SMALL CELL LUNG CANCER

Molecular Pathology OF THE

SMALL CELL LUNG CANCER

INTRODUCTION

The small cell lung cancer is an epithelial malignant tumor made up of small cells, with cytoplasm poor, marginal, with fine, granular appearance and lack of nucleoli. It has a high rate of mitosis and extensive necrosis. It differs through a very high nuclear-cytoplasmic ratio (1).

So far no precursors are not known, as well as for the lung cancer with neuroendocrine cells. The diffuse neuroendocrine hyperplasia is not considered pre-neoplastic lesion (1).

The lung neuroendocrine neoplasms are a wide range of entities phenotypic, biologically distinct, starting from the typical and atypical carcinoids up to small cell lung cancer and lung cancer with neuroendocrine cells.

The neuroendocrine appearance is highlighted through immuno-histochemistry and electron microscopy (2).

Small cell lung cancer forms simultaneously part of the neuroendocrine tumors with neuroendocrine cell

THE MECHANISM OF ACTION AND MECHANISM OF RESISTENCE OCCURENCE IN THE TREATMENT WITH TYROSINE-KINASE INHIBITORS

IULIAN POPESCU, PhD, MD

The Clinical Department of Radiobiology from the Fundeni Clinical Institute,

e-mail: popdociul@yahoo.com

Alina Halpern, PhD,  "Sf. Stefan" Hospital, Bucharest

ABSTRACT

Since 2000 a new era has begun in the treatment of lung adeno-carcinoma (ADC), which will improve, diversify, enrich the chemotherapy treatment of lung cancer (PA) which becomes the targeted treatment for a heterogeneous disease. The tyrosine-kinase inhibitors (ITK) have effect only upon ADC with EGFR mutations.

The most frequent mutations are at the level of the 19th exon  through deletion and at the level of the 21st exon  through punctiform mutations (T858R)

The EGFR and Kopi mutations, after the stimulation of ligands, undergo a homo or heterodimerization, leading to the autophosphorylation of the ATP / EGFR group, which in turn activate the pathways: PI3K/AKT, JAK/STAT and Ras/MAPK which further lead to cellular growth, survival and proliferation. The ITK blocks the ATP- EGFR phosphorylation, leading to the increase of cellular apoptosis. But after a period

THE EPITHELIAL MESENCHYMAL TRANSITION - MAIN FACTORS AND ITS INSTALLATION MECHANISM

POPESCU IULIAN, PhD, MD,

The Radiobiology Department of the Clinical Institute in Fundeni Bucharest

E-mail: popdociul@yahoo.com

ALINA HALPERN, PhD "St. Stefan" Hospital, Bucharest

ABSTRACT

The metastatic progression is responsible for most deaths from cancer in humans. For achieving this it is necessary to convert the epithelial phenotype of cancer cells into the mesenchymal phenotype that favours metastasis. This transformation, which is transient, is called Epithelial-Mesenchymal Transition (EMT).

The epithelial cancerous cells are characterized by immobility, apical-basal polarity, strong junctions of desmozomes, an interaction between the cell and extracellular matrix and an increased expression of cell adhesion markers, where E-cadherin plays the main role.

The mesenchymal cell is mobile, multi-polar, fusiform aspect, does not make strong cell-cell contacts, it can invade and express multiple markers, which confers these properties.

The TEM process is a complex mechanism involving changes in the expression, distribution and /or function of several proteins. Among the main factors, we distinguish:

THE CANCER STEM CELLS AND LUNG CANCER

POPESCU IULIAN PhD,MD, Clinical Department of Radio-Biology at the Fundeni Clinical Institute in Bucharest

e-mail popdociul @yahoo.com

Dr. ALINA HALPERN PhD, SF.ŞTEFAN Hospital  Bucharest

It is well recognized that lung localization of the cancer is one with the weakest therapeutic results, with all scientific conquests as concerns the therapies obtained from 1950 until today. Surviving more than 5 years is below 15%, compared to results from other localizations (99% in prostate cancer, 86% in breast cancer, 66% for colon cancer, 30% in ENT sphere cancer). In lung cancer encouraging results have been obtained in the possibility of increasing the survival time without relapse (disease free survival), but not also concerning the overall survival. The main task in the treatment of lung cancer remains the prolongation of overall survival and

THE MOLECULAR PATHOLOGY OF THE CHRONIC OBSTRUCTIVE BRONCHOPNEUMOPATHY

POPESCU IULIAN PhD, MD, Clinical Department of Radiobiology

FUNDENI CLINICAL HOSPITAL OF BUCHAREST

e-mail: popdociul@yahoo.com

Dr.ALINA HALPERN - PhD

The Lung Disease Hospital "Sf. Stefan", Bucharest

ABSTRACT.

THE CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) is characterized by the progressive airways narrowing and air flow limitation and related to an abnormal inflammatory process. In the inflammatory process take part: the structural cells, cells of the inherited and adaptive immunity: neutrophils, macrophages, T lymphocytes with the predominance of the Tc1 cells. Under the action of the etiologic factors multiple inflammatory mediators are released with the help of the transcription factor NFkappaB. These play a key role in orchestrating the chronic inflammation through their chemotactic and proinflammatory action. The chronic inflammation progresses in a very complex manner through the interaction of the native and adaptive immunity cells with the inflammation cytokines and mediators. The molecular basis of inflammation enlargement of is not well known, but it is - in part - genetically determined.

MOLECULAR PATHOLOGY DATA: ABOUT THE PATHOGENIC MECHANISMS OF THE INTERSTITIAL LUNG FIBROSIS

POPESCU IULIAN  PhD, MD
The Clinical Department of Radiobiology from the Fundeni Clinical Institute
popdociul@yahoo.com

Alina Halpern  PhD, 3rd Department of "Sf. Stefan" Hospital, Bucharest

 

Definition The history of etiological data

Interstitial lung diseases are a heterogeneous group of disorders, either idiopathic or related to aggressions or inflammatory causes where the place of agression is the lung interstitium.

To this kind belong: the idiopathic interstitial pneumonia, granulomatous disorders and other lung afections.

The most important, most common is the Idiopathic Lung Fibrosis, which has a severe prognostic, similar to lung cancer (1, 2, 3). It is a specific form of interstitial pneumonia, leading to chronic fibrosis of