For symptomatic relief of carcinoid syndrome:

- Octreotide (a somatostatin analogue which decreases the secretion of serotonin by the tumor and, secondarily, decreases the breakdown product of serotonin (5-HIAA))

- Telotristat ethyl (Xermelo) along with a somatostatin analogue in patients not responding to somatostatin analogue monotherapy. It is a tryptophan hydroxylase inhibitor and reduces the production of serotonin.

- Peptide receptor radionuclide therapy (PRRT) with lutetium-177, yttrium-90 or indium-111 labeled to octreotate is highly effective

- Methysergide maleate (antiserotonin agent but not used because of the serious side effect of retroperitoneal fibrosis)

- Cyproheptadine (an antihistamine drug with antiserotonergic effects)

Alternative treatment for qualifying candidates:

- Surgical resection of tumor and chemotherapy (5-FU and doxorubicin)

- Endovascular, chemoembolization, targeted chemotherapy directly delivered to the liver through special catheters mixed with embolic beads (particles that block blood vessels), used for patients with liver metastases.

The only treatment for MWS is only symptomatic, with multidisciplinary management

Surgery remains the front-line therapy for HNPCC. There is an ongoing controversy over the benefit of 5-fluorouracil-based adjuvant therapies for HNPCC-related colorectal tumours, particularly those in stages I and II.

Disease progression is difficult to ascertain because the disease can metastasize anywhere in the body and can be too small to identify with any current technology. Markers of the condition such as chromogranin-A are imperfect indicators of disease progression.

The first goal of treatment is to correct dehydration. Fluids are often given through a vein (intravenous fluids) to replace fluids lost in diarrhea.

The next goal is to slow the diarrhea. Some medications can help control diarrhea. Octreotide, which is a human-made form of the natural hormone somatostatin, blocks the action of VIP.

The best chance for a cure is surgery to remove the tumor. If the tumor has not spread to other organs, surgery can often cure the condition.

For metastatic disease, peptide receptor radionuclide therapy (PRRT) can be highly effective. This treatment involves attaching a radionuclide (Lutetium-177 or Yttrium-90) to a somatostatin analogue (octreotate or octreotide). This is a novel way to deliver high doses of beta radiation to kill tumours.

Some people seem to respond to a combination chemo called capecitabine and temozolomide but there is no report that it totally cured people from vipoma.

Treatment for FAP depends on the genotype. Most individuals with the APC mutation will develop colon cancer by the age of 40, although the less-common attenuated version typically manifests later in life (40–70). Accordingly, in many cases, prophylactic surgery may be recommended before the age of 25, or upon detection if actively monitored. There are several surgical options that involve the removal of either the colon or both the colon and rectum.

- Rectum involved: the rectum and part or all of the colon are removed. The patient may require an ileostomy (permanent stoma where stool goes into a bag on the abdomen) or have an ileo-anal pouch reconstruction. The decision to remove the rectum depends on the number of polyps in the rectum as well as the family history. If the rectum has few polyps, the colon is partly or fully removed and the small bowel (ileum) can be directly connected to the rectum instead (ileorectal anastomosis).

- Rectum not involved: the portion of the colon manifesting polyps can be removed and the ends 'rejoined' (partial colectomy), a surgery that has a substantial healing time, but leaves quality of life largely intact.

Prophylactic colectomy is indicated if more than a hundred polyps are present, if there are severely dysplastic polyps, or if multiple polyps larger than 1 cm are present.

Treatment for the two milder forms of FAP may be substantially different from the more usual variant, as the number of polyps are far fewer, allowing more options.

Various medications are being investigated for slowing malignant degeneration of polyps, most prominently the non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDS have been shown to significantly decrease the number of polyps but do not usually alter management since there are still too many polyps to be followed and treated endoscopically.

Surgery, if feasible, is the only curative therapy. If the tumor has metastasized (most commonly, to the liver) and is considered incurable, there are some promising treatment modalities, such as radiolabeled octreotide (e.g. Lutetium (Lu) DOTA-octreotate) or the radiopharmaceutical 131I-mIBG (meta iodo benzyl guanidine) for arresting the growth of the tumors and prolonging survival in patients with liver metastases, though these are currently experimental.

Chemotherapy is of little benefit and is generally not indicated. Octreotide or Lanreotide (somatostatin analogues) may decrease the secretory activity of the carcinoid, and may also have an anti-proliferative effect. Interferon treatment is also effective, and usually combined with somatostatin analogues.

As the metastatic potential of a coincidental carcinoid is probably low, the current recommendation is for follow up in 3 months with CT or MRI, labs for tumor markers such as serotonin, and a history and physical, with annual physicals thereafter.

Prior to reaching the advanced stages of colorectal cancer, the polyps are confined to the inner wall and thickness of the intestinal tract and do not metastasize or 'spread'. So provided FAP is detected and controlled either at the pre-cancerous stage or when any cancerous polyps are still internal to the intestinal tract, surgery has a very high success rate of preventing or removing cancer, without recurrence, since the locations giving rise to cancer are physically removed "in toto" by the surgery.

Following surgery, if a partial colectomy has been performed, colonoscopic surveillance of the remaining colon is necessary as the individual still has a risk of developing colon cancer. However, if this happened, it would be a fresh incident from polyps developing anew in the unremoved part of the colon subsequent to surgery, rather than a return or metastasis of any cancer removed by the original surgery.

SMA syndrome can present in acute, acquired form (e.g. abruptly emerging within an inpatient stay following scoliosis surgery) as well as chronic form (i.e. developing throughout the course of a lifetime and advancing due to environmental triggers, life changes, or other illnesses). According to a number of recent sources, at least 70% of cases can typically be treated with medical treatment, while the rest require surgical treatment.

Medical treatment is attempted first in many cases. In some cases, emergency surgery is necessary upon presentation. A six-week trial of medical treatment is recommended in pediatric cases. The goal of medical treatment for SMA Syndrome is resolution of underlying conditions and weight gain. Medical treatment may involve nasogastric tube placement for duodenal and gastric decompression, mobilization into the prone or left lateral decubitus position, the reversal or removal of the precipitating factor with proper nutrition and replacement of fluid and electrolytes, either by surgically inserted jejunal feeding tube, nasogastric intubation, or peripherally inserted central catheter (PICC line) administering total parenteral nutrition (TPN). Pro-motility agents such as metoclopramide may also be beneficial. Symptoms may improve after restoration of weight, except when reversed peristalsis persists, or if regained fat refuses to accumulate within the mesenteric angle. Most patients seem to benefit from nutritional support with hyperalimentation irrespective of disease history.

If medical treatment fails, or is not feasible due to severe illness, surgical intervention is required. The most common operation for SMA syndrome, duodenojejunostomy, was first proposed in 1907 by Bloodgood. Performed as either an open surgery or laparoscopically, duodenojejunostomy involves the creation of an anastomosis between the duodenum and the jejunum, bypassing the compression caused by the AA and the SMA. Less common surgical treatments for SMA syndrome include Roux-en-Y duodenojejunostomy, gastrojejunostomy, anterior transposition of the third portion of the duodenum, intestinal derotation, division of the ligament of Treitz (Strong's operation), and transposition of the SMA. Both transposition of the SMA and lysis of the duodenal suspensory muscle have the advantage that they do not involve the creation of an intestinal anastomosis.

The possible persistence of symptoms after surgical bypass can be traced to the remaining prominence of reversed peristalsis in contrast to direct peristalsis, although the precipitating factor (the duodenal compression) has been bypassed or relieved. Reversed peristalsis has been shown to respond to duodenal circular drainage—a complex and invasive open surgical procedure originally implemented and performed in China.

In some cases, SMA Syndrome may occur alongside a serious, life-threatening condition such as cancer or AIDS. Even in these cases, though, treatment of the SMA Syndrome can lead to a reduction in symptoms and an increased quality of life.

Surgery can usually cure VIPomas. However, in one-third to one-half of patients, the tumor has spread by the time of diagnosis and cannot be cured.

Corticosteroids are the mainstay of therapy with a 90% response rate in some studies. Appropriate duration of steroid treatment is unknown and relapse often necessitates long term treatment. Various steroid sparing agents e.g. sodium cromoglycate (a stabilizer of mast cell membranes), ketotifen (an antihistamine), and montelukast (a selective, competitive leukotriene receptor antagonist) have been proposed, centering on an allergic hypothesis, with mixed results. An elimination diet may be successful if a limited number of food allergies are identified.

Treatment options include:

1. Therapies to eliminate the underlying cancer, such as chemotherapy, radiation and surgery.

2. Therapies to reduce or slow neurological degeneration. In this scenario, rapid diagnosis and treatment are critical for the patient to have the best chance of recovery. Since these disorders are relatively rare, few doctors have seen or treated paraneoplastic neurological disorders (PNDs). Therefore, PND patients should consult with a specialist with experience in diagnosing and treating paraneoplastic neurological disorders.

A specific prognosis for those afflicted with paraneoplastic syndromes links to each unique case presented. Thus, prognosis for paraneoplastic syndromes may vary greatly. For example, paraneoplastic pemphigus often included infection as a major cause of death. Paraneoplastic pemphigus is one of the three major subtypes that affects IgG autoantibodies that are characteristically raised against desmoglein 1 and desmoglein 3 (which are cell-cell adhesion molecules found in desmosomes). Underlying cancer or irreversible system impairment, seen in acute heart failure or kidney failure, may result in death as well.

The main treatment modalities are surgery, embolization and radiotherapy.

Even if the tumor has advanced and metastasized, making curative surgery infeasible, surgery often has a role in neuroendocrine cancers for palliation of symptoms and possibly increased lifespan.

Cholecystectomy is recommended if there is a consideration of long-term treatment with somatostatin analogs.

In secretory tumors, somatostatin analogs given subcutaneously or intramuscularly alleviate symptoms by blocking hormone release. A consensus review has reported on the use of somatostatin analogs for GEP-NETs.

These medications may also anatomically stabilize or shrink tumors, as suggested by the PROMID study (Placebo-controlled prospective randomized study on the antiproliferative efficacy of Octreotide LAR in patients with metastatic neuroendocrine MIDgut tumors): at least in this subset of NETs, average tumor stabilization was 14.3 months compared to 6 months for placebo.

The CLARINET study (a randomized, double-blind, placebo-controlled study on the antiproliferative effects of lanreotide in patients with enteropancreatic neuroendocrine tumors) further demonstrated the antiproliferative potential of lanreotide, a somatostatin analog and recently approved FDA treatment for GEP-NETS. In this study, lanreotide showed a statistically significant improvement in progression-free survival, meeting its primary endpoint. The disease in sixty five percent of patients treated with lanreotide in the study had not progressed or caused death at 96 weeks, the same was true of 33% of patients on placebo. This represented a 53% reduction in risk of disease progression or death with lanreotide based on a hazard ratio of .47.

Lanreotide is the first and only FDA approved antitumor therapy demonstrating a statistically significant progression-free survival benefit in a combined population of patients with GEP-NETS.

Other medications that block particular secretory effects can sometimes relieve symptoms.

Clinical trials of protein kinase inhibitors, which block the abnormal kinase proteins involved in the development and growth of medullary cancer cells, showed clear evidence of response in 10-30% of patients. In the majority of responders there has been less than a 30% decrease in tumor mass, yet the responses have been durable; responses have been stable for periods exceeding 3 years. The major side effects of this class of drug include hypertension, nausea, diarrhea, some cardiac electrical abnormalities, and thrombotic or bleeding episodes.

Vandetanib, trade name Caprelsa, was the first drug (April 2011) to be approved by US Food and Drug Administration (FDA) for treatment of late-stage (metastatic) medullary thyroid cancer in adult patients who are ineligible for surgery.

Cabozantinib, trade name Cometriq, was granted marketing approval (November 2012) by the U.S. FDA for this indication. Cabozantinib which is a potent inhibitor of RET, MET and VEGF was evaluated in a double-blind placebo controlled trial. It was shown to improve overall survival by 5 months for the treated cohort vs. placebo, which was not statistically significant. However, cabozantinib was particularly effective in patients with the RET M918T mutation, extending overall survival by roughly 2 years, doubling survival vs. untreated patient (4 years vs. 2 year). Treatment with cabozantinib did require many dose reduction to mitigate side effects. It has been suggested that the trial dose of 140 mg was excessive, particularly in lower body mass patients. Ongoing trials have been scheduled to identify more optimal dosing regimes. Activity has been observed, in practice at doeses of 1.2 mg/kg.

There have been 30 cases of Marden-Walker Syndrome reported since 1966. The first case of this was in 1966 a female infant was diagnosed with blepharophimosis, joint contractures, arachnodactyly and growth development delay. She ended up passing at 3 months due to pneumonia.

In general, treatment for PanNET encompasses the same array of options as other neuroendocrine tumors, as discussed in that main article. However, there are some specific differences, which are discussed here.

In functioning PanNETs, octreotide is usually recommended prior to biopsy or surgery but is generally avoided in insulinomas to avoid profound hypoglycemia.

PanNETs in MEN1 are often multiple, and thus require different treatment and surveillance strategies.

Some PanNETs are more responsive to chemotherapy than are gastroenteric carcinoid tumors. Several agents have shown activity. In well differentiated PanNETs, chemotherapy is generally reserved for when there are no other treatment options. Combinations of several medicines have been used, such as doxorubicin with streptozocin and fluorouracil (5-FU) and capecitabine with temozolomide. Although marginally effective in well-differentiated PETs, cisplatin with etoposide has some activity in poorly differentiated neuroendocrine cancers (PDNECs), particularly if the PDNEC has an extremely high Ki-67 score of over 50%.

Several targeted therapy agents have been approved in PanNETs by the FDA based on improved progression-free survival (PFS):

- everolimus (Afinitor) is labeled for treatment of progressive neuroendocrine tumors of pancreatic origin in patients with unresectable, locally advanced or metastatic disease. The safety and effectiveness of everolimus in carcinoid tumors have not been established.

- sunitinib (Sutent) is labeled for treatment of progressive, well-differentiated pancreatic neuroendocrine tumors in patients with unresectable locally advanced or metastatic disease. Sutent also has approval from the European Commission for the treatment of 'unresectable or metastatic, well-differentiated pancreatic neuroendocrine tumors with disease progression in adults'. A phase III study of sunitinib treatment in well differentiated pNET that had worsened within the past 12 months (either advanced or metastatic disease) showed that sunitinib treatment improved progression-free survival (11.4 months vs. 5.5 months), overall survival, and the objective response rate (9.3% vs. 0.0%) when compared with placebo.

External beam radiotherapy is recommended when there is a high risk of regional recurrence, even after optimum surgical treatment. In this study, patients treated with external beam radiation were compared to a control group. Disease control with radiation was far superior in the group receiving radiation. The authors of the study [14] wrote: "in 40 high risk patients (microscopic residual disease, extraglandular invasion, or lymph node involvement), the local/regional relapse free rate was 86% at 10 years with postoperative external beam radiation (25 patients), and 52% for those with no postoperative external radiation (p = 0.049). To optimize local/regional tumor control, we therefore continue to advise external beam radiation in patients at high risk of local/regional relapse."

Unlike other differentiated thyroid carcinoma, there is no role for radioiodine treatment in medullary-type disease.

Feingold syndrome (also called oculodigitoesophagoduodenal syndrome) is a rare autosomal dominant hereditary disorder. It is named after Murray Feingold, an American physician who first described the syndrome in 1975. Until 2003, at least 79 patients have been reported worldwide.

Feingold syndrome is marked by various combinations of microcephaly, limb malformations, esophageal and duodenal atresias, and sometimes learning disability or mental retardation.

Treating PPB depends on the size and location of the tumor, whether the cancer has spread, and the child's overall health. Surgery is the main treatment for PPB. The main goal of surgery is to remove the tumor. If the tumor is too large to be completely removed, or if it's not possible to completely remove the tumor, surgery may be performed after chemotherapy. Because PPB can return after treatment, regular screening for possible recurrence should continue for 48 to 60 months, after diagnosis.

Because of its extreme rarity, there have been no controlled clinical trials of treatment regimens for FA and, as a result, there are no evidence-based treatment guidelines. Complete surgical resection is the treatment of choice in FA, as it is in nearly all forms of lung cancer.

Anecdotal reports suggest that FA is rarely highly sensitive to cytotoxic drugs or radiation. Case reports suggest that chemotherapy with UFT may be useful in FA.

Prostate cancer is the second most common urological malignancy to be associated with paraneoplastic syndromes after renal cell carcinoma. Paraneoplastic syndromes of this nature tend to occur in the setting of late stage and aggressive tumors with poor overall outcomes (endocrine manifestations, neurological entities, dermatological conditions, and other syndromes). A vast majority of prostate cancer cases (over 70%) document paraneoplastic syndrome as a major clinical manifestation of prostate cancer; and interestingly (under 20%), the syndrome as an initial sign of disease progression to the castrate-resistant state. Urologist researchers identify serum markers that are associated with the syndrome in order to specific what type of therapies may work most effectively.

Paraneoplastic neurological syndromes may be related immune checkpoint inhibitors (ICIs), one of the underlying causes in inflammatory central nervous system diseases (CNS). The central idea around such research pinpoints treatment strategies to combat cancer related outcomes in the clinical arena, specifically ICIs. Research suggests that patients who are treated with ICIs are more susceptible to CNS disease (since the mechanism of ICIs induces adverse effects on the CNS due to augmented immune responses and neurotoxicity). The purpose of this exploration was to shed light on immunotherapies and distinguishing between neurotoxicity and brain metastasis in the early stages of treatment. In other research, scientists have found that paraneoplastic peripheral nerve disorders (autoantibodies linked to multifocal motor neuropathy) may provide important clinical manifestations. This is especially important for patients who experience inflammatory neuropathies since solid tumors are often associated with peripheral nerve disorders. CV2 autoantibodies, which target dihydropyriminase-related protein 5 (DRP5, or CRMP5) are also associated with a variety of paraneoplastic neurological syndromes, including sensorimotor polyneuropathies. Interestingly, patients undergoing immune therapies or tumor removal respond very well to antibodies that target CASPR2 (to treat nerve hyperexcitability and neuromyotonia).

In the case of paraneoplastic Cushing's syndrome arising from a small cel carcinoma of the endometrium, paraneoplastic syndrome has been seen to interfere with standard treatments and lead to unexpected complications and clinical course. The purpose of this clinical case demonstrates the aggressive nature of the neuroendocrine small cell carcinoma with rapid invasion and extra-uterine spread. The researchers raise recognition for timely recognition of paraneoplastic syndrome, which in this particular case use a combinatorial therapy of etoposide and cisplatin chemotherapy to save the 32-year old female patient's life (presented with persistent migraine-like headache, palpitations, progressive nausea and vomiting, photo- and sonobia, menometrorrhagia and concomitant general fatigue).

treatment to be directed towards the findings in investigation if it is found to be AMAG immunosupressive drugs and chemotherapy with antineoplastic drugs.

In case of confirmed malignancy of stomach complete or step ladder or stage ladder resection of gastric or stomach to be done.