Factors that contribute to the development of hypopharyngeal cancer include:

- Smoking

- Chewing tobacco

- Heavy alcohol use

- Poor diet

Smoking, like lung cancer, can cause hypopharyngeal cancer because it contains carcinogens that alter the DNA or RNA in a dividing cell. These alterations may change a normal DNA sequence to an oncogene, a gene that causes cancer after exposure to a carcinogen.

Squamous cells, a type of cell that lines hollow organs like the throat, mouth, lungs, and outer layer of skin, are particularly vulnerable when exposed to cigarette smoke.

Chewing tobacco can have the same effects as smoking and is also linked to hypopharyngeal cancer. The chewing tobacco is placed into the mouth, leaving it exposed to enzymes, like amylase, which partly digests the carcinogenic material. Saliva is swallowed, along with the cancer-promoting material, which passes through the hypopharynx on its way to the esophagus.

Heavy alcohol use is linked to Hypopharyngeal Cancer as well. Alcohol damages the lining of the hypopharynx, increasing the amount of chemicals that are allowed to seep into the underlying membranes. Heavy alcohol use is also associated with nutritional deficiencies.

A disease called Plummer-Vinson syndrome, a genetic disorder that causes a long-term iron deficiency, may also lead to Hypopharyngeal Cancer. Other factors like a deficiency in certain vitamins also appear to contribute to this type of cancer.

Hypopharyngeal cancer is a disease in which malignant cells grow in the hypopharynx (the area where the larynx and esophagus meet).

It first forms in the outer layer (epithelium) of the hypopharynx (last part of the pharynx), which is split into three areas. Progression of the disease is defined by the spread of cancer into one or more areas and into deeper tissues.

This type of cancer is rare. Only about 2,500 cases are seen in the US each year. Because of this, Hypopharyngeal Cancer is difficult to catch in its earliest stages and has one of the highest mortality rates of any head and neck cancer.

Treatment options vary and depend on the type and stage of cancer. Common treatments include surgery, chemotherapy, radiation therapy, amputation, and immunotherapy. A combination of therapies may be used. Knowledge and treatment of cancer have increased significantly in the past three decades. Survival rates have also increased due to the increase prevalence of canine cancer treatment centers and breakthroughs in targeted drug development. Canine cancer treatment has become an accepted clinical practice and access to treatment for owners has widely expanded recently. Cancer-targeting drugs most commonly function to inhibit excessive cell proliferation by attacking the replicating cells. However, there is still a prevalent pharmacy gap in veterinary oncology.

There is one canine tumor vaccine approved by the USDA, for preventing canine melanoma. The Oncept vaccine activates T-cell responses and antibodies against tumor-specific tyrosinase proteins. There is limited information about canine tumor antigens, which is the reason for the lack of tumor-specific vaccines and immunotherapy treatment plans for dogs.

Success of treatment depends on the form and extent of the cancer and the aggressiveness of the therapy. Early detection offers the best chance for successful treatment. The heterogeneity of tumors makes drug development increasingly complex, especially as new causes are discovered. No cure for cancer in canines exist.

Some dog owners opt for no treatment of the cancer at all, in which case palliative care, including pain relief, may be offered. Regardless of how treatment proceeds following a diagnosis, the quality of life of the pet is an important consideration. In cases where the cancer is not curable, there are still many things which can be done to alleviate the dog's pain. Good nutrition and care from the dog's owner can greatly enhance quality of life.

Surgery is the mainstay of treatment for clinically localized disease. In feasible cases, a partial cystectomy with "en-bloc" resection of the median umbilical ligament and umbilicus can achieve good results. In progressed stages, radiotherapy seems not to lead to sufficient response rates. However, chemotherapy regimes containing 5-FU (and Cisplatin) have been described to be useful in these cases. In recent years, targeted therapies have been demonstrated to be useful in reports of single cases. These agents included Sunitinib, Gefitinib, Bevacizumab and Cetuximab.

The median overall survival rate is about 50% in 5 years. Worse prognostic factors include the presence of residual tumor at the margin of the resection specimen (R+), invasion of the peritoneum and metastatic disease.

In the treatment of Kangri cancer, surgery is, most often, the first-line course of action to remove the primary tumor.

Most people with cancer of unknown primary origin have widely disseminated and incurable disease, although a few can be cured through treatment. With treatment, typical survival with CUP ranges from 6 to 16 months. Survival rates are lower in cases with visceral metastatic disease, ranging from 6 to 9 months. Survival rates are higher when the cancer is more limited to lymph nodes, pleura, or peritoneal metastasis, which ranges from 14 to 16 months. Long-term prognosis is somewhat better if a particular source of cancer is strongly suggested by clinical evidence.

CUP sometimes runs in families. It has been associated with familial lung, kidney, and colorectal cancers, which suggests that these sites may often be the origin of unidentifiable CUP cancers.

People with HPV-mediated oropharyngeal cancer tend to have higher survival rates. The prognosis for people with oropharyngeal cancer depends on the age and health of the person and the stage of the disease. It is important for people with oropharyngeal cancer to have follow-up exams for the rest of their lives, as cancer can occur in nearby areas. In addition, it is important to eliminate risk factors such as smoking and drinking alcohol, which increase the risk for second cancers.

While less studies have been completed examining deintensification in this setting, than in primary radical radiation for this cancer (see below), it is an area of active investigation. In one single institution study, a decision was made to reduce the radiation dose in high risk patients with HPV+OPC from 66 to 60 Gy, corresponding to the actual evidence, and follow up has shown no decrease in cancer control. Current trials, both in North America and Europe (such as ECOG 3311 and PATHOS) use 50 Gy as the comparison arm. The comparator of 50 Gy was chosen on the grounds of (i) the exquisite sensitivity of HPV+OPC to radiation, both "in vitro" and "in vivo"; ECOG 1308 showing excellent disease control at 54 Gy; and data suggesting that 50 Gy in 1.43 Gy (iso-effective dose 43 Gy in 2.0 Gy was sufficient to electively treat the neck. Other studies are evaluating doses as low as 30 Gy in high risk cases.

Chemotherapy has been used concurrently with radiation in this setting, as in primary treatment with radical radiation, particularly where pathological features indicated a higher risk of cancer recurrence. a number of studies have suggested that this does not improve local control, although adding toxicity.

Immunotherapy with immune checkpoint inhibitors is being investigated in head and neck cancers.

External beam radiotherapy has been used in one person to prevent the relapse and growth of tumor metastases to the head and neck regions. The prophylactic applications of radiation have been noted as “encouraging” in this one case, reducing some tumors and eliminating others.

Another study with a couple of the same authors found that radiotherapy after surgery helped with the reduction and cure of head and neck tumors in additional cases. The researchers suggest that external beam radiotherapy should be part of the treatment course for patients who have or at risk of developing tumors in the head and neck areas.

Treatment of invasive carcinoma of no special type (NST) depends on the size of the mass (size of the tumor measured in its longest direction):

- <4 cm mass: surgery to remove the main tumor mass and to sample the lymph nodes in the axilla. The stage of the tumor is ascertained after this first surgery. Adjuvant therapy (i.e., treatment after surgery) may include a combination of chemotherapy, radiotherapy, hormonal therapy (e.g., tamoxifen) and/or targeted therapy (e.g., trastuzumab). More surgery is occasionally needed to complete the removal of the initial tumor or to remove recurrences.

- 4 cm or larger mass: modified (a less aggressive form of radical mastectomy) radical mastectomy (because any malignant mass in excess of 4 cm in size exceeds the criteria for a lumpectomy) along with sampling of the lymph nodes in the axilla.

The treatment options offered to an individual patient are determined by the form, stage and location of the cancer, and also by the age, history of prior disease and general health of the patient. Not all patients are treated the same way.

Treatments of cancer in cats usually consists of diagnosis and observation of the tumor to determine its type and size, the development of a treatment plan, the associated goals on the part of the treatment methods, and the regular evaluation of the overall health of the pet.

The prevention of feline cancer mainly depends on the cat's diet and lifestyle, as well as an ability to detect early signs and symptoms of cancer prior to advancement to a further stage. If cancer is detected at an earlier stage, it has a higher chance of being treated, therefore lessening the chances of fatality. Taking domesticated cats for regular checkups to the veterinarian can help spot signs and symptoms of cancer early on and help maintain a healthy lifestyle. Further, due to advancements in research, prevention of certain types of feline illnesses remains possible. A widely known preventative of feline leukemia virus is the vaccine which was created in 1969. Subsequently, an immunofloures-cent antibody (IFA) test for the detection of FeLV in the blood of infected cats was formulated. The IFA test was mainly used to experiment the chances of felines being exposed to cancer. The results showed that 33% of cats who were exposed to FeLV related diseases were at a higher risk for acquiring it, while the cats that were left unexposed were left unaffected. FeLV is either spread through contagion or infection and once infected it is possible for cats to stay that way for the rest of their lives.

Interaction with other Cats

Interaction with other cats with strains or diseases related to FeLV can be a great risk factor for cats attaining FeLV themselves. Therefore, a main factor in prevention is keeping the affected cats in quarantine from the unaffected cats. Stray cats, or indoor/outdoor cats have been shown to be at a greater risk for acquiring FeLV, since they have a greater chance of interacting with other cats. Domesticated cats that are kept indoors are the least vulnerable to susceptible diseases.

Vaccines

Vaccines help the immune system fight off disease causing organisms, which is another key to prevention. However, vaccines can also cause tumors if not given properly. Vaccines should be given in the right rear leg to ease tumor removal process. Vaccines given in the neck or in between the shoulder blades are most likely to cause tumors and are difficult to remove, which can be fatal to cats. Reducing the number of vaccinations given to a cat may also decrease the risk for it developing a tumor.

Spaying and Neutering

Spaying and neutering holds many advantages to cats, including lowering the risk for developing cancer. Neutering male cats makes them less subjected to testicular cancer, FeLV, and FIV. Spaying female cats lowers the risk for mammary cancer, ovarian, or uterine cancer, as it prevents them from going into heat. Female cats should be spayed before their first heat, as each cycle of heat creates a greater risk for mammary cancer. Spaying a female cat requires the removal of the ovaries and uterus, which would eliminate their chances of developing cancer in these areas.

Exposure to Sun

The risk of skin cancer increases when a cat is exposed to direct sunlight for prolonged periods. White cats, or cats with white faces and ears, should not be allowed out on sunny days. Between the hours of 10:00 am to 4:00 pm, it is recommended to keep domesticated cats indoors, as the sun is at its highest peak between these times. Sun block is also available for cats, which can help prevent skin irritation, and a veterinarian should be contacted to find out which brands are appropriate and to use on cats.

Exposure to Secondhand Smoke

Cats living in a smoker’s household are three times more likely to develop lymphoma. Compared to living in a smoke-free environment, cats exposed to secondhand smoke also have a greater chance of developing squamous cell carcinoma or mouth cancer. Cancer is also developed mostly due to the cat's grooming habits. As cats lick themselves while they groom, they increase chances of taking in the toxic, cancer-causing carcinogens that gather on their fur, which are then exposed to their mucus membranes.

Lifestyle

Providing a cat with the healthiest lifestyle possible is the key to prevention. Decreasing the amount of toxins, including household cleaning products, providing fresh and whole foods, clean and purified water, and reducing the amount of indoor pollution can help cats live a longer and healthier life. To lessen susceptibility to diseases, domesticated cats should be kept inside the household for most of their lives to reduce the risk of interacting with other stray cats that could be infected with diseases.

Carcinoma "in situ" is, by definition, a localized phenomenon, with no potential for metastasis unless it progresses into cancer. Therefore, its removal eliminates the risk of subsequent progression into a life-threatening condition.

Some forms of CIS (e.g., colon polyps and polypoid tumours of the bladder) can be removed using an endoscope, without conventional surgical resection. Dysplasia of the uterine cervix is removed by excision (cutting it out) or by burning with a laser. Bowen's disease of the skin is removed by excision. Other forms require major surgery, the best known being intraductal carcinoma of the breast (also treated with radiotherapy). One of the most dangerous forms of CIS is the "pneumonic form" of BAC of the lung, which can require extensive surgical removal of large parts of the lung. When too large, it often cannot be completely removed, with eventual disease progression and death of the patient.

Some studies in Australia, Brazil and Germany pointed to alcohol-containing mouthwashes as also being potential causes. The claim was that constant exposure to these alcohol-containing rinses, even in the absence of smoking and drinking, leads to significant increases in the development of oral cancer. However, studies conducted in 1985, 1995, and 2003 summarize that alcohol-containing mouth rinses are not associated with oral cancer. In a March 2009 brief, the American Dental Association said "the available evidence does not support a connection between oral cancer and alcohol-containing mouthrinse". A 2008 study suggests that acetaldehyde (a breakdown product of alcohol) is implicated in oral cancer, but this study specifically focused on abusers of alcohol and made no reference to mouthwash. Any connection between oral cancer and mouthwash is tenuous without further investigation.

Invasive carcinoma of no special type (NST) also known as invasive ductal carcinoma or ductal NOS and previously known as invasive ductal carcinoma, not otherwise specified (NOS) is a group of breast cancers that do not have the "specific differentiating features". Those that have these features belong to other types.

In this group are: pleomorphic carcinoma, carcinoma with osteoclast-like stromal giant cells, carcinoma with choriocarcinomatous features, and carcinoma with melanotic features. It is a diagnosis of exclusion, which means that for the diagnosis to be made all the other specific types must be ruled out.

Familial and genetic factors are identified in 5-15% of childhood cancer cases. In <5-10% of cases, there are known environmental exposures and exogenous factors, such as prenatal exposure to tobacco, X-rays, or certain medications. For the remaining 75-90% of cases, however, the individual causes remain unknown. In most cases, as in carcinogenesis in general, the cancers are assumed to involve multiple risk factors and variables.

Aspects that make the risk factors of childhood cancer different from those seen in adult cancers include:

- Different, and sometimes unique, exposures to environmental hazards. Children must often rely on adults to protect them from toxic environmental agents.

- Immature physiological systems to clear or metabolize environmental substances

- The growth and development of children in phases known as "developmental windows" result in certain "critical windows of vulnerability".

Also, a longer life expectancy in children avails for a longer time to manifest cancer processes with long latency periods, increasing the risk of developing some cancer types later in life.

There are preventable causes of childhood malignancy, such as delivery overuse and misuse of ionizing radiation through computed tomography scans when the test is not indicated or when adult protocols are used.

The probability of xerostomia at one year increases by 5% for every 1Gy increase in dose to the parotid gland. Doses above 25–30 Gy are associated with moderate to severe xerostomia. Similar considerations apply to the submandibular gland, but xerostomia is less common if only one parotid gland is included in the radiated field and the contralateral submandibular gland is spared (less than 39 Gy) In the same manner, radiation dose to the pharyngeal constrictor muscles, larynx, and cricopharyngeal inlet determine the risk of dysphagia (and hence dependence on gastrostomy tube feeds). The threshold for this toxicity is volume-dependent at 55–60 Gy, with moderate to severe impairment of swallowing, including aspiration, stricture and feeding tube dependence above a mean dose of 47 Gy, with a recommended dose to the inferior constrictor of less than 41 Gy. Dose-toxicity relationships for the superior and middle constrictors are steep, with a 20% increase in the probability of dysphagia for each 10 Gy. For late dysphagia, threshold mean total constrictor doses, to limit rates of greater than or equal to grade 2 and 3 below 5% were 58 and 61 Gy respectively. For grade 2 dysphagia, the rate increased by 3.4% per Gy. Doses above 30 Gy to the thyroid are associated with moderate to severe hypothyroidism. Subjective, patient-reported outcomes of quality of life also correlate with radiation dose received.

Altered fractionation schemes, such as RTOG 9003 and RTOG 0129 have not conferred additional benefit. Radiation dose recommendations were largely determined empirically in clinical studies with few HPV+OPC patients, and have remained unchanged for half a century, making it difficult to determine the optimum dose for this subgroup. A common approach uses 70 Gy bilaterally and anteriorly, such as RTOG 9003 (1991–1997) and RTOG 0129 (2002–2005). For lateralized tonsil cancer unilateral neck radiation is usually prescribed, but for tongue base primaries bilateral neck radiation is more common, but unilateral radiation may be used where tongue base lesions are lateralised.

Children with cancer are at risk for developing various cognitive or learning problems. These difficulties may be related to brain injury stemming from the cancer itself, such as a brain tumor or central nervous system metastasis or from side effects of cancer treatments such as chemotherapy and radiation therapy. Studies have shown that chemo and radiation therapies may damage brain white matter and disrupt brain activity.

The risk factors that can increase the risk of developing oropharyngeal cancer are:

- Smoking and chewing tobacco

- Heavy alcohol use

- A diet low in fruits and vegetables

- Chewing betel quid, a stimulant commonly used in parts of Asia

- Mucosal infection with human papilloma virus (HPV) (HPV-mediated oropharyngeal cancer)

- HPV infection

- Plummer-Vinson syndrome

- Poor nutrition

- Asbestos exposure

Certain genetic changes including: P53 mutation and CDKN2A (p16) mutations.

High-risk lesions:

- Erythroplakia

- Speckled erythroplakia

- Chronic hyperplastic candidiasis

Medium-risk lesions:

- Oral submucosal fibrosis

- Syphilitic glossitis

- Sideropenic dysphagia (or Paterson-Kelly-Brown syndrome)

Low-risk lesions:

- Oral lichen planus

- Discoid lupus erythematosus

- Discoid keratosis congenita

Cancer prevalence in dogs increases with age and certain breeds are more susceptible to specific kinds of cancers. Millions of dogs develop spontaneous tumors each year. Boxers, Boston Terriers and Golden Retrievers are among the breeds that most commonly develop mast cell tumors. Large and giant breeds, like Great Danes, Rottweilers, Greyhound and Saint Bernards, are much more likely to develop bone cancer than smaller breeds. Lymphoma occurs at increased rates in Bernese Mountain dogs, bulldogs, and boxers. It is important for the owner to be familiar with the diseases to which their specific breed of dog might have a breed predisposition.

Infection with human papillomavirus (HPV), particularly type 16 (there are over 180 types), is a known risk factor and independent causative factor for oral cancer. A fast-growing segment of those diagnosed does not present with the historic stereotypical demographics. Historically that has been people over 50, blacks over whites 2 to 1, males over females 3 to 1, and 75% of the time people who have used tobacco products or are heavy users of alcohol. This new and rapidly growing sub population between 30 and 50 years old, is predominantly nonsmoking, white, and males slightly outnumber females. Recent research from multiple peer-reviewed journal articles indicates that HPV16 is the primary risk factor in this new population of oral cancer victims. HPV16 (along with HPV18) is the same virus responsible for the vast majority of all cervical cancers and is the most common sexually transmitted infection in the US. Oral cancer in this group tends to favor the tonsil and tonsillar pillars, base of the tongue, and the oropharynx. Recent data suggest that individuals that come to the disease from this particular cause have a significant survival advantage, as the disease responds better to radiation treatments than tobacco caused disease.

Cancer prevention is defined as active measures to decrease cancer risk. The vast majority of cancer cases are due to environmental risk factors. Many of these environmental factors are controllable lifestyle choices. Thus, cancer is generally preventable. Between 70% and 90% of common cancers are due to environmental factors and therefore potentially preventable.

Greater than 30% of cancer deaths could be prevented by avoiding risk factors including: tobacco, excess weight/obesity, poor diet, physical inactivity, alcohol, sexually transmitted infections and air pollution. Not all environmental causes are controllable, such as naturally occurring background radiation and cancers caused through hereditary genetic disorders and thus are not preventable via personal behavior.