Goal: To analyze the tumor response to NACT in patients with aggressive biological subtypes of stage II–III breast cancer based on the contemporary scoring systems for residual pathological stage evaluation and the residual cancer burden according to the RCB system.

Materials and methods: A total of 172 women with stage II–III breast cancer of aggressive biological subtypes (triple negative in 34,3 %; HER2‑positive tumors in 28,5 %; luminal B Her2‑negative BC in 37,2 %) were included in this analysis. The median age of the patients was 47 years (24–81 years); сT2 was the predominant tumor size (65,1 %); 69,8 % of patients had regional lymph node involvement; 62,8 % of patients had G3 tumor; Ki67 ≥ 30 % was found in 90,7 % of cases. All patients received neoadjuvant chemotherapy (NACT) with concomitant anti-HER2 blockade in case of HER2‑positive tumors followed by surgery. Morphological assessment included evaluation of the residual pathological stage and the residual cancer burden according to the RCB system.

Results: Total pathological complete response (no evidence of residual invasive tumor in the breast and lymph nodes — tpCR) was observed in 69 of 172 patients (40,1 %), which corresponded to the уpT0N0 pathological stage and RCB class 0. The highest tpCR rate was achieved in patients with HER2‑positive cancer (63 % in non-luminal HER2‑positive subtype and 59.1 % in luminal HER2 + BC) and triple negative cancer (50,8 %). Meanwhile, the tpCR rate in patients with luminal HER2‑negative BC was only 15,6 %, p < 0.0001.

The proportions of the RCB classes in the whole sample were 6,4 % (RCB-I), 30,2 % (RCB-II), 23,3 % (RCB-III), and differed significantly between the biological subtypes. RCB class I was nearly absent in the triple negative cancer group (1,7 % only), the residual tumor corresponded to RCB classes II and III in 25,4 % and 23,7 % of cases, respectively. In the HER2‑positive cancer group, the percentage of patients with RCB class I residual tumors was 9,1 % and 11,0 % in luminal and non-luminal cancers, respectively. One of four patients had RCB class II; RCB class III was found only in 9 % of luminal HER2‑positive cancer cases and in no patients with non-luminal HER2‑positive subtype. Most patients with luminal B HER2‑negative BC had RCB II and III: 39,1 % and 37,5 % of cases, respectively, p < 0.0001.

Conclusions: patients with aggressive biological BC subtypes differed significantly not only in the rates of the total pathological complete response to NACT, but also in the distribution of residual cancer burden classes, which can be translated into the disease prognosis.

Breast cancer with skin involvement is one of the least studied and at the same time difficult to treat forms of cancer. Despite the achievements of modern diagnostics, many issues related to skin edema severity evaluation and quantitative assessment of changes associated with neoadjuvant drug therapy often cause a number of difficulties. In turn, this can lead to both incorrect staging and «overtreatment» of patients, as well as subjectivity in assessing the response to the treatment. Various approaches have been proposed to calculate the severity of edema, but they have not been widely accepted. This article presents our method developed for determining the area of skin edema, which in the future will allow individualizing approaches to treatment.

T3–4N0M0 breast cancer is rather rare among all breast cancers. The clinical features of these tumors and their biological nature are poorly studied in the scientific literature. In this study we showed that patients with T3N0M0 and T4N0M0 tumors revealed a number of common clinical features, comorbidities and biological characteristics of the tumor. At the same time carcinomas differed in their aggressiveness and the course of the disease. The history was shorter and the average tumor size was larger among patients from T3N0M0 group than in the T4N0M0 group, which indicates a higher tumor growth rate. Also, mean proliferation index ki-67 was higher in the T3N0M0 group than in the T4N0M0 group. The proportion of triple-negative and luminal B Her2‑negative biological subtypes was the largest in both the T3N0M0 and T4N0M0 groups. More than 50 % of women with T3–4N0M0 tumors had carcinomas with zero or low expression of hormonal receptors. Thus, such tumors were more aggressive and potentially highly sensitive to systemic chemotherapy in a significant proportion of patients with T3–4N0M0 breast cancer in our study.

Liver metastases is the most common type of colorectal cancer progression. Patients who have undergone surgical resection of liver metastases and received systemic antineoplastic therapy demonstrate the highest survival rates. Recog‑ nizing the oligometastatic disease as an individual entity has allowed identification of patients with advanced cancer who may benefit the most from the use of local treatment options. There are several methods of local treatment that can be currently used for the treatment of liver metastases: surgical resection, stereotactic radiation therapy, radiofrequency or microwave ablation, irreversible electroporation, and cryodestruction. The aim of our review is to provide a comparative assessment of the effectiveness, advantages and disadvantages of these techniques.

The most widespread infectious factors causing malignant neoplasms are human papillomaviruses (HPV). HPV geno‑ type 16 is often involved in the carcinogenesis of oropharyngeal squamous cell carcinoma, which occurs in 80 % of cases. The viral proteins E5, E6, and E7 are the main drivers responsible for the initiation and progression of cancer through the stimulation of cell proliferation, cell survival, inhibition of cell apoptosis and modulation of keratinocyte differentiation. The early promoter is initiated upstream of E6 independently of cell differentiation and synthesizes transcripts that are translated early in the viral life cycle. The launch of the late promoter depends on cell differentiation and activated for production transcripts that induce translation of the L1 and L2 proteins. During the entry of the virus into the cell, the L1 protein attaches to heparan sulfate proteoglycans (HSPG) on the extracellular matrix, after which the virus enters the cell by micropinocytosis. The interaction with HSPG is considered the initial contact that promotes conformational changes in the capsid, allowing the transfer of the virion to the secondary entry receptor. Cell division plays an important role in the delivery of the viral genome to the nucleus. HPV moves through the cytoplasm in the lumen of transport vesicles, which originate from the Golgi complex, line up along microtubules and are transmitted to condensed chromosomes. It is believed that the integration of the HPV genome increases the expression of HPV oncogenes in the cell, which contributes to uncontrolled cell proliferation and significant DNA damage. Integrated transcripts may be more stable and oncogenic than episomal-derived HPV transcripts.