hello everyone welcome to this short tutorial from pathology made simple at ilo pathology the topic which i am discussing today is lung cancer this is the part one of two part series on lung cancer right okay in this part we will be discussing in detail about the epidemiology of lung cancer the ato pathogenesis the various precursor lesions of lung cancers and then we'll conclude with classification of lung cancers now lung cancer currently is the most frequently diagnosed major cancer worldwide this is the most common cause of cancer mortality worldwide you know it occurs between the
ages 55 and 84 years and the peak incidence is in the seventh and eighth decade of life that's around 65 and 74 years okay and what is important to understand is lung cancer is very strongly linked to cigarette smoking now what is that which causes lung cancer when somebody you know inhales tobacco the various components of tobacco particularly these polycyclic hydrocarbons and nitrogens these are potent carcinogens okay the polycyclic hydrocarbons they bind to the nuclear dna and then they cause mutations so basically polycyclic hydrocarbons are mutagenic okay now once there is mutation the benzopyrene compounds
take over these benzopyrene compounds they act as tumor promoters so the components which are implicated in lung cancer in tobacco are polycyclic hydrocarbons and nitrogens these are potent carcinogens okay etiopathogenesis as i told you tobacco smoking is implicated in 80 to 90 percent of lung cancers it has a there is a linear correlation between the frequency of lung cancer and cigarette smoking when i say cigarette smoking we calc we talk in terms of pack years what is this package and how it is calculated the packages are basically calculated by multiplying the number of packs of
cigarettes smoked per day by the number of years the person has smoked let me make it very simple if i say one pack here that means the individual that particular person has been smoking one pack per day for one year one pack of cigarettes contained 20 cigarettes so that means smoking 20 cigarettes per day for one year now having known the concept of pac care we should know who are referred to as heavy smokers okay because heavy smokers they have very high incidence very very high chances that these individuals develop lung cancer who are all
called heavy smokers heavy smokers are the ones who smoke two packs a day for 20 years that means 40 cigarettes per day for 20 long years the risk of developing lung carcinoma in these heavy smokers are is 60 times greater than in non-smokers having said that not all smokers will develop lung cancer they they occur in only around 10 to 15 percent of smokers now why does this happen that's because there might be some other factors there will be some other predisposing factors you know and the environmental factors or the genetic factors may be implicated
which predisposes these new smokers for the development of lung cancer okay for strain for some strange reasons women are more susceptible to tobacco than men okay but one thing is very sure cessation of smoking decreases the risk of lung cancer significantly but then it does not come back to the that of a non-smoker level right now another thing you need to understand is the concept of passive smokers and secondhand smoke okay both of the both of these are same which basically means that these individuals are exposed to environmental tobacco smoke now nobody knows as to
what is the safe level of exposure there is no safe level of exposure and the cause of lung cancers in non-smokers is basically because of passive smoking or secondhand smoking now moving on to uh continuing with heater pathogens the first one what we taught what we talked about is tobacco smoking right the next one is industrial hazards what does that mean exposure to asbestos arsenic chromium uranium nickel and vinyl chloride are implicated in the development of lung cancer of course high dose ionizing radiation exposure to high dose ionizing radiation is implicated in development of cancers
because these ionizing radiation are mutagenic the third one is air pollution air pollution per se does not cause lung cancer but it adds to the risk in smokers now what does that do chronic exposure to air particles in smog they sort of irritate the lung parenchyma and then they result in long-standing inflammation and repair and we know that the tissue being inflamed often you know they are at increased risk of development of cancer moving on further acquired mutations what are these these mutations are driver mutations these are oncogenic driver mutations which means to say that
these are the mutations which leads to the development of cancer which leads to the progression of cancer what are the mutations which we see in lung cancer before that let us see the concept lung cancers for a clinician he wants to know whether he is dealing with a small cell cancer or a small cell carcinoma or a non-small cell carcinoma okay because small cell carcinomas are susceptible to radiation treatment these are very highly aggressive whereas non-small cell carcinomas have an indolent course they are managed by surgical approach surgical treatment okay among non-small cell carcinomas you
have adenocarcinoma and squamous cell carcinoma small cell carcinoma has the highest mutational burden these cancers are the ones which have many mitosis highest mutational burden the most common mutation implicated here is tp53 and retinoblastoma these are tumor suppressor genes the mutations involving tp53 and retinoblastoma gene okay of course there will be deletion of the short term of chromosome number three now adenocarcinoma is the most common type of lung carcinoma it is the most common type of carcinoma in people who do do not smoke at all right so what are the mutations you find in adrenal
carcinomas what are the mutations which is which are implicated in adenocarcinomas are gain of function mutations in the genes encoding these things the epidermal growth factor receptor the alk you know the braf mutations so all these you know gain of function mutations are implicated in the development of adenocarcinoma moving on to square muscle carcinoma there will be deletion of the short term of chromosome number three and nine which is implicated in you know involvement of this particular gene cd kn2 gene cdkn2a gene of course there will be t tp53 mutation as in the case of
small cell carcinoma apart from that there is also amplification of the gene encoding fibroblast growth factor receptor one okay these are the mutations in these genes involved in lung cancers now lung cancers in non-smokers are those who never smoke we have talked about it right those who never spoke they are exposed for passive smoking or secondhand smoking most often found in women adenocarcinoma is the most common type of lung cancers those who do not smoke are never smokers okay and they are the ones who are more likely to have eg fr mutations epidermal growth factor
receptor gene mutations and almost always they do not have k rash mutations okay in the earlier slide we saw that k rash mutations are seen in adenocarcinomas but then they are the ones which is seen in smokers but then these cases who are never smokers they don't find keras mutations now let us move on to understand what are the precursor lesions are pre-invasive lesions what are precursor lesions the lesions which might progress towards development of invasive or frank malignancy but having said that it does not imply that the progression of cancer is inevitable not all
precursor lesions progresses to invasive cancer okay now what are the pricker solutions in the lung cancer they are atypical adenomatous hyperplasia adenocarcinoma in situ squamous dysplasia and carcinoma in situ and lastly diffuse idiopathic pulmonary neuroendocrine cell hyperplasia now what is atypical adenomatous hypoplasia it it is basically the presence of dysplastic pneumocytes this plastic type 2 pneumocytes which are lining the alveolar walls so this is how atypical adenomatous hypoplasia looks like look at look at this these are this plastic pneumocytes which are lining the alveolar wall they are atypical adenomatous hyperplasia the second one is adenocarcinoma
in situ previously this was referred to as bronchiolo alveolar carcinoma now in the present who classification it's called as adenocarcinoma in situ they are compo they are they're more than a typical adenomatous hypoplasia they are composed entirely of this plastic cells their cancerous cells you know they grow along the pre-existing alveolar septa look at this these are the adenocarcinomatous cell or the malignant cells growing along the alveolar septa so that is adenocarcinoma in situ because they do not demonstrate invasion to call it as an invasive carcinoma they do not have lymph node metastasis or hemogeneous
metastasis nor invasion that's why they are adenocarcinoma in situ the third precursor lesion is squamous dysplasia and carcinoma in situ okay look at this you can find that there is varying grades of dysplasia here this is mild dysplasia and this is very high grade dysplasia to even carcinoma in situ okay so this is a precursor for squamous cell carcinoma and lastly the last precursor lesion is diffuse idiopathic pulmonary cell hyperplasia in the normal lung you find you know neuroendocrine cells what are neuroendocrine cells these are the cells which have both the properties of the nerve
cell as well as the endocrine cell okay they are normally present in singles or clusters whenever there is hyperplasia without any cause that is why they are referred to as idiopathic without cause diffuse idiopathic pulmonary neuroendocrine cell hyperplasia they are implicated in neuroendocrine tumors so these are the four precursor or pre-invasive lesions note that all of these or any of these will not progress to cancer compulsorily it is not inevitable let us see what are the what are all the cell of origins of lung cancer by now you would have known that you know neuroendocrine
cells are the ones which progresses are these are the cells of origin for small cell carcinomas the basal cells in the major bronchi major bronchi is lined by pseudostratified selenated color narrate they undergo squamous metaplasia then dysplasia so the basal cells in these major bronchi are the ones which progresses to square muscle carcinoma whereas the mucous glands in terminal bronchioles the cells of the glandular structures in the terminal bronchioles are implicated in adenocarcinoma they are the cells of origin for adenocarcinoma and lastly the classification of lung tumors very simple classification they are classified as adenocarcinoma
and their variants okay i'm just giving you a simpler classification adenocarcinoma and variants the square muscle carcinoma and thirdly neuroendocrine tumors the whole three variants which i we which we just discussed the cell of origin right among neuroendocrine cell tumors the small cell carcinoma is most important they are very aggressive again large cell neuroendocrine carcinoma and carcinoid these are low grade uh malignant epithelial tumors and lastly other lung cancers like you know they can be large cell carcinoma which do not have pictures of adenoma and squamous they can be combination of adrenal and squamous adenosine
they can be sarcomatoid or they can be salivary gland type tumors so this this is just a just of a simplified version of classification of lung tumors so with this i have complete completed the epidemiology the idiopathogenesis precursor lesions and classification in this part one in the part two i'll be discussing in detail about all these types of lung cancers the clinical features the paraneoplastic syndromes associated with lung cancers and also we'll discuss about neuroendocrine tumors thanks for watching if you have liked this video hit the like button do comment don't forget to subscribe because
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