Complications
Arrhythmias
Pulmonary edema
Peripheral emboli
Spread (metastasis) of the tumor
Blockage of the mitral heart valve
Stroke
Fusiform cerebral aneurysms

Causes
Myxomata are the most common type of adult primary heart tumor. Most myxomata arise sporadically (90%), and only about 10% are thought to arise due to inheritance.About 10% of myxomata are inherited, as in Carney syndrome. Such tumors are called familial myxomata. They tend to occur in more than one part of the heart at a time, and often cause symptoms at a younger age than other myxomata. Other abnormalities are observed in people with Carney syndrome include skin myxomata, pigmentation, endocrine hyperactivity, schwannomas and epithelioid blue nevi. Myxomata are more common in women than men. Diagnosis
A doctor will listen to the heart with a stethoscope. A "tumor plop" (a sound related to movement of the tumor), abnormal heart sounds, or a murmur similar to the mid-diastolic rumble of mitral stenosis may be heard. These sounds may change when the patient changes position.Right atrial myxomata rarely produce symptoms until they have grown to be at least 13 cm (about 5 inches) wide.Tests may include:
Echocardiogram and Doppler study
Chest x-ray
CT scan of chest
Heart MRI
Left heart angiography
Right heart angiography
ECG—may show atrial fibrillationBlood tests:

Blood tests: An FBC may show anemia and increased WBCs (white blood cells). The erythrocyte sedimentation rate (ESR) is usually increased. Blood tests: An FBC may show anemia and increased WBCs (white blood cells). The erythrocyte sedimentation rate (ESR) is usually increased. Treatment
The surgery is treatment of choice, tumor must be surgically removed. Some patients will also need their mitral valve replaced.
These activating factors are known to be important for malignant transformation and progression. mTOR is particularly important in the biology of renal cancer (RCC) owing to its function in regulating HIF-1a levels. Mutation or loss of the von Hippel Lindau tumor-suppressor gene is common in RCC and is manifested by reduced degradation of HIF-1a. In RCC tumors, activated mTOR further exacerbates accumulation of HIF-1a by increasing synthesis of this transcription factor and its angiogenic target gene products. Efficacy
In an international three-arm phase III study with 626 previously untreated, poor-prognosis patients, temsirolimus, interferon-α and the combination of both agents was compared. Median overall survival improved significantly in the temsirolimus group (10.9 months) compared with interferon-α group (7.3 months) and the combination group (8.4 months). Further studies are needed to determine the role of temsirolimus in the first-line treatment of patients with a more favorable prognosis, how it can be combined with other targeted agents and as sequential therapy with sunitinib or sorafenib. Adverse reactions
The toxicity profile is based on what was found in the phase III trial. adverse reaction
fatigue
skin rash
mucositis
hematologic abnormalities
hemoglobin decreased
lymphocytes decreased
laboratory abnormalities
triglycerides increased
glucose increased
phosphorus decreasedTemsirolimus has been generally well tolerated in clinical settings by patients with advanced RCC. In patients with RCC, the adverse effect profile of temsirolimus is primarily metabolic in nature, with minimal impact on QoL compared with the commonly seen side-effects with oral multikinase inhibitors. Temsirolimus high level of specificity for mTOR likely contributes to the tolerability of temsirolimus. However, temsirolimus increases mortality in cancer patients.