A proto-oncogene are genes that help control cell growth

A proto-oncogene are genes that help control cell growth

A proto-oncogene are genes that help control cell growth. The functions of a proto-oncogene can be extensive in what they can do. First, they can kick start the cell division. They play a role in differentiation of a cell. And lastly, they help with cell death (Robertson). These are also considered normal genes. Once the gene is mutated it becomes an oncogene. The gene that may possibly be mutated could be the HER-2/neu gene. This is a type of gene amplification. This is a mutation where there are more copies then normal of a gene. In this specific case it causes rapid reproduction of the cell (Porth, Carol, and Kathryn J. Gaspard).
The mutated proto-oncogene could have caused the cells to grow by no longer having control of the cell proliferation. In the HER-2/neu gene there is to many copies of this gene. This can raise the levels of proteins to an unhealthy level. With protein levels to high this can cause more cell reproduction at a faster then normal rate. This explains the cells growth (Porth, Carol, and Kathryn J. Gaspard, 137). This means with the unregulated cell growth there becomes to many cells. With too many cells this becomes a mass. That would explain the tumor.

Tamoxifen is an antiestrogen drug that is used as a hormone therapy for breast cancer. When levels of estrogen are too high this can cause the start of cancer or help it metastasize. Hormone therapy in general is used before surgery, after surgery or for individuals at a high risk for breast cancer. With this being an antiestrogen drug, it blocks the effect of estrogen. With this drug it blocks estrogen only in the breasts. This helps the cancer to stop growing and metastasizing (Hormone Therapy for Breast Cancer).
Cancer treatment where an antibody attaches to a tumor is called Monoclonal antibody drugs. The way these antibodies work can vary. They tag the cancer cell so that they can be destroyed. Monoclonal antibodies can weaken the membrane of the cancer cell and cause destruction. They can also function in many other ways (Monoclonal Antibody drugs for Cancer: How they work). In this situation we are considering toxin-linked monoclonal. This treatment still has the antibody that attaches to the cancer cell. With there being a toxin attached it has a little different of effect. Once the antibody latches to the cell the toxin attached can enter the cell. When the toxin is pushed into the cell it can help destroy it. This treatment is focusing directly on the cancer cell and not on healthy cells (Taber, Clarence, Wilbur,152).
A lumpectomy is used to remove the cancerous part of the breast with some of the healthy tissue included. This option is generally used for women in early stages of breast cancer (Lumpectomy Mayo Clinic). When radiation and lumpectomy are used together this is used to get rid of the remaining cancer cells (Lumpectomy Plus Radiation).
The treatment that would work the best would be a monoclonal antibody with a toxin attached. If we used a monoclonal antibody it could attach to the HER-2/neu gene and stop the over production of this tumor cell (Porth, Carol, and Kathryn J. Gaspard, 137). With this treatment the monoclonal antibody would attach to the HER-2/neu gene. Once it was attached the toxin associated with this antibody would then infect the inside of the cell. The toxin would then destroy the cell. Between the monoclonal antibody tagging these defective genes and the toxin helping destroy them this would get rid of the cancerous cells. With this treatment it would help kill newly produced HER-2/neu genes and keep the tumor from growing. As well as it would help shrink the tumor by killing these genes already present. Therefore, this would make an excellent treatment for this woman. Tamoxifen would not make a very good treatment. While it would block the effect of estrogen and keeping the tumor from growing it would not be attacking the tumor. As for a lumpectomy with radiation this would be a poor treatment option as well. We do not know what stage of breast cancer she is in or if she even has good margins for surgery. If the monoclonal with a toxin attached could work this would be the best option because there is no invasive surgery with all the risks and complications that can come with that. Therefore they should give her this treatment method.

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The gene p53 main function is to look for damaged DNA and either fix the issue or begin the process of cell death. If the levels of p53 are decreased, then the DNA is not being fixed or disposed of. In damaged radiation or chemotherapy cancer cells the gene p53 assists in their cell death (Porth, Carol, Kathryn J. Gaspard, 138). Therefore, if there is a deficiency in this p53 protein then DNA is not being fixed or disposed of and certain cancer treatments are not going to be as effective. With the lack of p53 protein there are many dangers. There is going to be an accumulation of bad DNA in many cells. With the lack of cell death not only is the DNA bad but there will form a mass from these cells not being disposed of in the way they were meant to.
For someone with multiple types of cancer cells and deficient in p53 protein it’s understandable why both cancer cells are present. The gene p53 initiates cell apoptosis in damaged or mutated cells. In this deficiency there is not much cell death happening in DNA damaged cells. These damaged DNA cells can possibly become many different types of mutated cancer cells. This can be a problem with mutated DNA and no cancer cell death. There is also the uncontrollable proliferation as well. This means a mass of mutated cells and nothing dying. In the end leading to multiple cell types in a growing tumor.
The third women is the most likely to have more primary cancer throughout her body. With the deficiency of p53 she is gathering damaged DNA in her breast. Without the p53 protein to fix DNA damage or decide that the DNA it is beyond repair the collecting of this mutated DNA has become a mass. This mass would be classified as a tumor (TP53 gene). This explains the tumor formation. Since she has breast cancer already and deficient p53 protein she is at risk for cancer elsewhere. With the lack of this protein the DNA can be mutated elsewhere in her body. If she continues to have mutations, increased cell growth and less cell death she can have tumor formation elsewhere in her body.
The most common classification of skin cancer is basal cell carcinoma. This cancer generally appears on the face or surrounding areas, but it can still appear other places. The appearance of basal cell carcinoma has a few different characteristics. The change in appearance can be a fleshy tone, white or pink lesions on the surface of the skin. These lesions tend to bleed. The lesion may also have a darker color to it such as brown, black or blue (Basal Cell Carcinoma). It is not flush to the skin it is elevated. Other types of this cancer can appear to be red and patchy. These tend to happen on the trunk of the body as opposed to the face. The least common form of this cancer is called morpheaform basal cell carcinoma. It is usually undefined border and looks similarly to a scar.
Squamous cell carcinoma is a form of skin cancer that can be present anywhere on the skin. This is a cancer that can spread but is not as dangerous as melanoma. Some of the symptoms of this cancer involve nodules, sores and patches. They can vary in the feel of the skin being firm, flat, raised or rough. As for the color they tend to be red (Squamous Cell Carcinoma of the Skin).
Melanoma is the deadliest type of skin cancer. This cancer starts in the cells that give the pigment to an individual’s skin. This skin cancer can appear anywhere even where there is rare sun exposure. One of the most common signs is an existing mole changing in appearance. Moles that may be cancer can be evaluated by the ABCDE characteristics (Melanoma).
The ABCDE rule is a good guide for assessing skin cancer. First, is asymmetrical where it looks lopsided or unbalanced in shape. An uneven border that looks like there are scratches or grooves. Then the color of the growth if it is multicolored, dark and light in the same growth. The size or the diameter of the growth if it is a fourth of an inch or larger then that is something to get checked. Last, is evolution which is when any of these characteristics change. If the growth becomes bigger or the color becomes darker or uneven in color (Melanoma).
The similarities between benign and malignant are limited. They both are growths that are not supposed to occur. Depending on their locations either once can be dangerous. They both lack normal cell regulatory functions. There composition in tissue are the same in either tumor they both have two types of possible tissue. One possibility being specialized cells that make a certain tissue. The other being the structural tissue within the body (Porth..,130).
Benign tumors are classified as noncancerous and do not metastasis. They grow at a slow rate, they can stop growing or become smaller. They cannot control the reproduction of the cell. They do keep the ability of cell differentiation. With keeping this ability, the cells of these tumors are like the tissue that they came from. A fibrous capsule forms in these tumors because of the slow growth rate. The fibrous capsule then provides a good margin for the removal of a benign tumor (Porth…,131).
Malignant tumors unlike benign tumors are cancerous and have the potential to metastasis. They grow at a fast rate. They use all the blood supply they can as they grow and eventually do not have enough to supply them. There are two different types of malignant tumors. There are malignant tumors in the blood and lymph, which travel throughout the body. These are called hematologic cancers. There are solid tumors in a certain area of the body. These typically affect specific organs and tissues. With the rapid growth rate and no fibrous capsule, it is hard in these tumors to see where it starts and ends. These tumors also have levels of cell differentiation to completely differentiated to not very differentiated. (Porth…,132).
The skin consists of three main layers the epidermis, the dermis and the hypodermis. The epidermis is the outermost portion of the skin. It has five sublayers that make up the epidermis and help protection the human body. The middle layer is the dermis. The dermis is divided into two layers. The papillary layer and the reticular layer. The innermost layer is the hypodermis.
In the epidermis you have the five sublayers. From innermost to outermost they are basal cell layer, squamous cell layer, stratum granulosum, stratum lucidum, and the stratum corneum. With Seth’s cancer being basal cell carcinoma we would be focusing on the epidermis and these five sublayers. Basal cells arise for the innermost sublayer the basal cell layer (Skin Cancer: Carcinoma ; Melanoma). They are pushed to the surface as new cells form. These are the cells that basal cell carcinoma arises from.
A proto-oncogene is a normal gene if they are mutated or become defective it then becomes an oncogene. There are many adverse reaction that come with these mutated genes. This can cause the reproduction of cells without any guidelines to follow how much or when like in normal genes. Apoptosis does not occur at the rate it’s supposed to (Roberston). These genes are associated in over activity.
Oncogenes are no longer a normal cell. They are mutated, dysfunctional or defective genes that are no longer coded correctly. These mutated genes can be caused by a single change in the nucleotide base. An example of this is the ras proto-oncogene. There is only one change in the sequence, yet this causes increased cell growth (Porth…137). Without them being normal genes, they cause abnormal things to happen. They grow to many cells and they do not die so they come a mass. These genes are believed to be related to cancer for these reasons.
Some of the primary risks Seth presents with is the time he spends in the sun. Consistently surfing as a hobby and as an instructor that is a lot of time in the sun. With being Scandinavian descent and having light skin leaves an individual more prone to sun damage. Age and gender can play a factor into his prognosis as well. With his age of being thirty eight and being a male increase his odds of having basal cell carcinoma. The description of the growth in color and blood vessels being present fit the characteristics of this cancer. The fact it would scab over and bleed all contribute this to being the most common type of basal cell carcinoma. Lastly, the placement of the growth being on his face which is a place that has high exposure to the sun. All these factors can contribute to his basal cell carcinoma (Basal Cell Carcinoma Mayo clinic).
Seth only presents with some of the risk cancers for skin cancer. If an individual has had radiation therapy for another ailment this can increase the odds for skin cancer. Having a history in the family of skin cancer. Certain medications such as immune-suppressant drugs. Exposure to arsenic in higher levels can leave a person more susceptible to cancer (Basal Cell Carcinoma). A personal history of skin cancer. Once you have these cancer cells you can be more prone to having it again. Not only is spending time in the sun put you at risk but having sun burns increases the odds (Squamous Cell Carcinoma). These are some of the other risks of skin cancer.
There are many treatment options for cancer including surgical excision, chemotherapy and radiation. Surgery can be used in the case of removing an entire neoplasm. It can also be used to remove some of a tumor so other treatments can have a greater effect on the cancer (surgery to treat cancer). This is good option when there are good margin lines for an entire tumor. It is also helpful in take bits and pieces if used with other treatments as well. Chemotherapy is usually used in conjunction with other treatments. This treatment works by helping slow the growth, shrinking tumors and avoid its return (Chemotherapy To Treat Cancer). Killing cancer cells is how radiation therapy is used in cancer. The radiation damages DNA (Radiation Therapy to Treat Cancer). When DNA becomes damaged this is a good example for someone who still had p53 protein. This protein would decide how damaged the DNA is and either fix it or cause it to die. When this process happens, it kills the cancer cells.
Treatment options for each of the skin cancers can differ and overlap in some areas. In basal cell carcinoma the most common treatment is electrodesiccation. This is when they scrape at the cancerous spot remove the cancer cells. Although mohns surgery is used frequently when growths reappear. This method has a high cure rate. There is the option of excision. Having it cut out with some healthy skin to be sure all the cancer was retrieved. Other methods include radiation and Cryotherapy. Immune response modifiers and topical chemotherapy are other choices if the cancer is not to deep in the skin (Treating Basal Cell Carcinoma).
Treatment for squamous cell cancer may vary. It will depend on a patient. Their health, age, the severity of the cancer will depend on the course of treatment. The same treatment options apply for this cancer as it does for basal cell carcinoma. These include in-office treatments like mohns surgery, excisional surgery, and electrosurgery. Cryosurgery is also considered to freeze and kill the cancer cells. Some of these processes are repeated to ensure all the cancer cells have be eliminated. Other treatment options include photodynamic therapy as well a few other treatments that the Food and Drug Administration has not approved (Squamous Cell Cancer).
Melanoma is the most dangerous of the skin cancers. This leaves these cancer treatments on the more serious side. One treatment option can be surgery with chemotherapy. Once the cancerous portion is removed, chemo can be given to kill any left behind cancer cells. In melanoma external radiation therapy can be used where radiation is targeting the cancer on the outside of the body. The immune system in the patient can also be an effective tool to fight the cancer this is called immunotherapy. In immunotherapy interferons, interleukin and tumor necrosis factor can be used. There are also the options of clinical trials. These are the treatments that can be used for melanoma.
Chemotherapy can have a lot of adverse reactions and side effects. Two of these side effects are hair loss and nausea. Chemotherapy can cause hair loss when the drug destroys the follicles. Even though this may be a side effect depending on the chemo or the person there is the potential for it to not happen to everyone. It can happen on a case by case basis depending on the individual (Hair Loss). The cells in the hair follicle are not proliferating in the way they are supposed to (Porth..,151). That is the technical term of what is happening.
Chemotherapy also causes nausea and vomiting in some of its patients. There is a part of the brain doctors believe controls vomiting. This is referred to as the chemoreceptor trigger center (Porth..151). Once this area in the brain is targeted it effects other areas in the body like the esophagus and stomach (Understanding Nausea and Vomiting). Those areas then start a reaction that leads to nausea and vomiting. Nausea and vomiting symptoms also depend on the type of chemo drugs that are being taken. There are classifications depending on the emetic potential how likely these symptoms may occur (Understanding Nausea and Vomiting).


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