Symptoms And Treatment Of Lung Adenocarcinomas

What are lung cancers? Lung cancers are the abnormal cells which grow in uncontrolled manner in one or both lungs. They do not function as normal lung cells and do not develop into healthy lung tissue. The abnormal cells can grow, form tumours and interfere with the normal functions of the lung (Lungcancer.org, 2015). Lung cancers can be divided into two major types, namely non-small cell lung cancers (NSCLC) and small cell lung cancers (SCLC). NSCLC can be further classified into three main subtypes, namely adenocarcinoma, squamous-cell carcinoma and large-cell carcinoma (Longo & Harrison, 2012). Lung cancers can be diagnosed by chest X-ray, computerised tomography (CT) scan, positron emission tomography-computerised tomography (PET-CT) scan, bronchoscopy and biopsy (Nhs.uk, 2015). Unfortunately, lung cancers are often diagnosed at the later stages. This is due to the unrecognisable symptoms and warning signs at the earlier stages. NSCLC are often diagnosed at stage IV which accounts for 30-40% of cases whereas 60% of SCLC is diagnosed at stage IV. Lung cancer usually originates from the cells lining the bronchi, bronchioles and alveoli. Carcinogens especially tobacco smoke will alter the gene expression of the normal human lung cells, resulting in cell mutation. The proto-oncogenes will be converted to mutated form, oncogenes. Mutation leads to the decreased expression of the tumour suppressor genes. This results in uncontrolled cell proliferation, cell

However, there are stages in the lives of all humans when the body finds itself in a position where it is no longer able to defend itself against ailments and diseases and eventually may even lose the battle. One such disease which claims many lives every year in this manner is Cancer. So far so, there has been no cure for Cancer but some medicines and treatments are now available which can slow down and in some cases can even alter the effects of Cancer, depending on the stage at which the disease is at that moment. For this paper however we would concentrate on Lung Cancer and its effects.

There are two important type of genes responsible for the development or cancer namely tumor suppressor because their normal function is

Lung cancer is a genetic and acquired disease. Lung cancer is genetic because cancer in general is caused by changes to the genes that control the way our cells function, especially how they grow and divide. All of these changes include mutations in the DNA that makes up our genes. Genetic changes that increase cancer risk can be inherited from our parents, if the changes are presents in germ cells. Which are the reproductive cells of the body, those are the eggs and the sperm. Lung cancer is also acquired because as the result of errors that occur as cells divide a person’s lifetime or exposure to certain chemicals. Some examples of these chemicals are found in tobacco smoke, radiation, UV rays from the sun that damage DNA. “In general, cancer cells have more genetic changes than normal cells. But each person’s cancer has a unique combination of genetic alterations.” Some of these changes may be the result of cancer, rather than the cause. As the cancer continues to grow, additional changes will occur. Even within the same tumor, cancer cells may have different genetic changes.

Compare and contrast tumour suppressor genes and proto-oncogenes. Discuss an example of how recent advances in our understanding of these genes have led to the development of a novel therapy that is being used in the treatment of human cancer.

The methods of obtaining the cancerous epithelial samples from various areas was a clear way of observing both the level of amplification of CCND1 and the presence of cancer within those tumors or samples. The FISH technique was fitting to localize the specific DNA sequences related to the cause and effect of amplification. Epithelial tissues which contained some development of cancer cells were studied. The researchers used samples that were stored at the University Medical Center Hamburg-Eppendorf, making sure to used samples from areas distant from one another (Burandt, et. al). Taking samples from various areas helped to further see the effect of various amount of amplification of the protein and how it affected the epithelial tissues at different stages.

As generations of diseases and cures continue to be created, the increase of cancer multiply each day. Although there are many recurring cancers through genes and natural behavior, lung cancer is one of the recurrent cancers that continue to grow; either it has to do with natural behavior or genetics. Lung cancer begins to occur when cells in your lungs begin to grow uncontrollably. This disease is infectious and severe because not only will the cancer affect your lungs which affects your breathing, but also spread throughout your body and affect other organs as well

Most thyroid tumors can be readily diagnosed using histopathologic criteria, which allow the pathologist to differentiate benign from malignant lesions and guarantee an accurate classification for the majority of the variants of carcinomas derived from follicular epithelial cells. However, in most cases, the pathologist is confronted with thyroid lesions in which the distinction between benign and malignant can be quite subtle. The decision favoring one or another has clinical consequences and implies different modalities of treatment. For this reason, the approach to these challenging tumors should include ancillary techniques, immunohistochemistry and molecular profiling, that can improve the standard morphologic assessment (3).

Birt-Hogg Dubé (BHD) syndrome is a rare autosomal dominant condition that’s characterized by the development of benign skin tumors and lung cysts. Moreover, these manifestations increase patients’ risk to develop renal cell carcinoma (RCC) and/or pneumothorax. Germline mutations in the Folliculin (FLCN) gene are responsible for patients to express the clinical hallmarks of BHD. Most of the BHD patient population contain mutations in the FLCN gene at exon 11, a disease-causing mutational hotspot. Research has shown mutations in FLCN are predicted to cause truncations of the gene resulting in its loss-of-function, resembling the function of a tumor suppressor. Furthermore, BHD clinical hallmarks are similar to the clinical manifestation caused by mutations in tumor suppressor, TSC1/2, such as: facial hamartomas and RCC. Although FLCN is predicted to be a tumor suppressor, the exact function of FLCN still remains unknown.

An irritant, such as cigarette smoke, effects the cells of the epithelium lining. Initially the body can repair the cell, but with repeated exposure the cells of the lungs become damaged and grow uncontrollably. P53 is a gene for various downstream targets that are involved in cell progression, DNA repair and regulation of cells that undergo apoptosis. Mutations to P53 hinder its normal tumor suppressing capabilities. Therefore, DNA damage remains unchecked, faulty cells proceed through the cell cycle and apoptosis is invaded. All these factors create a genetic condition where the cell is more susceptible to further mutation. If the cancer grows large enough, it can affect the organ by closing off the aveoli, leading to shortness of

Aberrant expression of p16INK4a, either high or low, is found frequently in human cancers (Table 1). In colon cancer, two different patterns of p16INK4a overexpression have been reported. The first pattern is related to senescence in serrated adenomas, which have malignant transformation associated with p16INK4a downregulation (Refs. 138, 139). The second pattern is characterized by a very low p16INK4a immunostaining in normal mucosa, with a progressively higher expression in aberrant crypt foci, non-serrated adenomas, primary carcinomas and metastatic tumors (Ref. 87). A similar pattern was observed in skin cancer where p16INK4a expression increases from relatively low levels in pre-malignant lesions to high levels in in situ and infiltrating carcinomas (Ref. 140). In breast cancer, p16INK4a was negative or low in normal ductal epithelium, but a progressive increase was found in benign lesions and carcinoma (Refs. 88, 89). Increased nuclear p16INK4a protein expression compared with normal epithelium has been reported in pre-neoplastic and tumor tissues of the gallbladder (Ref. 141). Therefore, inactivation of

|Specific Purpose: |To inform readers on the causes, effects and treatments of lung cancer. |

Individuals with a family history of lung cancer are at approximately two to threefold increased risk of developing this disease. (Chen & Kaphingst, 2011)

Adenocarcinoma has been predominantly present in male smokers, however its occurrence in women, non-smokers, and young patients (below age 40) has been increasing as well (3). Consequently, mutations and gene alterations that may be targeted to treat adenocarcinoma are being highly studied, which include: epidermal growth factor receptor (EGFR), anaplastic lymphoma receptor tyrosine kinase (ALK), thyroid transcription factor 1 (TTF-1), Napsin A, v-raf murine sarcoma viral oncogene homolog B1 (BRAF), v-erb-b2 erythroblastic leukaemia viral oncogene homolog 2 (HER2), c-ros oncogene 1 receptor tyrosine kinase (ROS1), and rearranged during transfection (RET) (4). The EGFR gene mutations seem to be most significant in adenocarcinomas, specifically deletions in Exon 19, and point mutations in Exon 21 (5). Similarly, almost 5% of all NSCLCs are associated with a rearrangement in the ALK

Molecular studies are aimed at improving the microscopic understanding of various pathologies and aid in better diagnosis and treatment. Cancer genetics assists to improvise clinical outcomes by directing therapy towards the molecular mechanism and targets associated with malignant growth, transformation and metastasis. Cancer biomarkers are substances or alterations as a specific response to that particular cancer and that indicates the presence or prognosis of cancer. This chapter correlated the expression analysis of the Wnt pathway genes to the various