Jump to content

Cancer treatment

From Wikipedia, the free encyclopedia
(Redirected from Antitumor)

Cancer treatment
A patient prepared for radiation therapy
SpecialtyOncology
ICD-10-PCS110000053

Cancer treatments are a wide range of treatments available for the many different types of cancer, with each cancer type needing its own specific treatment.[1] Treatments can include surgery, chemotherapy, radiation therapy, hormonal therapy, targeted therapy including small-molecule drugs or monoclonal antibodies,[2] and PARP inhibitors such as olaparib.[3] Other therapies include hyperthermia, immunotherapy, photodynamic therapy, and stem-cell therapy.[4] Most commonly cancer treatment involves a series of separate therapies such as chemotherapy before surgery.[4] Angiogenesis inhibitors are sometimes used to enhance the effects of immunotherapies.[5]

The choice of therapy depends upon the location and grade of the tumor and the stage of the disease, as well as the general state of the patient. Biomarker testing can help to determine the type of cancer, and indicate the best therapy.[6] A number of experimental cancer treatments are continuously under development. In 2023 it was estimated that one in five people will be diagnosed with cancer at some point in their lifetime.[1]

The primary goal of cancer treatment is to either cure the cancer by its complete removal, or to considerably prolong the life of the individual. Palliative care is involved when the prognosis is poor and the cancer termed as terminal. There are many types of cancer, and many of these can be successfully treated if detected early enough.[1]

Types of treatments

[edit]

The treatment of cancer has undergone evolutionary changes as understanding of the underlying biological processes has increased. Tumor removal surgeries have been documented in ancient Egypt, hormone therapy and radiation therapy were developed in the late 19th century. Chemotherapy, immunotherapy and newer targeted therapies are products of the 20th century. As new information about the biology of cancer emerges, treatments will be developed and modified to increase effectiveness, precision, survivability, and quality of life.

Surgery

[edit]

Malignant tumours can be cured if entirely removed by surgery. But if the cancer has already spread (metastasized) to other sites, complete surgical excision is usually impossible. In the Halstedian model of cancer progression, tumors grow locally, then spread to the lymph nodes, then to the rest of the body. This has given rise to the popularity of local-only treatments such as surgery for small cancers. Even small localized tumors are increasingly recognized as possessing metastatic potential.

Examples of surgical procedures for cancer include mastectomy, and lumpectomy for breast cancer, prostatectomy for prostate cancer, and lung cancer surgery for non-small cell lung cancer. The goal of the surgery can be either the removal of only the tumor, the entire organ, or part of the organ.[7] A single cancer cell is invisible to the naked eye but can regrow into a new tumor, a process called recurrence. For this reason, the pathologist will examine the surgical specimen to determine if a margin of healthy tissue is present, thus decreasing the chance that microscopic cancer cells are left in the patient.

In addition to removal of the primary tumor, surgery is often necessary for staging, e.g. determining the extent of the disease and whether it has metastasized to regional lymph nodes. Staging is a major determinant of prognosis and of the need for adjuvant therapy. Occasionally, surgery is necessary to control symptoms, such as spinal cord compression or bowel obstruction. This is referred to as palliative treatment.

Surgery may be performed before or after other forms of treatment. Treatment before surgery is often described as neoadjuvant. In breast cancer, the survival rate of patients who receive neoadjuvant chemotherapy are no different from those who are treated following surgery.[8] Giving chemotherapy earlier allows oncologists to evaluate the effectiveness of the therapy, and may make removal of the tumor easier. However, the survival advantages of neoadjuvant treatment in lung cancer are less clear.

Radiation therapy

[edit]
Main article: Radiation therapy
See also: Radiosurgery

Radiation therapy (radiotherapy) is the use of ionizing radiation to kill cancer cells and shrink tumors by damaging their DNA causing cellular death.[9] Radiation therapy can either damage DNA directly or create charged particles (free radicals) within the cells that can in turn damage the DNA. Radiation therapy can be administered externally via external beam radiotherapy or internally via brachytherapy. The effects of radiation therapy are localised and confined to the region being treated. Although radiation damages both cancer cells and normal cells, most normal cells can recover from the effects of radiation and function properly. The goal of radiation therapy is to damage as many cancer cells as possible, while limiting harm to nearby healthy tissue. Hence, it is given in many fractions, allowing healthy tissue to recover between fractions.

Radiation therapy may be used to treat almost every type of solid tumor, and may also be used to treat leukemia and lymphoma. Radiation dose to each site depends on a number of factors, including the radio sensitivity of each cancer type and whether there are tissues and organs nearby that may be damaged by radiation. Thus, as with every form of treatment, radiation therapy is not without its side effects.

Radiation therapy can lead to dry mouth from exposure of salivary glands to radiation, resulting in decreased saliva secretion. Post therapy, the salivary glands will resume functioning but rarely in the same fashion. Dry mouth caused by radiation can be a permanent problem.[10]

Chemotherapy

[edit]
Main article: Chemotherapy

Chemotherapy is the treatment of cancer with drugs ("anticancer drugs") that can destroy cancer cells. Chemotherapy can be given in a variety of ways such as injections into the muscles, skin, artery, or vein, or it could even be taken by mouth in the form of a pill.[11] In current usage, the term "chemotherapy" usually refers to cytotoxic drugs which affect rapidly dividing cells in general, in contrast with targeted therapy (see below). Chemotherapy drugs interfere with cell division in various possible ways, e.g. with the duplication of DNA or the separation of newly formed chromosomes. Most forms of chemotherapy target all rapidly dividing cells and are not specific to cancer cells, although some degree of specificity may come from the inability of many cancer cells to repair DNA damage, while normal cells generally can. Hence, chemotherapy has the potential to harm healthy tissue, especially those tissues that have a high replacement rate (e.g. intestinal lining). These cells usually repair themselves after chemotherapy.

Because some drugs work better together than alone, two or more drugs are often given at the same time. This is called "combination chemotherapy"; most chemotherapy regimens are given in a combination.[12]

Since chemotherapy affects the whole body, it can have a wide range of side effects. Patients often find that they start losing their hair since the drugs that are combatting the cancer cells also attack the cells in the hair roots. This powerful treatment can also lead to fatigue, loss of appetite, and vomiting depending on the person.[11]

The treatment of some leukaemias and lymphomas requires the use of high-dose chemotherapy, and total body irradiation (TBI). This treatment ablates the bone marrow, and hence the body's ability to recover and repopulate the blood. For this reason, bone marrow, or peripheral blood stem cell harvesting is carried out before the ablative part of the therapy, to enable "rescue" after the treatment has been given. This is known as autologous stem cell transplantation.

Targeted therapies

[edit]
Main article: Targeted therapy

Targeted therapy, which first became available in the late 1990s, has had a significant impact in the treatment of some types of cancer, and is currently a very active research area. This constitutes the use of agents specific for the deregulated proteins of cancer cells. Small molecule drugs are targeted therapy drugs that are generally inhibitors of enzymatic domains on mutated, overexpressed, or otherwise critical proteins within the cancer cell. Prominent examples are the tyrosine kinase inhibitors imatinib (Gleevec/Glivec) and gefitinib (Iressa).

Monoclonal antibody therapy is another strategy in which the therapeutic agent is an antibody which specifically binds to a protein on the surface of the cancer cells. Examples include the anti-HER2/neu antibody trastuzumab (Herceptin) used in breast cancer, and the anti-CD20 antibody rituximab, used in a variety of B-cell malignancies.

Targeted therapy can also involve small peptides as "homing devices" which can bind to cell surface receptors or affected extracellular matrix surrounding the tumor. Radionuclides which are attached to these peptides (e.g. RGDs) eventually kill the cancer cell if the nuclide decays in the vicinity of the cell. Especially oligo- or multimers of these binding motifs are of great interest, since this can lead to enhanced tumor specificity and avidity.

Photodynamic therapy (PDT) is a ternary treatment for cancer involving a photosensitizer, tissue oxygen, and light (often using lasers[13]). PDT can be used as treatment for basal cell carcinoma (BCC) or lung cancer; PDT can also be useful in removing traces of malignant tissue after surgical removal of large tumors.[14] In February 2019, medical scientists announced that iridium attached to albumin, creating a photosensitized molecule, can penetrate cancer cells and, after being irradiated with light, destroy the cancer cells.[15][16]

High-energy therapeutic ultrasound could increase higher-density anti-cancer drug load and nanomedicines to target tumor sites by 20x fold higher than traditional target cancer therapy.[17]

Targeted therapies under pre-clinical development as potential cancer treatments include morpholino splice switching oligonucleotides, which induce ERG exon skipping in prostate cancer models,[18] multitargeted kinase inhibitors that inhibit the PI3K[19] with other pathways including MEK[20] and PIM,[21] and inhibitors of NF-κB in models of chemotherapy resistance.[22][23][24]

Immunotherapy

[edit]
A renal cell carcinoma (lower left) in a kidney
Main article: Cancer immunotherapy
Further information: Bladder cancer § Immunotherapy

Cancer immunotherapy refers to a diverse set of therapeutic strategies designed to induce the patient's own immune system to fight the tumor. Contemporary methods for generating an immune response against tumors include intravesical BCG immunotherapy for superficial bladder cancer, and use of interferons and other cytokines to induce an immune response in renal cell carcinoma and melanoma patients. Cancer vaccines to generate specific immune responses are the subject of intensive research for a number of tumors, notably malignant melanoma and renal cell carcinoma. Sipuleucel-T is a vaccine-like strategy for prostate cancer in which dendritic cells from the patient are loaded with prostatic acid phosphatase peptides to induce a specific immune response against prostate-derived cells. It gained FDA approval in 2010.

Allogeneic hematopoietic stem cell transplantation (usually from the bone marrow) from a genetically non-identical donor can be considered a form of immunotherapy, since the donor's immune cells will often attack the tumor in a phenomenon known as graft-versus-tumor effect. For this reason, allogeneic HSCT leads to a higher cure rate than autologous transplantation for several cancer types, although the side effects are also more severe.

The cell based immunotherapy in which the patients own natural killer cells (NKs) and cytotoxic T cells are used has been in practice in Japan since 1990. NK cells and TCs primarily kill the cancer cells when they are developed. This treatment is given together with the other modes of treatment such as surgery, radiotherapy or chemotherapy and termed autologous immune enhancement therapy (AIET).[25][26]

Immune checkpoint therapy focuses on two immune checkpoint proteins, cytotoxic T-lymphocyte associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1). Under normal conditions, the immune system utilizes checkpoint proteins as negative feedback mechanisms to return to homeostasis once pathogens have been cleared from the body. In a tumor microenvironment, cancer cells can commandeer this physiological regulatory system to "put a brake" on the anti-cancer immune response and evade immune surveillance.[27] 2018 Nobel Prize in medicine is awarded to Dr. James Allison of University of Texas MD Anderson Cancer Center in U.S. and Dr. Tasuku Honjo Kyoto University in Japan for their contributions in advance of PD-1 and CTLA-4 immune checkpoint therapy.[28]

Hormonal therapy

[edit]
Main article: Hormonal therapy (oncology)

The growth of some cancers can be inhibited by providing or blocking certain hormones. Common examples of hormone-sensitive tumors include certain types of breast and prostate cancers. Blocking estrogen or testosterone is often an important additional treatment. In certain cancers, administration of hormone agonists, such as progestogens may be therapeutically beneficial. Although the side effects from hormone therapy vary depending on the type, patients can experience symptoms such as hot flashes, nausea, and fatigue.[29]

Angiogenesis inhibitors

[edit]
Main article: Angiogenesis inhibitor

Angiogenesis inhibitors prevent the extensive growth of blood vessels (angiogenesis) that tumors need to survive and grow. Continued growth allows the invasion of cells into neighbouring tissues, and metastasis into distal tissues.[30] There are many approved angiogenesis inhibitors including bevacizumab, axitinib, and cabozantinib.[30]

Flavonoids have been shown to downregulate the angiogenic stimulation of VEGF and Hypoxia-inducible factor (HIF) but none have reached clinical trials.[31]

Exercise prescription

[edit]
Main article: Exercise prescription

Exercise prescription is becoming a mainstream adjunct treatment for cancer,[32] based on studies which show that exercise (compared to no exercise) is associated with reduced recurrence rates, improved mortality outcomes, reduction of side effects from traditional cancer treatments.[33][34] Although it is uncertain whether improved outcomes with exercise are correlated or causative, the benefit-risk ratio of including exercise as part of cancer treatment is large,[35] as exercise has further benefits (e.g. cardiovascular, mental health) without major risks, although there is a small risk of overuse injury if added too aggressively.[36] Exercise physiologists and exercise medicine specialists can assist oncologists and primary care practitioners with exercise prescription in cancer patients.

Walking is usually an excellent exercise option as an adjunct cancer treatment.

Synthetic lethality

[edit]
Main article: Synthetic lethality

Synthetic lethality arises when a combination of deficiencies in the expression of two or more genes leads to cell death, whereas a deficiency in only one of these genes does not. The deficiencies can arise through mutations, epigenetic alterations or inhibitors of one or both of the genes.

Cancer cells are frequently deficient in a DNA repair gene.[37][38] (Also see DNA repair deficiency in cancer.) This DNA repair defect either may be due to mutation or, often, epigenetic silencing (see epigenetic silencing of DNA repair). If this DNA repair defect is in one of seven DNA repair pathways (see DNA repair pathways), and a compensating DNA repair pathway is inhibited, then the tumor cells may be killed by synthetic lethality. Non-tumorous cells, with the initial pathway intact, can survive.

Ovarian cancer

[edit]
Main article: Ovarian cancer

Mutations in DNA repair genes BRCA1 or BRCA2 (active in homologous recombinational repair) are synthetically lethal with inhibition of DNA repair gene PARP1 (active in the base excision repair and in the microhomology-mediated end joining pathways of DNA repair).[39][40]

Ovarian cancers have a mutational defect in BRCA1 in about 18% of patients (13% germline mutations and 5% somatic mutations) (see BRCA1). Olaparib, a PARP inhibitor, was approved in 2014 by the US FDA for use in BRCA-associated ovarian cancer that had previously been treated with chemotherapy.[41] The FDA, in 2016, also approved the PARP inhibitor rucaparib to treat women with advanced ovarian cancer who have already been treated with at least two chemotherapies and have a BRCA1 or BRCA2 gene mutation.[42]

Colon cancer

[edit]
Main article: Colorectal cancer

In colon cancer, epigenetic defects in the WRN gene appear to be synthetically lethal with inactivation of TOP1. In particular, irinotecan inactivation of TOP1 was synthetically lethal with deficient expression of the DNA repair WRN gene in patients with colon cancer.[43] In a 2006 study, 45 patients had colonic tumors with hypermethylated WRN gene promoters (silenced WRN expression), and 43 patients had tumors with unmethylated WRN gene promoters, so that WRN protein expression was high.[43] Irinotecan was more strongly beneficial for patients with hypermethylated WRN promoters (39.4 months survival) than for those with unmethylated WRN promoters (20.7 months survival). The WRN gene promoter is hypermethylated in about 38% of colorectal cancers.[43]

There are five different stages of colon cancer, and these five stages all have treatment:

  • Stage 0, is where the patient is required to undergo surgery to remove the polyp (American Cancer Society[44]).
  • Stage 1, depending on the location of the cancer in the colon and lymph nodes, the patient undergoes surgery just like Stage 0.
  • Stage 2 patients undergoes removing nearby lymph nodes, but depending on what the doctor says, the patent might have to undergo chemotherapy after surgery (if the cancer is at higher risk of coming back).
  • Stage 3, is where the cancer has spread all throughout the lymph nodes but not yet to other organs or body parts. When getting to this stage, Surgery is conducted on the colon and lymph nodes, then the doctor orders Chemotherapy (FOLFOX or CapeOx) to treat the colon cancer in the location needed (American Cancer Society[44]). The last a patient can get is Stage 4.
  • Stage 4 patients only undergo surgery if it is for the prevention of the cancer, along with pain relief. If the pain continues with these two options, the doctor might recommended radiation therapy. The main treatment strategy is chemotherapy due to how aggressive the cancer becomes in this stage, not only to the colon but to the lymph nodes.

Symptom control and palliative care

[edit]
Further information: Cancer pain § Management

Although the control of the symptoms of cancer is not typically thought of as a treatment directed at the cancer, it is an important determinant of the quality of life of cancer patients, and plays an important role in the decision whether the patient is able to undergo other treatments. In general, doctors have the therapeutic skills to reduce pain including, chemotherapy-induced nausea and vomiting, diarrhea, hemorrhage and other common problems in cancer patients. The multidisciplinary specialty of palliative care has increased specifically in response to the symptom control needs for these groups of patients.

Pain medication, such as morphine, oxycodone, and antiemetics are drugs to suppress nausea and vomiting. These are very commonly used in patients with cancer-related symptoms. Improved antiemetics such as ondansetron and analogues, as well as aprepitant have made aggressive treatments much more feasible in cancer patients.

Cancer pain can be associated with continuing tissue damage due to the disease process, or the treatment (i.e. surgery, radiation, chemotherapy). There is always a role for environmental factors and affective disturbances in the genesis of pain behaviors, However these are not usually the predominant etiologic factors in patients with cancer pain. Some patients with severe pain associated with cancer are nearing the end of their lives, but in all cases, palliative therapies should be used to control the pain. Issues such as the social stigma of using opioids and health care consumption can be concerns and may need to be addressed for the person to feel comfortable taking the medications required to control his or her symptoms. The typical strategy for cancer pain management is to get the patient as comfortable as possible using the least amount of medications possible, even if that means using opioids, surgery, and physical measures.

Historically, doctors were reluctant to prescribe narcotics to terminal cancer patients due to addiction and respiratory function suppression. The palliative care movement, a more recent offshoot of the hospice movement, has engendered more widespread support for preemptive pain treatment for cancer patients. The World Health Organization also noted uncontrolled cancer pain as a worldwide problem and established a "ladder" as a guideline for how practitioners should treat pain in patients who have cancer

Cancer-related fatigue is a very common symptom of cancer, and there are a number of approaches put forward for helping with this.[45]

Mental struggles/pain

[edit]

Cancer patients undergo many obstacles and one of these includes mental strain. It is very common for cancer patients to become stressed, overwhelmed, uncertain, and even depressed.[46] The use of chemo is a very harsh treatment causing the cells of the body to die. Physical effects like this do not only inflict pain but also cause patients to become mentally exhausted and want to give up. For a lot of reasons including these, hospitals offer many types of therapy and mental healing. Some of these include yoga, meditation, communication therapy, and spiritual ideas.[47] All of these are meant to calm and relax the mind, or to give hope for the patients that may feel drained.

Insomnia

[edit]

A common disorder experienced by people that have survived cancer treatments is insomnia. Almost 60% of cancer survivors experience insomnia, and if it is not treated properly it can have long term effects on physiological and physical health.[48] Insomnia is defined as dissatisfaction with sleep duration or quality and difficulties initiating or maintaining sleep.[49] Insomnia can heavily reduce one's quality of life. Cognitive behavioral therapy has been seen to reduce insomnia and depression for cancer survivors.[50]

Muscle strength

[edit]

Decreased muscle strength is a common side effect to many different cancer treatments. Because of this, exercise is very important especially in the first year after treatment. It has been shown that yoga, water exercise, and pilates can improve the emotional well-being and quality of life of breast cancer survivors.[51]

Hospice care

[edit]

Hospice care provides palliative care at home, or in a dedicated hospice institution, for a person with an advanced illness termed as terminal.[52] Untreated cancer will prove terminal, and sometimes a choice is made to forgo treatment and its unpleasant side effects, and opt instead for hospice care. Hospice care aims to provide support for the person's medical, emotional, social, practical, psychological, and spiritual needs.[52]

Advance care planning (ACP) can help a person to decide for themself their future care wishes as they approach end of life.[53] ACP helps adults at any stage of health to decide, and record in writing, their wishes for medical treatment preferences, and future wants, preferably as previously discussed with relatives or carers.[53]

Research

[edit]
Main article: Experimental cancer treatment

Clinical trials, also called research studies, test new treatments in people with cancer. The goal of this research is to find better ways to treat cancer and help cancer patients. Clinical trials test many types of treatment such as new drugs, new approaches to surgery or radiation therapy, new combinations of treatments, or new methods such as gene therapy.

A clinical trial is one of the final stages of a long and careful cancer research process. The search for new treatments begins in the laboratory, where scientists first develop and test new ideas. If an approach seems promising, the next step may be testing a treatment in animals to see how it affects cancer in a living being and whether it has harmful effects. Of course, treatments that work well in the lab or in animals do not always work well in people. Studies are done with cancer patients to find out whether promising treatments are safe and effective.

Patients who take part may be helped personally by the treatment they receive. They get up-to-date care from cancer experts, and they receive either a new treatment being tested or the best available standard treatment for their cancer. At the same time, new treatments also may have unknown risks, but if a new treatment proves effective or more effective than standard treatment, study patients who receive it may be among the first to benefit. There is no guarantee that a new treatment being tested or a standard treatment will produce good results. In children with cancer, a survey of trials found that those enrolled in trials were on average not more likely to do better or worse than those on standard treatment; this confirms that success or failure of an experimental treatment cannot be predicted.[54]

Exosome research

[edit]

Exosomes are lipid-covered microvesicles shed by solid tumors into bodily fluids, such as blood and urine. Current research is being done attempting to use exosomes as a detection and monitoring method for a variety of cancers.[55] The hope is to be able to detect cancer with a high sensitivity and specificity via detection of specific exosomes in the blood or urine. The same process can also be used to more accurately monitor a patient's treatment progress. Enzyme linked lectin specific assay or ELLSA Archived 13 July 2011 at the Wayback Machine has been proven to directly detect melanoma derived exosomes from fluid samples.[56] Previously, exosomes had been measured by total protein content in purified samples and by indirect immunomodulatory effects. ELLSA directly measures exosome particles in complex solutions, and has already been found capable of detecting exosomes from other sources, including ovarian cancer and tuberculosis-infected macrophages.

Exosomes, secreted by tumors, are also believed to be responsible for triggering programmed cell death (apoptosis) of immune cells; interrupting T-cell signaling required to mount an immune response; inhibiting the production of anti-cancer cytokines, and has implications in the spread of metastasis and allowing for angiogenesis.[57] Studies are currently being done with "Lectin affinity plasmapheresis" (LAP),[56] LAP is a blood filtration method which selectively targets the tumor based exosomes and removes them from the bloodstream. It is believed that decreasing the tumor-secreted exosomes in a patient's bloodstream will slow down progression of the cancer while at the same time increasing the patients own immune response.

Complementary and alternative

[edit]
Main article: Alternative cancer treatments

Complementary and alternative medicine (CAM) treatments are the diverse group of medical and health care systems, practices, and products that are not part of conventional medicine and have not been shown to be effective.[58] "Complementary medicine" refers to methods and substances used along with conventional medicine, while "alternative medicine" refers to compounds used instead of conventional medicine.[59] CAM use is common among people with cancer; a 2000 study found that 69% of cancer patients had used at least one CAM therapy as part of their cancer treatment.[60] Most complementary and alternative medicines for cancer have not been rigorously studied or tested. Some alternative treatments which have been investigated and shown to be ineffective continue to be marketed and promoted.[61]

Special circumstances

[edit]

In pregnancy

[edit]

The incidence of pregnancy-associated cancer has risen due to the increasing age of pregnant mothers.[62] Cancers may also be detected incidentally during maternal screening.[62]

Cancer treatment needs to be selected to do least harm to both the woman and her embryo/fetus. In some cases a therapeutic abortion may be recommended.

Radiation therapy is out of the question, and chemotherapy always poses the risk of miscarriage and congenital malformations.[63] Little is known about the effects of medications on the child.

Even if a drug has been tested as not crossing the placenta to reach the child, some cancer forms can harm the placenta and make the drug pass over it anyway.[63] Some forms of skin cancer may even metastasize to the child's body.[63]

Diagnosis is also made more difficult, since computed tomography is infeasible because of its high radiation dose. Still, magnetic resonance imaging works normally.[63] However, contrast media cannot be used, since they cross the placenta.[63]

As a consequence of the difficulties to properly diagnose and treat cancer during pregnancy, the alternative methods are either to perform a Cesarean section when the child is viable in order to begin a more aggressive cancer treatment, or, if the cancer is malignant enough that the mother is unlikely to be able to wait that long, to perform an abortion in order to treat the cancer.[63]

In utero

[edit]

Fetal tumors are sometimes diagnosed while still in utero. Teratoma is the most common type of fetal tumor, and usually is benign. In some cases these are surgically treated while the fetus is still in the uterus.

Society and culture

[edit]

Racial and social disparities

[edit]

Cancer is a significant issue that is affecting the world. Specifically in the U.S., 1,735,350 new cases of cancer, and 609,640 deaths were expected by the end of 2018. Adequate treatment can prevent many cancer deaths but there are racial and social disparities in treatments which has a significant factor in high death rates. Minorities are more likely to receive inadequate treatment while white patients are more likely to receive efficient treatments in a timely manner.[64] Having satisfactory treatment in a timely manner can increase the patient's likelihood of survival. It has been shown that chances of survival are significantly greater for white patients than for African American patients.[64]

The annual average mortality of patients with colorectal cancer between 1992 and 2000 was 27 and 18.5 per 100,000 white patients and 35.4 and 25.3 per 100,000 black patients. In a journal that analyzed multiple studies testing racial disparities when treating colorectal cancer found contradicting findings. The US Veterans Administration and an adjuvant trial found that there was no evidence to support racial differences in treating colorectal cancer. However, two studies suggested that African American patients received less satisfactory and poorer quality treatment compared to white patients.[65] One of these studies specifically was provided by the Center for Intramural Research. They found that black patients were 41% less likely to receive colorectal treatment and were more likely to be hospitalized in a teaching hospital with less certified physicians compared to white patients. Furthermore, black patients were more likely to be diagnosed with oncologic sequelae, which is a severity of the illness in result of poorly treated cancer. Lastly, for every 1,000 patients in the hospital, there were 137.4 black patient deaths and 95.6 white patient deaths.[66]

An article in a breast cancer journal analyzed the disparities of breast cancer treatments in the Appalachian Mountains. African American women were found to be three times more likely to die compared to Asians and two times more likely to die compared to white women.[67] According to the study, African American women are at a survival disadvantage compared to other races.[68][67] Black women are also more likely to receive less successful treatment than white women by not receiving surgery or therapy. Furthermore, the US National Cancer Institute panel identified breast cancer treatments, given to black women, as inappropriate and not adequate compared to the treatment given to white women.[69]

From these studies, researchers have noted that there are definite disparities in the treatment of cancer, specifically who has access to the best treatment and can receive it in a timely manner. This eventually leads to disparities between who dies from cancer and who is more likely to survive.

The cause of these disparities is generally that African Americans have less medical care coverage, insurance and access cancer centers than other races.[70] For an example, black patients with breast cancer and colorectal cancer were shown to be more likely to have Medicaid or no insurance compared to other races.[66] The location of the health care facility also plays a role in why African Americans receive less treatment in comparison to other races.[70][66] However, some studies say that African Americans do not trust doctors and do not always seek the help they need and that this explains why fewer African Americans receive treatment.[71] Others suggest that African Americans seek more treatment than whites and that it is simply a lack of the resources available to them.[71] In this case, analyzing these studies will identify the treatment disparities and look to prevent them by discovering potential causes of these disparities.

Public perception

[edit]

Despite recognition of improvements in outcomes, visceral fear of the disease is ubiquitous, and people may have to struggle to control it.[72]

Among lung cancer patients, stigma, shame, social isolation, and discrimination are common.[73] Such patients are sometimes told that they deserve cancer because of their smoking. Those patients also may have feelings of guilt for having cancer.[74][75][76] Stigma in cervical cancer was predominantly driven by fear of social judgment and rejection, self-blame, and shame, with notable negative influences from gender and social norms, as both human papillomavirus infection and cervical cancer were stigmatized due to the perception that they arise from reckless behavior such as having multiple sexual partners or neglecting screening.[77] Resilience may be a potent protective mechanism against stigmatization.[78] Resilience in context of cancer treatment is patient's physiological and psychological capacity to effectively adapt, recover, and maintain optimal functioning in the face of the medical challenges. It encompasses the ability to cope with and overcome adversity, maintain emotional well-being, and promote overall health and healing.[79]

See also

[edit]

References

[edit]
  1. ^ a b c "Cancer". www.who.int. Retrieved 9 November 2023.
  2. ^ "Targeted Therapy for Cancer - NCI". www.cancer.gov. 15 August 2014. Retrieved 7 November 2023.
  3. ^ Research Cf (11 March 2022). "FDA approves olaparib for adjuvant treatment of high-risk early breast cancer". FDA. Retrieved 10 November 2023.
  4. ^ a b "Types of Cancer Treatment - NCI". www.cancer.gov. 31 July 2017. Retrieved 7 November 2023.
  5. ^ Fukumura D, Kloepper J, Amoozgar Z, Duda DG, Jain RK (May 2018). "Enhancing cancer immunotherapy using antiangiogenics: opportunities and challenges". Nat Rev Clin Oncol. 15 (5): 325–340. doi:10.1038/nrclinonc.2018.29. PMC 5921900. PMID 29508855.
  6. ^ "Biomarker Testing for Cancer Treatment - NCI". www.cancer.gov. 5 October 2017. Retrieved 7 November 2023.
  7. ^ Subotic S, Wyler S, Bachmann A (August 2012). "Surgical Treatment of Localised Renal Cancer". European Urology Supplements. 11 (3): 60–65. doi:10.1016/j.eursup.2012.04.002.
  8. ^ Mieog JS, van der Hage JA, van de Velde CJ (October 2007). "Neoadjuvant chemotherapy for operable breast cancer". The British Journal of Surgery. 94 (10): 1189–200. doi:10.1002/bjs.5894. PMID 17701939. S2CID 34216395.
  9. ^ Baskar R, Lee KA, Yeo R, Yeoh KW (2012). "Cancer and radiation therapy: current advances and future directions". Int J Med Sci. 9 (3): 193–9. doi:10.7150/ijms.3635. PMC 3298009. PMID 22408567.
  10. ^ "Sore mouth and problems with your teeth". www.cancerresearchuk.org. Retrieved 11 November 2023.
  11. ^ a b "Chemotherapy: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 1 November 2022.
  12. ^ Takimoto CH, Calvo E (2008). "Principles of Oncologic Pharmacotherapy". In Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (eds.). Cancer Management: A Multidisciplinary Approach (11 ed.). Archived from the original on 4 October 2013. Retrieved 14 November 2009.
  13. ^ Duarte, F J (Ed.), Tunable Laser Applications (CRC, New York, 2009) Chapters 5, 7, 8.
  14. ^ Dolmans DE, Fukumura D, Jain RK (May 2003). "Photodynamic therapy for cancer". Nature Reviews. Cancer. 3 (5): 380–7. doi:10.1038/nrc1071. PMID 12724736. S2CID 205467056.
  15. ^ University of Warwick (3 February 2019). "Simply shining light on dinosaur metal compound kills cancer cells". EurekAlert!. Retrieved 3 February 2019.
  16. ^ Zhang, Pingyu, et al. (15 December 2018). "Nucleus-Targeted Organoiridium–Albumin Conjugate for Photodynamic Cancer Therapy". Angewandte Chemie. 58 (8): 2350–2354. doi:10.1002/anie.201813002. PMC 6468315. PMID 30552796.
  17. ^ Mo S, Carlisle R, Laga R, Myers R, Graham S, Cawood R, Ulbrich K, Seymour L, Coussios CC (July 2015). "Increasing the density of nanomedicines improves their ultrasound-mediated delivery to tumours". Journal of Controlled Release. 210 (10): 10–8. doi:10.1016/j.jconrel.2015.05.265. PMID 25975831.
  18. ^ Li L, Hobson L, Perry L, Clark B, Heavey S, Haider A, Sridhar A, Shaw G, Kelly J, Freeman A, Wilson I, Whitaker H, Nurmemmedov E, Oltean S, Porazinski S, Ladomery M (15 September 2020). "Targeting the ERG oncogene with splice-switching oligonucleotides as a novel therapeutic strategy in prostate cancer". British Journal of Cancer. 123 (6): 1024–1032. doi:10.1038/s41416-020-0951-2. PMC 7493922. PMID 32581342. S2CID 220049871.
  19. ^ Heavey S, O'Byrne KJ, Gately K (April 2014). "Strategies for co-targeting the PI3K/AKT/mTOR pathway in NSCLC". Cancer Treatment Reviews. 40 (3): 445–456. doi:10.1016/j.ctrv.2013.08.006. PMID 24055012.
  20. ^ Heavey S, Cuffe S, Finn S, Young V, Ryan R, Nicholson S, Leonard N, McVeigh N, Barr M, O'Byrne K, Gately K (29 November 2016). "In pursuit of synergy: An investigation of the PI3K/mTOR/MEK co-targeted inhibition strategy in NSCLC". Oncotarget. 7 (48): 79526–79543. doi:10.18632/oncotarget.12755. PMC 5346733. PMID 27765909.
  21. ^ Luszczak S, Kumar C, Sathyadevan VK, Simpson BS, Gately KA, Whitaker HC, Heavey S (December 2020). "PIM kinase inhibition: co-targeted therapeutic approaches in prostate cancer". Signal Transduction and Targeted Therapy. 5 (1): 7. doi:10.1038/s41392-020-0109-y. PMC 6992635. PMID 32296034.
  22. ^ Ryan SL, Beard S, Barr MP, Umezawa K, Heavey S, Godwin P, Gray SG, Cormican D, Finn SP, Gately KA, Davies AM, Thompson EW, Richard DJ, O'Byrne KJ, Adams MN, Baird AM (September 2019). "Targeting NF-κB-mediated inflammatory pathways in cisplatin-resistant NSCLC" (PDF). Lung Cancer. 135: 217–227. doi:10.1016/j.lungcan.2019.07.006. PMID 31446998. S2CID 199025494.
  23. ^ Heavey S, Godwin P, Baird AM, Barr MP, Umezawa K, Cuffe S, Finn SP, O'Byrne KJ, Gately K (10 October 2014). "Strategic targeting of the PI3K–NFκB axis in cisplatin-resistant NSCLC". Cancer Biology & Therapy. 15 (10): 1367–1377. doi:10.4161/cbt.29841. PMC 4130730. PMID 25025901.
  24. ^ Godwin P, Baird AM, Heavey S, Barr MP, O'Byrne KJ, Gately K (2013). "Targeting Nuclear Factor-Kappa B to Overcome Resistance to Chemotherapy". Frontiers in Oncology. 3: 120. doi:10.3389/fonc.2013.00120. PMC 3655421. PMID 23720710.
  25. ^ Damodar S, Terunuma H, Sheriff AK, Farzana L, Manjunath S, Senthilkumar R, Shastikumar G, Abraham S. "Autologous Immune Enhancement Therapy (AIET) for a Case of Acute Myeloid Leukemia (AML) - Our Experience" in "Proceedings of the Annual Symposium on Regenerative Medicine(PASRM)". Journal of Stem Cells and Regenerative Medicine. 1 (1): 40–56. 26 December 2006. doi:10.46582/jsrm.0101007. PMC 3907960. PMID 24692861. S2CID 27569762.
  26. ^ Sivaraman G, Pandian A, Baskar S, Senthil K, Senthilnagarajan R, Srinivasan V, Dedeepiya V, Abraham S (2008). "Autologous Immune Enhancement therapy for Advanced Carcinoma of Pancreas-A Case Report". Journal of Stem Cells & Regenerative Medicine. 4 (1): 13. PMID 24693028.
  27. ^ Buchbinder EI, Desai A (February 2016). "CTLA-4 and PD-1 Pathways: Similarities, Differences, and Implications of Their Inhibition". American Journal of Clinical Oncology. 39 (1): 98–106. doi:10.1097/COC.0000000000000239. PMC 4892769. PMID 26558876.
  28. ^ Ledford H, Else H, Warren M (October 2018). "Cancer immunologists scoop medicine Nobel prize". Nature. 562 (7725): 20–21. Bibcode:2018Natur.562...20L. doi:10.1038/d41586-018-06751-0. PMID 30279600.
  29. ^ "Hormone Therapy for Cancer - NCI". www.cancer.gov. 29 April 2015. Retrieved 30 October 2022.
  30. ^ a b "Angiogenesis Inhibitors - NCI". www.cancer.gov. 1 May 2018. Retrieved 10 November 2023.
  31. ^ Al-Khayri JM, Sahana GR, Nagella P, Joseph BV, Alessa FM, Al-Mssallem MQ (May 2022). "Flavonoids as Potential Anti-Inflammatory Molecules: A Review". Molecules. 27 (9): 2901. doi:10.3390/molecules27092901. PMC 9100260. PMID 35566252.
  32. ^ Ashcraft KA, Warner AB, Jones LW, Dewhirst MW (January 2019). "Exercise as Adjunct Therapy in Cancer". Seminars in Radiation Oncology. 29 (1): 16–24. doi:10.1016/j.semradonc.2018.10.001. PMC 6656408. PMID 30573180.
  33. ^ Christensen JF, Simonsen C, Hojman P (13 December 2018). "Exercise Training in Cancer Control and Treatment". Comprehensive Physiology. 9 (1): 165–205. doi:10.1002/cphy.c180016. PMID 30549018. S2CID 56492477.
  34. ^ Cormie P, Zopf EM, Zhang X, Schmitz KH (1 January 2017). "The Impact of Exercise on Cancer Mortality, Recurrence, and Treatment-Related Adverse Effects". Epidemiologic Reviews. 39 (1): 71–92. doi:10.1093/epirev/mxx007. PMID 28453622.
  35. ^ Cormie P, Trevaskis M, Thornton-Benko E, Zopf EM (April 2020). "Exercise medicine in cancer care". Australian Journal of General Practice. 49 (4): 169–174. doi:10.31128/AJGP-08-19-5027. PMID 32233341. S2CID 214751316.
  36. ^ Orchard JW (April 2020). "Prescribing and dosing exercise in primary care". Australian Journal of General Practice. 49 (4): 182–186. doi:10.31128/AJGP-10-19-5110. PMID 32233343. S2CID 214749061.
  37. ^ Kennedy RD, D'Andrea AD (August 2006). "DNA repair pathways in clinical practice: lessons from pediatric cancer susceptibility syndromes". Journal of Clinical Oncology. 24 (23): 3799–808. doi:10.1200/JCO.2005.05.4171. PMID 16896009.
  38. ^ Shaheen M, Allen C, Nickoloff JA, Hromas R (June 2011). "Synthetic lethality: exploiting the addiction of cancer to DNA repair". Blood. 117 (23): 6074–82. doi:10.1182/blood-2011-01-313734. PMID 21441464.
  39. ^ Ledermann J, Harter P, Gourley C, Friedlander M, Vergote I, Rustin G, Scott CL, Meier W, Shapira-Frommer R, Safra T, Matei D, Fielding A, Spencer S, Dougherty B, Orr M, Hodgson D, Barrett JC, Matulonis U (July 2014). "Olaparib maintenance therapy in patients with platinum-sensitive relapsed serous ovarian cancer: a preplanned retrospective analysis of outcomes by BRCA status in a randomised phase 2 trial". The Lancet. Oncology. 15 (8): 852–61. doi:10.1016/S1470-2045(14)70228-1. PMID 24882434.
  40. ^ Ding X, Ray Chaudhuri A, Callen E, Pang Y, Biswas K, Klarmann KD, Martin BK, Burkett S, Cleveland L, Stauffer S, Sullivan T, Dewan A, Marks H, Tubbs AT, Wong N, Buehler E, Akagi K, Martin SE, Keller JR, Nussenzweig A, Sharan SK (August 2016). "Synthetic viability by BRCA2 and PARP1/ARTD1 deficiencies". Nature Communications. 7: 12425. Bibcode:2016NatCo...712425D. doi:10.1038/ncomms12425. PMC 4979061. PMID 27498558.
  41. ^ Yao S (19 December 2014). "FDA approves Lynparza to treat advanced ovarian cancer: First LDT companion diagnostic test also approved to identify appropriate patients". U.S. Food and Drug Administration.
  42. ^ Commissioner Oo (18 March 2019). "Press Announcements - FDA grants accelerated approval to new treatment for advanced ovarian cancer". www.fda.gov.
  43. ^ a b c Agrelo R, Cheng WH, Setien F, Ropero S, Espada J, Fraga MF, Herranz M, Paz MF, Sanchez-Cespedes M, Artiga MJ, Guerrero D, Castells A, von Kobbe C, Bohr VA, Esteller M (June 2006). "Epigenetic inactivation of the premature aging Werner syndrome gene in human cancer". Proceedings of the National Academy of Sciences of the United States of America. 103 (23): 8822–7. Bibcode:2006PNAS..103.8822A. doi:10.1073/pnas.0600645103. PMC 1466544. PMID 16723399.
  44. ^ a b "American Cancer Society | Information and Resources about for Cancer: Breast, Colon, Lung, Prostate, Skin". www.cancer.org. Retrieved 19 April 2017.
  45. ^ "Managing and treating cancer fatigue". www.cancerresearchuk.org. Retrieved 12 November 2023.
  46. ^ Ong L, Visser M, Lammes F, de Haes J (September 2000). "Doctor–Patient communication and cancer patients' quality of life and satisfaction". Patient Education and Counseling. 41 (2): 145–156. doi:10.1016/S0738-3991(99)00108-1. PMID 12024540.
  47. ^ McClain CS, Rosenfeld B, Breitbart W (May 2003). "Effect of spiritual well-being on end-of-life despair in terminally-ill cancer patients". The Lancet. 361 (9369): 1603–1607. doi:10.1016/S0140-6736(03)13310-7. PMID 12747880. S2CID 17851580.
  48. ^ Garland SN, Xie SX, DuHamel K, Bao T, Li Q, Barg FK, Song S, Kantoff P, Gehrman P, Mao JJ (1 December 2019). "Acupuncture Versus Cognitive Behavioral Therapy for Insomnia in Cancer Survivors: A Randomized Clinical Trial". JNCI: Journal of the National Cancer Institute. 111 (12): 1323–1331. doi:10.1093/jnci/djz050. ISSN 0027-8874. PMC 6910189. PMID 31081899.
  49. ^ Morin CM, Drake CL, Harvey AG, Krystal AD, Manber R, Riemann D, Spiegelhalder K (3 September 2015). "Insomnia disorder". Nature Reviews Disease Primers. 1 (1): 15026. doi:10.1038/nrdp.2015.26. hdl:20.500.11794/67139. ISSN 2056-676X. PMID 27189779. S2CID 19868023.
  50. ^ Peoples AR, Garland SN, Pigeon WR, Perlis ML, Wolf JR, Heffner KL, Mustian KM, Heckler CE, Peppone LJ, Kamen CS, Morrow GR, Roscoe JA (15 January 2019). "Cognitive Behavioral Therapy for Insomnia Reduces Depression in Cancer Survivors". Journal of Clinical Sleep Medicine. 15 (1): 129–137. doi:10.5664/jcsm.7586. ISSN 1550-9389. PMC 6329536. PMID 30621831.
  51. ^ Odynets T, Briskin Y, Todorova V (January 2019). "Effects of Different Exercise Interventions on Quality of Life in Breast Cancer Patients: A Randomized Controlled Trial". Integrative Cancer Therapies. 18: 153473541988059. doi:10.1177/1534735419880598. ISSN 1534-7354. PMC 6801883. PMID 31625419.
  52. ^ a b "Hospice care". nhs.uk. 27 July 2023. Retrieved 12 November 2023.
  53. ^ a b "Gold Standard Framework - Advance Care Planning". www.goldstandardsframework.org.uk. Retrieved 12 November 2023.
  54. ^ Kumar A, Soares H, Wells R, Clarke M, Hozo I, Bleyer A, Reaman G, Chalmers I, Djulbegovic B (December 2005). "Are experimental treatments for cancer in children superior to established treatments? Observational study of randomised controlled trials by the Children's Oncology Group". BMJ. 331 (7528): 1295. doi:10.1136/bmj.38628.561123.7C. PMC 1298846. PMID 16299015.
  55. ^ Rabinowits G, Gerçel-Taylor C, Day JM, Taylor DD, Kloecker GH (January 2009). "Exosomal microRNA: a diagnostic marker for lung cancer". Clinical Lung Cancer. 10 (1): 42–6. doi:10.3816/CLC.2009.n.006. PMID 19289371.
  56. ^ a b "Aethlon Medical Announces Data Against Metastatic Melanoma - Sep 9, 2010". Aethlonmedical.investorroom.com. 9 September 2010. Archived from the original on 11 August 2011. Retrieved 21 June 2013.
  57. ^ Ichim TE, Zhong Z, Kaushal S, Zheng X, Ren X, Hao X, Joyce JA, Hanley HH, Riordan NH, Koropatnick J, Bogin V, Minev BR, Min WP, Tullis RH (July 2008). "Exosomes as a tumor immune escape mechanism: possible therapeutic implications". Journal of Translational Medicine. 6: 37. doi:10.1186/1479-5876-6-37. PMC 2504474. PMID 18644158.DOI: 10.1038/s41392-020-0205-z
  58. ^ Cassileth BR, Deng G (1 February 2004). "Complementary and Alternative Therapies for Cancer" (PDF). The Oncologist. 9 (1): 80–89. doi:10.1634/theoncologist.9-1-80. PMID 14755017. S2CID 6453919. Archived from the original (PDF) on 19 July 2018. Retrieved 24 June 2021.
  59. ^ What Is CAM? National Center for Complementary and Integrative Health. Retrieved 3 February 2008.
  60. ^ Richardson MA, Sanders T, Palmer JL, Greisinger A, Singletary SE (July 2000). "Complementary/alternative medicine use in a comprehensive cancer center and the implications for oncology". Journal of Clinical Oncology. 18 (13): 2505–14. doi:10.1200/JCO.2000.18.13.2505. PMID 10893280.
  61. ^ Vickers A (2004). "Alternative cancer cures: "unproven" or "disproven"?". CA: A Cancer Journal for Clinicians. 54 (2): 110–8. CiteSeerX 10.1.1.521.2180. doi:10.3322/canjclin.54.2.110. PMID 15061600. S2CID 35124492.
  62. ^ a b Harwin J, Jha P, Post A, Silverstein J, Van Loon K, Poder L (May 2023). "The radiologist's role in a multidisciplinary approach to cancer in pregnancy". Abdom Radiol (NY). 48 (5): 1605–1611. doi:10.1007/s00261-023-03809-0. PMC 10149443. PMID 36705722.
  63. ^ a b c d e f "Krebstherapie in der Schwangerschaft extrem schwierig" (in German). Curado. Associated Press. 20 February 2009. Archived from the original on 6 March 2016. Retrieved 6 June 2009.
  64. ^ a b Shugarman LR, Mack K, Sorbero ME, Tian H, Jain AK, Ashwood JS, Asch SM (2009). "Race and Sex Differences in the Receipt of Timely and Appropriate Lung Cancer Treatment". Medical Care. 47 (7): 774–781. doi:10.1097/MLR.0b013e3181a393fe. JSTOR 40221952. PMID 19536007. S2CID 12148999.
  65. ^ Bigby JA, Holmes MD (2005). "Disparities across the Breast Cancer Continuum". Cancer Causes & Control. 16 (1): 35–44. doi:10.1007/s10552-004-1263-1. JSTOR 20069438. PMID 15750856. S2CID 28887189.
  66. ^ a b c Ball JK, Elixhauser A (September 1996). "Treatment Differences Between Blacks and Whites with Colorectal Cancer". Medical Care. 34 (9): 970–984. doi:10.1097/00005650-199609000-00008. PMID 8792784.
  67. ^ a b Couto RA (2012). Ludke RL, Obermiller PJ (eds.). Appalachian Health and Well-Being. University Press of Kentucky. ISBN 9780813135861. JSTOR j.ctt2jcssn.
  68. ^ Holmes L, Opara F, Hossain J (2010). "A Five-Year Breast Cancer-Specific Survival Disadvantage of African American Women". African Journal of Reproductive Health. 14 (3): 195–200. JSTOR 41329740. PMID 21495613.
  69. ^ Diehr P, Yergan J, Chu J, Feigl P, Glaefke G, Moe R, Bergner M, Rodenbaugh J (1989). "Treatment Modality and Quality Differences for Black and White Breast-Cancer Patients Treated in Community Hospitals". Medical Care. 27 (10): 942–958. doi:10.1097/00005650-198910000-00005. JSTOR 3765483. PMID 2796413. S2CID 41540074.
  70. ^ a b Palmer RC, Schneider EC (2005). "Social Disparities across the Continuum of Colorectal Cancer: A Systematic Review". Cancer Causes & Control. 16 (1): 55–61. doi:10.1007/s10552-004-1253-3. JSTOR 20069440. PMID 15750858. S2CID 9426166.
  71. ^ a b Schnittker J, Pescosolido BA, Croghan TW (May 2005). "Are African Americans Really Less Willing to Use Health Care?". Social Problems. 52 (2): 255–271. doi:10.1525/sp.2005.52.2.255.
  72. ^ Robb KA, Simon AE, Miles A, Wardle J (July 2014). "Public perceptions of cancer: a qualitative study of the balance of positive and negative beliefs". BMJ Open. 4 (7): e005434. doi:10.1136/bmjopen-2014-005434. PMC 4120326. PMID 25011992.
  73. ^ Hamann HA, Ver Hoeve ES, Carter-Harris L, Studts JL, Ostroff JS (August 2018). "Multilevel Opportunities to Address Lung Cancer Stigma across the Cancer Control Continuum". J Thorac Oncol. 13 (8): 1062–1075. doi:10.1016/j.jtho.2018.05.014. PMC 6417494. PMID 29800746.
  74. ^ Knapp-Oliver S, Moyer A (2009). "Visibility and the Stigmatization of Cancer: Context Matters1". Journal of Applied Social Psychology. 39 (12): 2798–2808. doi:10.1111/j.1559-1816.2009.00550.x.
  75. ^ Knapp S, Marziliano A, Moyer A (July 2014). "Identity threat and stigma in cancer patients". Health Psychol Open. 1 (1): 2055102914552281. doi:10.1177/2055102914552281. PMC 5193175. PMID 28070343.
  76. ^ Knapp-Oliver S, Moyer A (2012). "Causal Attributions Predict Willingness to Support the Allocation of Funding to Lung Cancer Treatment Programs". Journal of Applied Social Psychology. 42 (10): 2368–2385. doi:10.1111/j.1559-1816.2012.00945.x.
  77. ^ Peterson CE, Silva A, Goben AH, Ongtengco NP, Hu EZ, Khanna D, Nussbaum ER, Jasenof IG, Kim SJ, Dykens JA (December 2021). "Stigma and cervical cancer prevention: A scoping review of the U.S. literature". Prev Med. 153: 106849. doi:10.1016/j.ypmed.2021.106849. PMID 34662598. S2CID 239027566.
  78. ^ Li S, Wang X, Wang M, Jiang Y, Mai Q, Wu J, Ye Z (October 2023). "Association between stigma and sleep quality in patients with breast cancer: A latent profile and mediation analysis". Eur J Oncol Nurs. 67: 102453. doi:10.1016/j.ejon.2023.102453. PMID 37951070. S2CID 264547634.
  79. ^ Sihvola S, Kuosmanen L, Kvist T (February 2022). "Resilience and related factors in colorectal cancer patients: A systematic review". Eur J Oncol Nurs. 56: 102079. doi:10.1016/j.ejon.2021.102079. PMID 34844135. S2CID 244559871.

Bibliography

[edit]
  • "Understanding What Cancer Is: Ancient Times to Present". www.cancer.org.
  • Chahine S, Urquhart R (October 2019). "A cross-sectional population-based survey looking at the impact of cancer survivorship care plans on meeting the needs of cancer survivors in the posttreatment stage". Supportive Care in Cancer. 27 (10): 3785–3792. doi:10.1007/s00520-019-04685-5. PMID 30721368. S2CID 59604164.
  • Colby DA, Shifren K (1 January 2013). "Optimism, mental health, and quality of life: A study among breast cancer patients". Psychology, Health & Medicine. 18 (1): 10–20. doi:10.1080/13548506.2012.686619. PMID 22690751. S2CID 205772143.
  • "How Does Radiation Therapy Work?" American Cancer Society. N.p., n.d. Web. 21 March 2017.
  • Piazza MF, Galletta M, Portoghese I, Pilia I, Ionta MT, Contu P, Mereu A, Campagna M (August 2017). "Meeting psychosocial and health information needs to ensure quality of cancer care in outpatients". European Journal of Oncology Nursing. 29: 98–105. doi:10.1016/j.ejon.2017.06.001. PMID 28720273.
  • Northouse LL (1 September 2012). "Helping Patients and Their Family Caregivers Cope With Cancer". Oncology Nursing Forum. 39 (5): 500–506. doi:10.1188/12.ONF.500-506. PMID 22940514. S2CID 21512508.
  • "Radiation Therapy for Brain Cancer | CTCA." CancerCenter.com. N.p., 1 January 0001. Web. 21 March 2017.
  • "Radiation Therapy for Cancer." National Cancer Institute. N.p., n.d. Web. 21 March 2017.
Retrieved from "https://wiki.riteme.site/w/index.php?title=Cancer_treatment&oldid=1261980771"