Pathogenesis of cancer - Сергей Шалин

Pathogenesis of cancer

Страниц

25

Год

2024

Книга обсуждает патогенез рака, указывая на необходимость определения первичной мутации ядерной ДНК генома предшественника раковых клеток. Автор предлагает теоретически обосновать, какая клетка может играть роль предшественника раковой клетки, учитывая функциональные возможности раковой клетки, полученные от соматической клетки, и патологическое состояние тканей, создающих оптимальные условия для появления злокачественной стволовой клетки, её роста и развития. Также рассматриваются ключевые понятия: инициирование, продвижение, моноциты, злокачественная стволовая клетка, мутация. Введение освещает многостадийный механизм возникновения и развития злокачественного процесса. Делается акцент на разделение злокачественных заболеваний на гемобластозы и солидные опухоли, где рассматривается цитогенез рака кроветворных и лимфоидных тканей, а также проблемы цитогенеза солидных опухолей. Отсутствие четкой представленности о происхождении злокачественных клеток затрагивается как слабый звено существующей теории.

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We can talk about the pathogenesis of cancer only by determining the primary mutation of the nuclear DNA of the genome of the precursor cell of the cancer cell. It is possible to theoretically substantiate which cell can lay claim to the role of a precursor cell of a cancer cell if we take into account the functional abilities of the cancer cell received from a somatic cell and the pathological state of the tissues that created optimal conditions for the emergence of a malignant stem cell, the growth and development of the malignant process. Key words: initiation, promotion, monocyte, malignant stem cell, mutation.

Key words: initiation, promotion, monocyte, malignant stem cell, mutation.

INTRODUCTION

Carcinogenesis or oncogenesis is a multi-stage mechanism of the emergence, growth and development of a malignant process. According to the modern theory of carcinogenesis, the occurrence of a malignant tumor is the result of the sequential accumulation of mutations in the somatic cells of the body that are not inherited. When the number of mutations becomes critical, the formation of a primary malignant stem cell occurs. The weak link of this theory is the absence of a cancer cell precursor cell. In a morphological study, it looks like this: a healthy normal cell, next to it a malignant cell, there is no transitional variant or precursor cell to a cancer cell.

MALIGNANT DISEASES

All human malignant diseases are divided into two main groups: hemoblastoses and solid tumors. The principle of division is based on the different localization of the malignant process and some similarity between malignant cells and normal cells of the microenvironment. The cytogenesis of malignant diseases of hematopoietic and lymphoid tissue is considered the most studied, which is based on the doctrine of stem and semi-stem precursor cells of hematopoiesis. Cytogenesis of solid tumors has not yet been studied; there is no clear idea from which progenitor cells malignant cells arise. That is why we will mainly consider issues related to solid tumors, drawing a possible analogy with hemoblastoses.

General signs of hemoblastoses and solid tumors.

1. Etiology: chemical agents (endo- and exocarcinogens), ionizing radiation.

2. Pathogenesis: nuclear DNA mutations and epigenetic changes – damage to the structure of the cell membrane and chemical processes in the cytoplasm of the cell. 3. Diagnostics: clinical, laboratory and instrumental research methods with mandatory morphological verification of the diagnosis (histological and cytological studies).

4. Complications: infectious, thrombotic, disruption of the normal mechanism of osteogenesis, gastrointestinal complications (nausea, vomiting, hiccups, constipation, diarrhea and mucositis), intoxication and psychological changes (anxiety, depression, aggressiveness and suicide).

5. Principles of pathogenetic therapy: influences that suppress the proliferation of malignant cells (X-ray, chemotherapy, hormone therapy and immunotherapy); vitamin therapy; auxiliary therapy (blood transfusion, relief of infection, treatment of thrombosis and bleeding); bone marrow transplantation.

6. Causes of death: cachexia, secondary infection, severe anemia, thromboembolic complications, massive bleeding and hemorrhage.