Lung cancer Flashcards
What is the only example of a benign lung neoplasm?
Pulmonary hamartoma
What is pulmonary hamartoma?
- The most common benign tumor of the lungs, AKA pulmonary chondroma (as this tumor has a lot of cartilage)
- A hamartoma is a normal component of the organs and tissues but arranged in a disorganized way, it arises due to the disorganization of cells where often cartilage is found in places where it should not be and its division will give rise to more disorganized cells leading to a hamartoma
- Usually asymptomatic and found accidently as a coin lesion
Where in the lungs does hamartoma occur?
At the periphery
Which tumors occur at the periphery of the lungs?
1) Pulmonary hamartoma
2) Pulmonary chondroma
3) Bronchioalveolar atypical adenomatous hyperplasia
4) Adenocarcinoma in situ
5) Adenocarcinoma
6) Large cell carcinoma
Which tumors occur at the center of the lungs?
1) Squamous dysplasia
2) Squamous cell carcinoma
3) Small cell lung carcinoma
4) The most common type of typical carcinoid
What is the pulmonary chondroma of carney?
- It is a syndrome found in young females which involves 3-types of tumors:
1) Chondroma in lungs
2) Tumor in the GIT (GIST)
3) Tumor in the ganglia or the adrenal glands (paraganglioma)
What is the difference between hamartoma and pulmonary chondroma of carney?
1) Hamartoma occurs in males while Carney’s triad occurs in young females
2) Hamartoma contains cartilage, fat, and smooth muscle cells, while carney has cartilage only
3) Hamartomas have a single tumor, while in Carney’s there are multiple tumors
What are some examples of pre-invasive lung neoplasms?
1) Squamous dysplasia
2) Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH)
3) Bronchial atypical adenomatous hyperplasia
4) Adenocarcinoma in situ
What is squamous dysplasia?
- It is a disordered proliferation of the cells where they acquire cancerous morphological features, but are unable to invade the surrounding tissues (with three grades: mild, moderate, and severe)
- It is a central lesion of the large airways, which is associated with obstructive lung disease (chronic bronchitis and bronchiectasis “cells change continuously due to inflammation then metaplasia then dysplasia”) and smoking (as smoking causes a change of the pseudostratified cells into squamous)
What are the types of squamous dysplasia lesions?
1) Flat
2) Nodular
3) Polypoid
Describe the pathological progression of squamous dysplasia
- Squamous cells are found in the trachea and bronchi via some sort of metaplasia
1) Hyperplasia of the basal cells of the pseudostratified cells
2) Squamous Metaplasia
3) Dysplasia, which will lead to squamous cell carcinoma
What is diffuse idiopathic pulmonary neuroendocrine cell hyperplasia?
1) Diffuse = Occurs in multiple places in the lungs (multifocal)
2) Idiopathic: No known cause
3) Neuro-endocrine cells: These cells are present throughout our body (especially in the lung and the GIT), and respond to neural stimulation by releasing hormones, in this cancer those type of cells will proliferate in the lungs without a nervous stimulation
Describe the pathophysiology of the DIPNECH
- The neuro-endocrine cells will increase without nervous stimulation
- Once they cross the basement membrane they become a tumor (less than 5mm), if it becomes greater than 5mm it will turn into a carcinoid tumor
What is bronchioalveolar atypical adenomatous hyperplasia?
1) atypical: not similar to the normal alveolar epithelium
2) hyperplasia: increase in number
3) Adenomatous: which means that if left untreated it will continue to divide and proliferate becoming an adenocarcinoma (the most common type of lung cancer)
- It is a precursor to adenocarcinoma in situ and invasive adenocarcinoma, that arises from progenitor cells, Clara cells, and type-2 pneumocytes
- It has no nodule, and it is multifocal with a Tan lesion at the periphery of the lungs (centri-acinar)
- It is <5mm in size
- The alveolar walls are thickened by fibrosis and lined by an interrupted proliferation of the tumor cells (Lepidic growth pattern along the alveolar septa)
From which types of lung cells do Bronchioalveolar atypical adenomatous hyperplasia arise?
1) Progenitor cells
2) Clara cells
3) Type-2 pneumocytes
What is adenocarcinoma in situ?
1) In situ: it does not spread “not invasive”
- It is a precursor for adenocarcinoma with two types mucinous and non-mucinous
- It has a single nodule at the periphery of the lungs that is 5-30mm in size
- The alveolar walls are thickened by fibrosis lined by uninterrupted proliferation of the tumor cells in a lepidic growth pattern
From which type of lung cells do adenocarcinoma arise?
1) Mucinous: arises from goblet cells
2) Non-mucinous: Arises from Clara cells and type-2 pneumocytes
What is meant by lepidic growth pattern?
The growth of abnormal cells along the alveolar septa without invading the stroma or pleura
What is the difference between adenocarcinoma in situ and bronchoalveolar atypical adenomatous hyperplasia?
1) AIS is larger in size by 5-30mm compared to below 5mm in the case of AAH
2) AIS can be mucin-producing in case it arises from the goblet cells other than that they are non-mucin-producing
3) AAH has an interrupted lepidic growth while AIS has an uninterrupted lepidic alveolar growth
4) AAH has no nodule while AIS has a nodule
What are the different types of invasive lung neoplasm?
1) Adenocarcinoma
- Most common
- Most common in women and in never smokers who are below 45 years old
2) Squamous cell carcinoma (Sq.CC)
- Strongest associated with smoking, and more common in men
3) Small cell carcinoma (SCLC “subtype of neuroendocrine carcinoma”)
- Strong association with smoking
4) Large cell carcinoma
How did adenocarcinoma replace small cell carcinoma as being the most common?
As tobacco companies created alternatives for cigarettes with smaller amounts of nicotine enabling us to inhale the smoke deep into our alveoli
- It affects females and never smokers more frequently, unknown etiology
Which lung cancer occurs in females and in never-smokers?
Adenocarcinoma
What are the risk factors of lung carcinoma?
1) Sex: More in females
2) Cigarette smoking
- 90% of lung cancers occur in smokers and those who recently quit
2) E-Cigarettes
3) IQOS (I Quit Ordinary Smoking)
4) Environmental factors
- Pollution
- Industrial asbestos, ionizing radiation
- Vitamin-A deficiency (needed to maintain the epithelium and if not it can lead to metaplasia)
5) Heredity
6) Pre-existing lung diseases (IPF, Asbestosis, Chronic bronchitis, Bronchiectasis)
Describe the pathogenesis of lung cancer
- Smoking-related carcinomas of the lungs arise stepwise by the accumulation of mutations
- Activation of Oncogenes:
1) Activation of K-RAS oncogene usually in adenocarcinoma, mucin secreting, and female smokers (K-RASSSSS, MUCCCCIN, SSSSSMOKER, SSSSSET)
2) Overexpression of EGFR (epidermal growth factor receptor), usually in adenocarcinoma in non-smoker females (women are responsible for the growth of a child “mnemonic”)
3) EML4-ALK fusion gene, in adenocarcinoma, young, non-smoker males
- Inhibition of tumor suppressor genes
1) Mutation of the p53 tumor suppressor gene
2) Mutation/deletion of the RB gene (mainly in SCLC)
