostics. A systematic search was performed in PubMed, Scopus, and Web of Science (2000-2025), covering case reports and clinical studies. The most frequently described PNS include paraneoplastic cerebellar degeneration, stiff-person syndrome, limbic encephalitis, and chronic inflammatory demyelinating polyneuropathy. Proper diagnosis differentiates disease progression from treatment complications. Notably, neurological symptoms may precede tumour detection by months and serve as early warning markers. In diagnosed cases, regular neurological follow-up enables earlier detection of new symptoms and better assessment of recurrence risk. Accurate interpretation of neurological signs requires close interdisciplinary collaboration, particularly with neurologists, who must maintain high diagnostic vigilance for atypical neurological presentations that may indicate an underlying malignancy.
Background: Colorectal cancer (CRC) remains a global health problem. It is the most common malignancy of the gastrointestinal tract, with a global incidence of over 1.9 million cases, making it the third most common cause of cancer-related deaths worldwide. The incidence is increasing particularly in low- and middle-income countries and among individuals under 50 years of age, with lifestyle and environmental factors contributing to this trend-many of which affect the gut microbiome. Main body: Advances in CRC treatment have introduced immunotherapy, particularly for tumours with mismatch repair deficiency (dMMR) and high microsatellite instability (MSI-H). This review explores the symbiotic relationship between the gut microbiome and immunotherapy in CRC. The human colon harbours a complex microbiome composed of diverse microbial species and vast genetic diversity, with structural, metabolic, and immunomodulatory functions. Dysbiosis, influenced by factors such as diet and lifestyle, contributes to CRC pathogenesis through inflammation and metabolic disruptions. Immunotherapy, specifically immune checkpoint inhibitors (ICIs), has revolutionized cancer treatment by enhancing T cell-mediated immune responses against cancer cells. In CRC, ICIs have demonstrated efficacy in MSI-H/dMMR tumours that represent less than 15% of all CRC cases. Challenges persist in treating microsatellite stable (MSS) CRC in regard to immunotherapy. Emerging evidence suggests that specific gut microbiota compositions influence the response to ICIs by modulating systemic immune responses and tumour microenvironments, potentially having a key role for MSS CRC patients. Strategies to manipulate the gut microbiome, including probiotics and faecal microbiota transplantation, hold promise in augmenting immunotherapy efficacy. Conclusion: The review underscores the potential of the gut microbiome as a predictive biomarker and therapeutic target in CRC immunotherapy. Ultimately, harnessing the therapeutic potential of the gut microbiome represents a promising avenue for enhancing immunotherapy outcomes and advancing personalized medicine in CRC care.
Paraneoplastic syndromes with ocular manifestations are rare but clinically significant immune-mediated disorders that may precede the diagnosis of malignancy. They arise from immune cross-reactivity between tumor and ocular antigens, leading to retinal or optic nerve damage through autoantibodies, cellular immunity, or soluble mediators. This narrative review summarizes current evidence on immunopathogenesis, clinical presentation, diagnostic approach, and oncologic implications. A literature search of PubMed, Scopus, and Web of Science was conducted for publications from January 2000 to September 10, 2025. Because of heterogeneity in study design and outcomes, the evidence was synthesized qualitatively. Ocular paraneoplastic syndromes most commonly present with subacute bilateral visual dysfunction, including vision loss, photopsias, scotomas, nyctalopia, and dyschromatopsia. Cancer-associated retinopathy is typically linked to antiretinal antibodies and rapid photoreceptor dysfunction, while melanoma-associated retinopathy is associated with metastatic melanoma, TRPM1 antibodies, and an electronegative electroretinogram. Paraneoplastic optic neuropathy, including CRMP5-associated forms, may mimic inflammatory or infectious optic nerve disease and requires careful differential diagnosis. Management relies on prompt detection and treatment of the underlying malignancy together with immunomodulatory therapy tailored to the ocular phenotype. Immune checkpoint inhibitors further complicate diagnosis and management, underscoring the need for multidisciplinary care.
Cancer remains one of the leading causes of death worldwide, and conventional therapies such as chemotherapy and radiotherapy often face major limitations including severe toxicity, non-specific targeting, and drug resistance. These drawbacks have emphasized the need for innovative and targeted treatment strategies in oncology. Immunotherapy has emerged as a breakthrough approach that utilizes the body?s immune system to identify and eliminate cancer cells, offering durable responses and improved patient survival. This review was conducted through an extensive analysis of recent research articles, clinical trial data, and FDA-approved reports published between 2016 and 2025. It provides a comprehensive overview of various immunotherapeutic modalities such as checkpoint inhibitors, CAR-T cell therapy, immune modulators, and combination approaches, while also addressing mechanisms of resistance that limit therapeutic success. Our review concludes that integrating immunotherapy with conventional cancer pharmacology offers enhanced efficacy, reduced toxicity, and paves the way for future personalized and combination-based treatment.
Insulinoma represents a benign, insulin-secreting neuroendocrine tumor of the beta cells of islets of Langerhans in the pancreas, which leads to frequent episodes of hypoglycemia. Surgery is the definite treatment. However, the perioperative treatment of patients with insulinoma is highly challenging. We present the perioperative management of a 46-year-old obese male patient with insulinoma. As the patient reported frequent severe hypoglycemia episodes, the main priority of the perioperative treatment was to prevent hypoglycemia before tumor resection and to control rebound hyperglycemia after tumor removal. Maintaining normoglycemia was challenging during the regular fasting period before abdominal surgery, as well as during the intervention, as general anaesthesia masks the symptoms of hypoglycemia. Obesity further complicated the anaesthetic management, due to expected difficult airway management and central venous access. Glycemia was monitored in 15-minute intervals during surgery and in 30-minute intervals postoperatively, and dysglycemia was corrected according to the trend of variations. As insulinoma is a rare phenomenon with an unpredictable clinical course, current reportings regarding the anaesthetic management of patients with this pathology are relatively lacking. Therefore, our case report could contribute to expanding the limited data about the perioperative treatment of patients with this condition.
Introduction. Desmoid type fibromatosis (DT) represents a rare benign tumor formation characterized by local aggressive behavior but an absence of metastatic potential. Histologically, they are often misdiagnosed, leading to unnecessary radical surgery. Even with proper diagnosis, there are different approaches and unclear protocols for the treatment of DT. Case report. The study presents the case of a 33-year-old male who presented to the emergency department with a large swelling of the abdominal wall that had been present for two years. An ultrasound was performed, and the abdominal swelling was described by the radiologist as a ventral hernia. After further radiological studies (CT scan and magnetic resonance imaging), a diagnosis of a tumor of the abdominal wall was established. A partial biopsy led to the diagnosis of sarcoma. Surgery was planned as the tumor was growing rapidly, reaching around 30 cm and causing necrosis of the abdominal wall skin. After the resection of 8.5 kg of tumor with clinically clear margins, the defect was reconstructed by placing a polypropylene mesh and using a darn nylon suture with a local rotational skin flap. In the postoperative days, an infection of the surgical wound developed. The infection resolved in two weeks without further complications. The definitive histopathological diagnosis was desmoid type fibromatosis. Conclusion. Active surveillance is now regarded as the most acceptable strategy for the treatment of DT. A better understanding of the genetic alterations underlying DT and the identification of prognostic factors that favor aggressive behavior will lead to the development of appropriate individual strategies and tailored therapy for each patient.
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.
Background: 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.Methods: 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.Results: 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 superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione-S-transferase (GST) activity compared to the control group. 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.Conclusion: Both applied doses induce animal models of acute doxorubicin induced oxidative stress and cardiotoxicity. 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.
Background: 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.Methods: 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.Results: 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.Conclusion: 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.
Background: Pheochromocytoma (PHEO) is a rare tumor of intraadrenal sympathetic origin. At least 25-30% of PHEOs have been found to be linked to germline or somatic mutations in the neurofibromin 1 (NF1) gene, which functions as a tumor suppressor. Despite the high frequency of NF1 gene mutations in PHEOs, the exact mechanism underlying the pathogenesis of these tumors has not yet been fully elucidated.Methods: A large-scale analysis of transcriptomic profiles and biological pathways associated with NF1-related PHEOs was conducted utilizing RNA-Seq and miRNA-Seq data from the The Cancer Genome Atlas (TCGA) project. The studied dataset comprised 143 patients with PHEOs.Results: 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 NF1 gene. The present study detected a decrease in the mRNA levels of NF1, as well as of its interacting partners, SPRED3 and EZR. A decreased expression of oncogenic microRNA miR-423-3p was also observed. Seven differentially expressed genes (SHC3, SHC1, STAT3, NF1, KSR1, NOS2, and ALDOC) were found to be overrepresented in a number of distinct biological pathways, including those associated with RAS and HIF-1 signaling, the pathway linked to the resistance to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, and the growth hormone-associated pathway. These findings suggest the deregulation of these pathways in NF1-mutated PHEOs.Conclusion: The results obtained demonstrate the consequences of NF1 gene mutations at the level of the transcriptome. Furthermore, they confirm a change in RAS signaling pathways in NF1-related PHEOs.
Background: Colorectal cancer (CRC) is one of the leading causes of cancer-related morbidity and mortality worldwide. Microsatellite instability (MSI) is a crucial biomarker with prognostic and predictive value, influencing treatment decisions in CRC. Methods: This retrospective study investigated the impact of the MSI status on clinical outcomes in 184 CRC patients treated at the Oncology Institute of Vojvodina between 2018 and 2023. The MSI status was determined using the immunohistochemical analysis of mismatch repair proteins. Results: Among the cohort, 75% of tumors were microsatellite-stable (MSS), 4.3% exhibited low MSI (MSI-L), and 20.6% displayed high MSI (MSI-H). MSI-H tumors were significantly associated with right-sided CRC, mucinous differentiation, and female gender (p<0.05). The survival analyses revealed that the MSI-H patients with stage II disease had significantly better disease-free survival (DFS) and overall survival (OS) than the MSS counterparts (p=0.024 and p=0.006, respectively). Conversely, the MSI-H status in stage II patients receiving adjuvant therapy was linked to shorter DFS (p=0.000), highlighting the limited benefit from 5-fluorouracil-based regimens. In stage III CRC, the MSI status did not significantly affect DFS or OS. Conclusion: These findings underscore the dual role of MSI as a favorable prognostic marker in early-stage CRC and a predictor of the reduced benefit from adjuvant chemotherapy in stage II disease. This study emphasizes the need for individualized treatment strategies based on the MSI status and supports the potential integration of immunotherapy in the adjuvant setting for MSI-H CRC.
Background: Toxoplasmosis, caused by Toxoplasma gondii, affects around 40% of the Iranian population and can be severe in vulnerable patients, such as those receiving chemotherapy. In this study, the titers of IgG and IgM antibodies in 92 children treated with chemotherapy have been compared with 92 matched controls. We also looked into the demographic and lifestyle factors in association with the antibody levels as a contribution to the development of improved preventive and management techniques. Methods: In this case-control study conducted at Shahid Madani Hospital, Khorramabad, Iran, blood samples of both groups were tested for IgG and IgM anti-Toxoplasma gondii antibodies by ELISA. The participants were selected randomly, and demographic, clinical, and lifestyle data were obtained from structured interviews and from the hospital records. Statistical analyses were performed using SPSS software, considering p-values less than 0.05 as significant. The approval for ethics was obtained, and an informed consent was provided by the guardians. Results: The results revealed that the prevalence of IgG antibodies was significantly higher in chemotherapy patients (35.9%) compared to the controls (14.1%), indicating a strong association between immunosuppression and elevated IgG levels (p = 0.001, OR = 2.026). No significant difference in IgM antibodies was found, suggesting that chemotherapy increases the risk of reactivation rather than new infections. Subgroup analysis showed that IgG positivity was more common in younger immunocompromised patients (under 10 years old). However, factors such as gender, residence, and dietary habits did not significantly affect IgG or IgM positivity. In the control group, urban residents had a higher IgG positivity rate than rural ones. Conclusion: In conclusion, pediatric patients who have undergone chemotherapy are more prone to chronic infection with Toxoplasma gondii. Serological tests and prevention measures must be carried out regularly to reduce the risk of reactivation in such patients.
Insulinoma represents a benign, insulin-secreting neuroendocrine tumor of the beta cells of islets of Langerhans in the pancreas, which leads to frequent episodes of hypoglycemia. Surgery is the definite treatment. However, the perioperative treatment of patients with insulinoma is highly challenging. We present the perioperative management of a 46-year-old obese male patient with insulinoma. As the patient reported frequent severe hypoglycemia episodes, the main priority of the perioperative treatment was to prevent hypoglycemia before tumor resection and to control rebound hyperglycemia after tumor removal. Maintaining normoglycemia was challenging during the regular fasting period before abdominal surgery, as well as during the intervention, as general anaesthesia masks the symptoms of hypoglycemia. Obesity further complicated the anaesthetic management, due to expected difficult airway management and central venous access. Glycemia was monitored in 15-minute intervals during surgery and in 30-minute intervals postoperatively, and dysglycemia was corrected according to the trend of variations. As insulinoma is a rare phenomenon with an unpredictable clinical course, current reportings regarding the anaesthetic management of patients with this pathology are relatively lacking. Therefore, our case report could contribute to expanding the limited data about the perioperative treatment of patients with this condition.
The effectiveness of anti-PD-1/PD-L1 targeted therapies focused on the antitumor immune response restoration in the treatment of melanoma and several other tumors has renewed trust in immunotherapy potential. Despite inspiring enthusiasm that led both to the expansion of indications for anti-PD-1/PD-L1 monoclonal antibodies and to an explosive growth in trials of new immune checkpoint inhibitors, a number of unresolved problems remain: relatively low response rates to existing drugs, development of acquired resistance, tumor progression and immune-mediated adverse events. Both the response to anti-checkpoint therapy and possible adverse reactions are based on quantitative and functional changes in malignant cell clones, tumor microenvironment and immune cells. An indispensable role in these interactions is played by regulatory T cells (Tregs), a heterogeneous population of CD4+ T lymphocytes capable of suppressing the immune response. It is known that, like conventional T cells, Tregs up-regulate several checkpoint receptors, including PD-1, TIM-3, LAG-3. However, the biological relevance of such expression and the consequences of Treg checkpoint blockade are vague, as data from in vitro and clinical observations are contradictory. Here, we reviewed the current understanding of inhibitory checkpoint receptor expression by Treg populations and their relationship with the effects of treatment with checkpoint inhibitors.
This study aimed to review the effects of different arm immobilization methods on set-up accuracy in photon and proton radiotherapy techniques for breast cancer with supraclavicular lymph node (LN) involvement. A systematic review was conducted using a comprehensive literature search of English-language sources from PubMed, Google Scholar, ScienceDirect, and Medline databases, with no restrictions on publication date. Two independent reviewers assessed and screened titles and abstracts for inclusion. Following screening and eligibility determination, 14 articles were included. Of these, 11 studies focused on photon radiotherapy (8 in the supine position and 3 in the prone position), while 3 studies examined proton radiotherapy. For the supine position, the "both hands above the head" method demonstrated superior set-up accuracy. In the prone position, the crawl position combined with the deep inspiration breath-hold (DIBH) method outperformed other approaches. In proton radiotherapy for breast cancer, both "hands-up" and "hands-down" methods yielded equivalent results.
Introduction: Paget's disease of the vulva is an intraepithelial adenocarcinoma, primarily arising from vulvar skin glands, with or without an underlying invasive adenocarcinoma. It brings low mortality and a high local recurrence rate and mainly affects postmenopausal women. Case outline: This is a case report of a 57-year-old postmenopausal woman, who had histopathological (HP) verified Extramammary Vulvar Paget's disease (EVPD) in 2014, and underwent a radical vulvectomy with a right-sided inguinofemoral lymphadenectomy and V-Y flap at the Oncology Institute of Vojvodina. Nine years later, in 2023, the patient was presented with a biopsy HP proven EVPD recurrence. The recurrence was surgically treated with vulvectomy and bilateral fasciocutaneous V-Y flaps reconstruction. The operative HP specimen proved the EVPD recurrence with atypical cells on one edge of the specimen. Due to the infection-complicated healing and wound dehiscence, the first reoperation was performed, which included wound debridement and left-sided rotational flap. We carried out the wound care and toileting in the postoperative course, with antibiotic treatment. Due to infection-complicated healing, tissue necrosis and consequent dehiscence, the second reoperation was performed, which included wound debridement with granulation tissue excochleation and Tiersch-type skin graft. Conclusion: The patient was discharged 21 days after the second reoperation in good condition. A regular oncological postsurgical follow-up on the 3th and 6th month revealed no recurrence or deterioration of the general condition or local findings. The patient subjectively feels well and has no complaints or unwanted effects of the applied treatment.
Background: Despite the progress in individualizing breast cancer therapy and achieving success in surgical and systemic treatment, the mortality remains high, which requires the search for new targets that can have a significant direct or indirect contribution to the development and prognosis of this disease. One such factor is vitamin D, which is deficient in most parts of the world, and its serum and receptor status have been extensively studied. Numerous studies have been published on the protective effects of vitamin D on breast cancer and other malignancies, risk of development, and treatment outcomes, in particular, increasing the sensitivity of tumors to systemic therapy, survival, and prognosis. Methods: The authors analyzed and systematized research data on the predictive effect of vitamin D on the prognosis and course of breast cancer, the manifestation of its "non-classical" effects in preclinical and clinical studies, and assessed the possible practical application of the results obtained at the molecular-cellular level. The results allow us to use vitamin D as an important marker for monitoring the skeletal system's state during and after breast cancer treatment. In addition, vitamin D and its analogues in combination with other cytostatic drugs can help search for possible new therapeutic targets. Conclusion: The presented results of vitamin D activity associated with the stages of carcinogenesis undoubtedly open up prospects for finding new possibilities for the treatment and prevention of breast cancer, creating prospects for further research to improve the prognosis and survival rates for such patients. The studied cytotoxic effects expand the field of clinical research on the "non-classical" properties of vitamin D and allow the integration of data on a potential antitumor agent for many malignant tumors.
Insidious, usually painless, and rare inguinoscrotal masses arising from paratesticular elements (spermatic cord, epididymis, tunica or the stroma) are known as paratesticular tumors. The overall incidence is less than 5%, and the total number of giant (>10cm) paratesticular liposarcomas is less than 300 cases recorded since 2020. We report a similar clinical dilemma of a giant scrotal mass managed via a wide local resection and close surveillance in a 61 year old male. However, owing to its rarity, there is no fixed treatment protocol; hence, a supplementary review of similar cases is discussed here.
Objective: The occurrence, development, invasion, and metastasis of tumors are closely linked to angiogenesis, which is reflected by tumor microvessel density. The aim is to analyze microvascular density (MVD) in groups of patients with high grade squamous intraepithelial lesions (H-SIL), and cervical carcinoma, and to compare MVD in relation to the degree of tumor differentiation, size, presence of lymphovascular invasion and lymph node metastases. Materials and methods: The study was retrospective, conducted on histopathological samples of 109 patients who underwent hysterectomy with/without adnexectomy. Patients were divided into two groups depending on the histopathological results: group A - patients with H-SIL, and B with cervical cancer. The control group included surgically treated patients with benign uterine diseases. Based on hematoxylin/eosine staining, representative sample was chosen for immunohistochemistry, and the analysis of CD34 antigen expression and measurement of MVD were done. Results: In order to subdivide groups according to the low (L) and high (H) MVD, in control, group A, and B, with mean MVDs 2.2; 9.85 and 17.19, respectively, a cut-off values were determined. In the control group, LMVD 100% was measured. There were 7 (21.21%) in group A and 29 patients (63.04%) in group B with HMVD. A statistically significant difference was confirmed by comparing HMVD and LMVD in cervical cancer patients with lymph nodes metastasis (p<0.029). In the subgroup of patients with other worse pathohistological prognostic factors, a tumor size greater than 2 cm, depth of stromal invasion >10 mm, infiltration of "isthmus" of the uterus, a difference with no statistical significance was confirmed. Conclusion: Invasive cervical cancers are characterised by a significantly higher mean values of MVD compared to H-SIL. Significantly more often, HMVD is associated with the presence of lymph node metastases and histopathological parameters of poor prognosis.
