Adrenocortical Carcinoma
Mitotane
Adrenocortical Adenoma
Adrenal Cortex
Carcinoma
Cushing Syndrome
Adrenocorticotropic Hormone
Hydrocortisone
Myelolipoma
Adrenal Glands
Adrenal Rest Tumor
Steroid 17-alpha-Hydroxylase
Carcinoma, Squamous Cell
Carcinoma, Hepatocellular
Feminization
Adrenocortical Hyperfunction
17-alpha-Hydroxyprogesterone
Li-Fraumeni Syndrome
Immunohistochemistry
Aldosterone
Steroidogenic Factor 1
Tumor Markers, Biological
Aromatase
Carcinoma in Situ
Dehydroepiandrosterone
Steroids
Tomography, X-Ray Computed
Prognosis
Incidental Findings
Carcinoma, Papillary
Tumor Cells, Cultured
Antineoplastic Agents, Hormonal
Neoplasm Staging
RNA, Messenger
Inhibins
Gene Expression Regulation, Neoplastic
Treatment Outcome
Fatal Outcome
YM116, 2-(1H-imidazol-4-ylmethyl)-9H-carbazole, decreases adrenal androgen synthesis by inhibiting C17-20 lyase activity in NCI-H295 human adrenocortical carcinoma cells. (1/185)
The concentrations of androstenedione and dehydroepiandrosterone, products of C17-20 lyase, in the medium after a 6-hr incubation of NCI-H295 cells were decreased by YM116 (2-(1H-imidazol-4-ylmethyl)-9H-carbazole) (IC50: 3.6 and 2.1 nM) and ketoconazole (IC50: 54.9 and 54.2 nM). 17Alpha-hydroxyprogesterone, a product of 17alpha-hydroxylase, was increased by YM116 (1-30 nM) and by ketoconazole (10-300 nM) and then was decreased at higher concentrations of both agents (IC50: 180 nM for YM116, 906 nM for ketoconazole), indicating that YM116 and ketoconazole were 50- and 16.5-fold more specific inhibitors of C17-20 lyase, respectively, than 17alpha-hydroxylase. Compatible with these findings, progesterone, a substrate of 17alpha-hydroxylase, was increased by these agents. Cortisol production was inhibited by YM116 and ketoconazole (IC50: 50.4 and 80.9 nM, respectively). YM116 was a 14-fold more potent inhibitor of androstenedione production than cortisol production, whereas ketoconazole was a nonselective inhibitor of the production of both steroids. YM116 and ketoconazole inhibited the C17-20 lyase activity in human testicular microsomes (IC50: 4.2 and 17 nM, respectively). These results demonstrate that YM116 reduces the synthesis of adrenal androgens by preferentially inhibiting C17-20 lyase activity. (+info)Comparison of expression and regulation of the high-density lipoprotein receptor SR-BI and the low-density lipoprotein receptor in human adrenocortical carcinoma NCI-H295 cells. (2/185)
In rodents, cholesterol for adrenal steroidogenesis is derived mainly from high-density lipoproteins (HDL) via the HDL receptor, scavenger receptor-BI (SR-BI). In humans cholesterol for steroidogenesis is considered to be derived from the low-density lipoprotein (LDL) receptor pathway, and the contribution of SR-BI to that is unknown. In the present study SR-BI expression and regulation by steroidogenic stimuli was analysed in human adrenocortical cells and compared with LDL receptor expression. In addition, the functional contribution of both receptors for cholesteryl ester delivery to human adrenocortical cells was compared. Northern blot and reverse transcription-PCR amplification and sequence analysis demonstrated the presence of SR-BI mRNA in foetal and adult human adrenal cortex. Furthermore, SR-BI mRNA was expressed to similar levels in human primary adrenocortical and adrenocortical carcinoma NCI-H295 cells, indicating its presence in the steroid-producing cells. Treatment of NCI-H295 cells with 8Br-cAMP, a stimulator of glucocorticoid synthesis via the protein kinase A second messenger signal transduction pathway, resulted in an increase of both SR-BI and LDL receptor mRNA levels in a time- and dose-dependent manner. The induction of SR-BI and LDL receptor by cAMP was independent of ongoing protein synthesis and occurred at the transcriptional level. Ligand blot experiments indicated that a protein of similar size to SR-BI is the major HDL-binding protein in NCI-H295 cells. Western blot analysis demonstrated that cAMP treatment increased the levels of LDL receptor and, to a lesser extent, SR-BI protein in NCI-H295 cells. Binding and uptake of cholesterol was quantitatively smaller from HDL than from LDL, both in basal as well as in cAMP-stimulated cells. Scatchard analysis under basal conditions indicated that NCI-H295 cells express twice as many specific binding sites for LDL than for HDL. Dissociation constant values (Kd; in nm) were approximately five times higher for HDL than for LDL, indicating a lower affinity of HDL compared with LDL. The combined effects of these two parameters and the low cholesteryl ester content of HDL subfraction 3 (HDL3) contributes to a lower cholesteryl ester uptake from HDL than from LDL by the NCI-H295 cells. In conclusion, both the SR-BI and LDL receptor genes are expressed in the human adrenal cortex and coordinately regulated by activators of glucocorticoid synthesis. In contrast to rodents, in human adrenocortical cells the HDL pathway of cholesterol delivery appears to be of lesser importance than the LDL pathway. Nevertheless, the SR-BI pathway may become of major importance in conditions of functional defects in the LDL receptor pathway. (+info)The expression of inhibin/activin subunits in the human adrenal cortex and its tumours. (3/185)
Inhibins and activins are dimeric proteins of the transforming growth factor-beta superfamily which have been shown to be expressed in the adrenal cortex. Recent studies have suggested a role for these peptides in the pathogenesis and/or function of adrenal tumours. To investigate further their physiological and pathological roles, we have documented immunoreactivity for inhibin alpha, betaA and betaB subunits in normal adult and fetal human adrenals, in hyperplastic adrenals and in adrenal tumours. In the normal and hyperplastic adult gland, diffuse immunopositivity was demonstrated for beta subunits, suggesting that activins (beta beta dimers) can be expressed in all zones. Inhibin alpha was limited to the zona reticularis and the innermost zona fasciculata in the normal gland, extending centripetally into the zona fasciculata in hyperplasia, supporting a role for ACTH in the regulation of expression, and suggesting that expression of inhibins (alpha beta dimers) is restricted. Immunopositivity for all three subunits was seen in both fetal and definitive zones of the fetal cortex, indicating that both inhibins and activins could be expressed in both. Immunopositivity for all three subunits was seen in most adrenocortical tumours. Loss of immunopositivity for inhibin alpha in a subgroup of carcinomas might indicate a role in tumour progression. The greater intensity of staining for inhibin alpha in tumours associated with Cushing's syndrome again suggests a link with cortisol production. (+info)Autocrine role of IGF-II in proliferation of human adrenocortical carcinoma NCI H295R cell line. (4/185)
In adrenocortical tumors, the malignant phenotype is associated with rearrangements (paternal isodisomy) at the 11p15 locus and IGF-II gene overexpression, strongly suggesting that the IGF system is a major determinant of adrenocortical tumor progression. The aim of this study was to validate an in vitro model for investigating the involvement of the IGF system in adrenocortical tumorigenesis. We analyzed the production of IGF mRNA and proteins, IGF-binding proteins (IGFBPs) and IGF receptors by the NCI H295R cell line, which is derived from a human adult adrenocortical carcinoma. H295R cells were shown to proliferate for a long period (26 days) in the absence of serum or any added growth factor. Northern blot analyses showed high IGF-II mRNA contents in H295R cells. The cells secreted large amounts of IGF-II protein (14 ng/10(6) cells per 48 h) although no IGF-I protein was detected. Western ligand blot analyses of conditioned media detected the presence of large amounts of a 34 kDa protein, which was identified as IGFBP-2 by immunoblotting. The presence of high-affinity binding sites for IGF-I and IGF-II on H295R cells was shown by binding experiments using radiolabeled IGFs and confirmed by reverse transcription PCR analyses showing type 1 and type 2 IGF receptors. Proliferation of H295R cells was inhibited by anti-IGF-II antibody (45%) and by anti-type 1 IGF receptor antibody (53%) indicating that IGF-II is an autocrine growth factor for these cells and that its effects are, at least in part, mediated by the type 1 IGF receptor. These findings confirm the involvement of the IGF system in adrenocortical tumors and suggest that the H295R cell line is a suitable in vitro model for studying the molecular mechanisms of adrenocortical tumor proliferation. (+info)Lack of response to octreotide in Cushing's syndrome due to metastatic adrenocortical carcinoma. (5/185)
Functional metastatic adrenocortical carcinoma is an uncommon cause of Cushing's syndrome, which rarely responds to conventional treatment. A patient presenting with Cushing's syndrome secondary to adrenocortical carcinoma underwent surgical resection. Postoperatively, she developed metastatic disease resistant to conventional chemotherapy. Octreotide, a somatostatin analogue which is effective in the treatment of several types of neuroendocrine tumour, was tried to ameliorate her secretory symptoms, but without any therapeutic effect. (+info)Analysis of genomic alterations in sporadic adrenocortical lesions. Gain of chromosome 17 is an early event in adrenocortical tumorigenesis. (6/185)
Genetic changes underlying the tumorigenesis of sporadic adrenocortical tumors are poorly characterized. To search for characteristic genomic imbalances involved in adrenocortical tumors, we examined 41 adrenocortical lesions (12 carcinomas, 23 adenomas, and 6 hyperplasias) by comparative genomic hybridization. Our results show that genetic alterations are more frequent in malignant than in benign lesions and that they rarely occur in hyperplastic lesions. The most frequent DNA copy number changes in adrenocortical carcinomas included losses of 1p21-31, 2q, 3p, 3q, 6q, 9p, and 11q14-qter, as well as gains and amplifications of 5q12, 9q32-qter, 12q, and 20q. The genomic aberrations prevalently occurring in adrenocortical adenomas were gains of 17q, 17p, and 9q32-qter. Gains found in 2 of 6 adrenocortical hyperplastic lesions involved chromosome 17 or 17q only. These data indicate that oncogenes determining the early tumorigenesis of adrenocortical tumors may exist on chromosome 17 and that the number of genomic alterations is closely associated with tumor behavior in adrenocortical tumors. (+info)Changes in neoplastic cell features and sensitivity to mitotane during mitotane-induced remission in a patient with recurrent, metastatic adrenocortical carcinoma. (7/185)
A 58-year-old man had adrenocortical carcinoma in the right adrenal gland. The tumour secreted excessive cortisol and dehydroepiandrosterone-sulphate (DHEA-S), and had invaded the right hepatic lobe and vena cava. Eleven months after surgical tumour resection, the serum DHEA-S levels again increased. Local tumour recurrence and a metastasis was found in the lung. Eleven months after surgery chemotherapy with mitotane (o,p'-DDD) was initiated. Twelve weeks of mitotane reduced serum DHEA-S levels and caused these tumours to disappear. The patient was then treated with low-dose mitotane (1.5-2.0 g/day) for 2 years. Serum levels of mitotane remained at less than 10 microg/ml. Although such low serum levels of mitotane and delayed initiation of mitotane after surgery have been proposed to weaken the antineoplastic effect of mitotane, the patient had a remission for 2 years. However, there was then local re-recurrence with an increase in serum DHEA-S and death 4 months later. The histological features of neoplastic cells were quite different comparing tumour resected at surgery and tumour at autopsy. The latter had more frequent mitotic nuclei. This tumour was initially sensitive to mitotane, but later became insensitive. (+info)Expression of inhibin alpha in adrenocortical tumours reflects the hormonal status of the neoplasm. (8/185)
Inhibins are gonadal glycoprotein hormones whose main endocrine function is to inhibit pituitary FSH secretion. In addition to testes and ovaries, other steroid-producing organs are sites of inhibin alpha subunit expression. To study the role of inhibins in human adrenal gland, we screened a panel of 150 adrenals (10 normal adrenals, 25 adrenocortical hyperplasias, 65 adrenocortical adenomas, 30 adrenocortical carcinomas and 20 phaeochromocytomas) for inhibin alpha expression. mRNA levels of inhibin alpha subunit were studied in 57 samples and all tissues were stained immunohistochemically with an inhibin alpha subunit-specific antibody. Inhibin alpha mRNA was detected in all adrenocortical tissues. Virilizing adenomas possessed a 10-fold higher median inhibin alpha mRNA expression than did normal adrenals. Bilaterally and nodularly hyperplastic adrenals and other than virilizing adrenocortical tumours had their median inhibin alpha mRNA levels close to those of normal adrenals. Immunohistochemically, inhibin alpha subunit was detectable in all normal and hyperplastic adrenals, as well as in 73% of the adrenocortical tumours. However, the percentage of inhibin alpha-positive cells varied greatly in different tumour types. The median percentage of positive cells was 10 in non-functional and Conn's adenomas, 30 in Cushing's adenomas and 75 in virilizing adenomas. In malignant adrenocortical tumours the median percentage of inhibin alpha-immunopositive cells was 20 in non-functional carcinomas, 30 in Conn's carcinomas, 65 in Cushing's carcinomas and 75 in virilizing carcinomas. All phaeochromocytomas were negative for inhibin alpha subunit both at the mRNA level and immunohistochemically. Our data show that inhibin alpha subunit is highly expressed in both normal and neoplastic androgen-producing adrenocortical cells, with less expression in cortisol-producing and hardly any in aldosterone-producing cells. This suggests a specific role for inhibins in the regulation of adrenal androgen production. We did not find any significant difference in inhibin alpha expression between benign and malignant adrenocortical tumours. Thus inhibin alpha gene does not seem to have a tumour suppressor role in human adrenal cortex. (+info)Adrenocortical carcinoma can be subdivided into three main types based on their histological features:
1. Typical adrenocortical carcinoma: This is the most common type and accounts for about 70% of all cases. It is characterized by a large, irregular tumor that grows in the cortex of the adrenal gland.
2. Adenomatous adrenocortical carcinoma: This type is less aggressive than typical adrenocortical carcinoma and accounts for about 20% of cases. It is characterized by a small, well-circumscribed tumor that grows in the cortex of the adrenal gland.
3. Adrenocortical sarcoma: This is the least common type and accounts for about 10% of cases. It is characterized by a rare, malignant tumor that grows in the cortex of the adrenal gland.
Adrenocortical carcinoma can cause a variety of symptoms, including abdominal pain, weight loss, fatigue, and skin changes. The diagnosis is typically made through a combination of imaging studies, such as CT scans and MRI, and tissue biopsy. Treatment options include surgery, chemotherapy, and radiation therapy, and the prognosis depends on the stage and aggressiveness of the tumor.
Overall, adrenocortical carcinoma is a rare and aggressive cancer that requires prompt diagnosis and treatment to improve patient outcomes.
Types of Adrenal Cortex Neoplasms:
1. Adrenocortical carcinoma (ACC): A rare and aggressive malignant tumor that originates in the adrenal cortex. It is often associated with virilization (excessive masculinization) in women.
2. Adrenocortical adenoma (ACA): A benign tumor that originates in the adrenal cortex. It is less common than ACC and may not cause any symptoms.
3. Pheochromocytoma: A rare tumor that originates in the adrenal medulla, which is the inner part of the adrenal gland. It can secrete excessive amounts of hormones that regulate blood pressure and heart rate.
4. Paraganglioma: A rare tumor that originates in the paraganglia, which are clusters of cells located near the adrenal glands. These tumors can produce excessive amounts of hormones and cause similar symptoms as pheochromocytoma.
Symptoms of Adrenal Cortex Neoplasms:
1. Virilization (excessive masculinization) in women, such as deepening of the voice, excessive body hair growth, and clitoral enlargement.
2. Headache, fatigue, and weight gain due to excessive production of steroid hormones.
3. High blood pressure and heart rate due to excessive production of catecholamines (hormones that regulate blood pressure and heart rate).
4. Abdominal pain, nausea, and vomiting due to the tumor's size and location.
Diagnosis of Adrenal Cortex Neoplasms:
1. Imaging tests such as CT scans or MRI to visualize the tumor and determine its size and location.
2. Laboratory tests to measure hormone levels in the blood, including cortisol, aldosterone, and catecholamines.
3. Biopsy to obtain a tissue sample for further examination under a microscope.
Treatment of Adrenal Cortex Neoplasms:
1. Surgery to remove the tumor, which is usually curative.
2. Medications to control symptoms such as high blood pressure and hormone levels.
3. Radiation therapy may be used in cases where surgery is not feasible or if there is a risk of recurrence.
Prognosis of Adrenal Cortex Neoplasms:
The prognosis for adrenal cortex neoplasms depends on the type and size of the tumor, as well as the extent of hormone production. In general, the prognosis is good for patients with benign tumors that are removed surgically. However, malignant tumors can have a poorer prognosis and may require additional treatments such as radiation therapy or chemotherapy.
Prevention of Adrenal Cortex Neoplasms:
There is no known prevention for adrenal cortex neoplasms, but early detection and treatment can improve outcomes. Regular monitoring of hormone levels and imaging tests can help detect tumors at an early stage.
Lifestyle Changes:
1. Reduce stress: High levels of cortisol can be caused by stress, so finding ways to manage stress can help prevent adrenal cortex neoplasms.
2. Maintain a healthy diet: Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains can help support overall health and well-being.
3. Exercise regularly: Regular physical activity can help reduce stress and improve overall health.
4. Get enough sleep: Aim for 7-8 hours of sleep per night to help regulate hormone levels.
5. Limit caffeine and alcohol: Both substances can disrupt hormone levels and contribute to the development of adrenal cortex neoplasms.
Adrenocortical adenomas are typically slow-growing and may not cause any symptoms in the early stages. However, as they grow, they can begin to produce excessive amounts of hormones such as cortisol and aldosterone, which can lead to a variety of symptoms including:
* Weight gain and central obesity
* Buffalo hump (a fat deposit on the back of the neck)
* Moon face (a rounded, full face)
* Stretch marks and thin skin
* Easy bruising and poor wound healing
* Fatigue, weakness, and decreased muscle mass
* Increased blood pressure and salt craving
* Decreased potassium levels
If the adenoma becomes large enough, it can also cause compression of nearby structures such as the surrounding blood vessels and nerves, leading to additional symptoms such as:
* Pain in the abdomen or flank
* Nausea and vomiting
* Feeling of fullness after eating only a small amount
* Fever and chills
If left untreated, adrenocortical adenomas can continue to grow and potentially lead to complications such as:
* Adrenal crisis (a life-threatening condition caused by the sudden release of large amounts of hormones into the bloodstream)
* Heart problems, such as hypertension and cardiac arrhythmias
* Kidney damage and failure
* Osteoporosis and bone fractures
The exact cause of adrenocortical adenomas is not known, but they are believed to be related to genetic mutations that occur during fetal development. They can also be associated with certain medical conditions such as familial adenomatous polyposis (FAP) and Li-Fraumeni syndrome.
The diagnosis of an adrenocortical adenoma is based on a combination of imaging studies, such as CT scans or MRI, and laboratory tests to assess hormone levels in the blood and urine. The imaging studies can help identify the size and location of the adenoma, while the laboratory tests can help confirm the presence of excess hormones in the body.
Treatment options for adrenocortical adenomas include:
* Surgery to remove the adenoma: This is the primary treatment for most adrenocortical adenomas. The surgery may be performed through a laparoscope (a thin tube with a camera and light on the end) or through an open incision in the abdomen.
* Radiation therapy: This may be used in cases where the adenoma cannot be removed completely by surgery or if it has spread to other parts of the body.
* Hormone therapy: Medications such as metyrapone or ketoconazole can be used to reduce hormone production by the adrenal gland.
It is important to note that not all adrenocortical adenomas are cancerous, and some may not require treatment. Your doctor will discuss the best course of treatment for you based on the specific characteristics of your adenoma and your overall health.
In summary, the diagnosis of an adrenocortical adenoma is based on a combination of imaging studies and laboratory tests, and treatment options include surgery, radiation therapy, and hormone therapy. It is important to work closely with your doctor to determine the best course of treatment for you.
There are several subtypes of carcinoma, including:
1. Adenocarcinoma: This type of carcinoma originates in glandular cells, which produce fluids or mucus. Examples include breast cancer, prostate cancer, and colon cancer.
2. Squamous cell carcinoma: This type of carcinoma originates in squamous cells, which are found on the surface layers of skin and mucous membranes. Examples include head and neck cancers, cervical cancer, and anal cancer.
3. Basal cell carcinoma: This type of carcinoma originates in the deepest layer of skin, called the basal layer. It is the most common type of skin cancer and tends to grow slowly.
4. Neuroendocrine carcinoma: This type of carcinoma originates in cells that produce hormones and neurotransmitters. Examples include lung cancer, pancreatic cancer, and thyroid cancer.
5. Small cell carcinoma: This type of carcinoma is a highly aggressive form of lung cancer that spreads quickly to other parts of the body.
The signs and symptoms of carcinoma depend on the location and stage of the cancer. Some common symptoms include:
* A lump or mass
* Pain
* Skin changes, such as a new mole or a change in the color or texture of the skin
* Changes in bowel or bladder habits
* Abnormal bleeding
The diagnosis of carcinoma typically involves a combination of imaging tests, such as X-rays, CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a small sample of tissue for examination under a microscope. Treatment options for carcinoma depend on the location and stage of the cancer and may include surgery, radiation therapy, chemotherapy, or a combination of these.
In conclusion, carcinoma is a type of cancer that originates in epithelial cells and can occur in various parts of the body. Early detection and treatment are important for improving outcomes.
References:
1. American Cancer Society. (2022). Carcinoma. Retrieved from
2. Mayo Clinic. (2022). Carcinoma. Retrieved from
3. MedlinePlus. (2022). Carcinoma. Retrieved from
Cushing syndrome is a rare hormonal disorder that occurs when the body produces too much cortisol, a steroid hormone produced by the adrenal gland. It can be caused by a variety of factors, including tumors, infections, and genetic conditions.
The symptoms of Cushing syndrome can vary depending on the cause and severity of the condition, but may include:
* Weight gain, particularly in the abdomen, face, and neck
* Fatigue and muscle weakness
* Poor sleep
* Mood changes, such as anxiety, depression, and irritability
* High blood pressure
* Easy bruising and thinning skin
* Osteoporosis or osteopenia
* Increased risk of infections
* Menstrual irregularities in women
* Hirsutism (excessive hair growth) in women
* Erectile dysfunction in men
Cushing syndrome can be difficult to diagnose, as the symptoms can be similar to other conditions. A healthcare provider will typically begin by taking a detailed medical history and performing a physical exam. They may also order several tests, including:
* Blood tests to measure cortisol levels and look for other hormonal imbalances
* Urine tests to check for abnormal steroid metabolites
* Imaging studies, such as CT or MRI scans, to look for tumors or other structural abnormalities
* Salivary cortisol testing to measure cortisol levels throughout the day
Treatment for Cushing syndrome depends on the underlying cause of the condition. In some cases, medication may be prescribed to reduce cortisol production or to treat symptoms such as high blood pressure or mood changes. Surgery may be necessary to remove a tumor or other structural abnormality. In addition, lifestyle changes such as diet and exercise may be recommended to help manage the condition.
It is important for individuals with Cushing syndrome to work closely with their healthcare provider to develop a treatment plan that is tailored to their specific needs and circumstances. With appropriate treatment, many people with Cushing syndrome can experience significant improvement in their symptoms and quality of life.
Some common types of adrenal gland neoplasms include:
1. Adrenocortical carcinoma: A rare and aggressive malignancy that arises in the outer layer of the adrenal cortex.
2. Adrenocortical adenoma: A benign tumor that arises in the outer layer of the adrenal cortex.
3. Pheochromocytoma: A rare tumor that arises in the inner part of the adrenal medulla and produces excessive amounts of hormones such as epinephrine and norepinephrine.
4. Paraganglioma: A rare tumor that arises in the sympathetic nervous system, often near the adrenal glands.
Symptoms of adrenal gland neoplasms can include:
* Weight gain or weight loss
* High blood pressure
* Fatigue
* Abdominal pain
* Headache
* Nausea and vomiting
* Palpitations
Diagnosis of adrenal gland neoplasms typically involves imaging tests such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and positron emission tomography (PET) scans, as well as hormone level assessments. Treatment options vary depending on the type and size of the tumor, and may include surgery, chemotherapy, and hormone therapy.
Myelolipomas are thought to arise from the mesoderm, which is one of the three primary germ layers (the others being ectoderm and endoderm) that give rise to all of the tissues in the body. The exact cause of myelolipoma is not well understood, but it is believed to be related to abnormal growth and development of the hematopoietic cells in the bone marrow.
Myelolipomas are usually slow-growing and may not cause any symptoms until they reach a significant size. When they do cause symptoms, they can include pain in the abdomen or pelvis, fever, weight loss, and fatigue. If a myelolipoma becomes infected, it can cause severe symptoms such as fever, chills, and abdominal pain.
Myelolipomas are usually diagnosed with the help of imaging tests such as CT scans or MRI scans. In some cases, a biopsy may be performed to confirm the diagnosis. Treatment for myelolipoma typically involves surgical removal of the tumor, and in some cases, radiation therapy or chemotherapy may be used to shrink the tumor before surgery. The prognosis for myelolipoma is generally good, and most patients with this condition can expect a complete recovery after treatment.
Also known as: Adrenal rest tumor, Adrenal cortical adenoma, Adrenocortical adenoma.
SCC typically appears as a firm, flat, or raised bump on the skin, and may be pink, red, or scaly. The cancer cells are usually well-differentiated, meaning they resemble normal squamous cells, but they can grow rapidly and invade surrounding tissues if left untreated.
SCC is more common in fair-skinned individuals and those who spend a lot of time in the sun, as UV radiation can damage the skin cells and increase the risk of cancer. The cancer can also spread to other parts of the body, such as lymph nodes or organs, and can be life-threatening if not treated promptly and effectively.
Treatment for SCC usually involves surgery to remove the cancerous tissue, and may also include radiation therapy or chemotherapy to kill any remaining cancer cells. Early detection and treatment are important to improve outcomes for patients with SCC.
The adrenal cortex is a layer of tissue that surrounds the adrenal gland and produces steroid hormones, such as cortisol and aldosterone. Adrenal cortex diseases are conditions that affect the adrenal cortex and disrupt the normal production of these hormones.
Types of Adrenal Cortex Diseases:
1. Cushing's Syndrome: This is a condition caused by an excess of cortisol in the body, often due to a tumor on the adrenal gland. Symptoms include weight gain, high blood pressure, and diabetes.
2. Addison's Disease: This is a condition where the adrenal glands do not produce enough cortisol and aldosterone, often due to an autoimmune disorder or injury to the glands. Symptoms include fatigue, weight loss, and low blood pressure.
3. Adrenal Insuficiency: This is a condition where the adrenal glands do not produce enough cortisol and aldosterone, often due to a genetic disorder or injury to the glands. Symptoms include fatigue, weight loss, and low blood pressure.
4. Adrenal Hyperplasia: This is a condition where the adrenal glands produce too much cortisol, often due to a genetic disorder. Symptoms include high blood pressure, obesity, and diabetes.
5. Adrenocortical Carcinoma: This is a rare type of cancer that affects the adrenal cortex. Symptoms include weight loss, high blood pressure, and abdominal pain.
Treatment Options for Adrenal Cortex Diseases:
1. Medications: Depending on the specific condition, medications such as steroids, anti-inflammatory drugs, or hormone replacement therapy may be prescribed to manage symptoms.
2. Surgery: In some cases, surgery may be necessary to remove a tumor or affected tissue.
3. Lifestyle Changes: Patients with adrenal cortex diseases may need to make lifestyle changes such as reducing stress, losing weight, and increasing physical activity.
4. Hormone Replacement Therapy: This is often necessary in cases where the adrenal glands are not producing enough hormones.
5. Radiation Therapy: This is a treatment option for patients with adrenocortical carcinoma.
Prognosis for Adrenal Cortex Diseases:
The prognosis for adrenal cortex diseases varies depending on the specific condition and the severity of symptoms. In general, early diagnosis and treatment can improve outcomes. However, some conditions such as adrenocortical carcinoma can be difficult to treat and may have a poor prognosis.
Complications of Adrenal Cortex Diseases:
1. High Blood Pressure: Many adrenal cortex diseases can cause high blood pressure, which can lead to complications such as heart disease and stroke.
2. Hormonal Imbalances: Adrenal cortex diseases can disrupt the balance of hormones in the body, leading to a range of symptoms and complications.
3. Weight Gain or Loss: Some adrenal cortex diseases can cause weight gain or loss, which can lead to other health problems such as joint pain and decreased mobility.
4. Fatigue and Weakness: Adrenal cortex diseases can cause fatigue and weakness, making it difficult to perform daily activities.
5. Depression and Anxiety: Hormonal imbalances and other symptoms of adrenal cortex diseases can lead to depression and anxiety.
6. Increased Risk of Infections: Adrenal insufficiency can increase the risk of infections such as pneumonia and meningitis.
7. Decreased Immune Function: Hormonal imbalances can weaken the immune system, making it more difficult to fight off infections.
8. Adrenal Crisis: In rare cases, adrenal cortex diseases can lead to an adrenal crisis, which is a life-threatening condition that requires immediate medical attention.
Prevention of Adrenal Cortex Diseases:
While some adrenal cortex diseases may be genetic and unavoidable, there are steps you can take to prevent or manage the symptoms. Here are some ways to prevent adrenal cortex diseases:
1. Maintain a Balanced Diet: Eating a balanced diet that includes essential nutrients such as vitamins, minerals, and protein can help maintain healthy adrenal function.
2. Reduce Stress: High levels of stress can disrupt hormone production in the adrenal glands. Practicing stress-reducing techniques such as meditation, yoga, or deep breathing exercises can help manage stress.
3. Get Enough Sleep: Getting enough sleep is essential for maintaining healthy adrenal function. Aim for 7-8 hours of sleep per night.
4. Stay Hydrated: Drinking enough water throughout the day can help prevent dehydration, which can affect adrenal function.
5. Exercise Regularly: Regular exercise can help improve adrenal function and overall health. Aim for at least 30 minutes of moderate-intensity exercise per day.
6. Avoid Toxins: Exposure to toxins such as pesticides, heavy metals, and pollution can damage the adrenal glands. Avoiding these toxins by using non-toxic household cleaners, personal care products, and avoiding exposure to pollution can help prevent adrenal cortex diseases.
7. Manage Medications: Certain medications such as corticosteroids can disrupt the normal function of the adrenal glands. Monitoring and managing medications with your healthcare provider can help prevent adrenal cortex diseases.
8. Get Regular Check-Ups: Regular check-ups with your healthcare provider can help identify any potential issues before they become serious.
While some adrenal cortex diseases may be unavoidable, taking these steps can help prevent or manage symptoms and maintain overall health. If you experience any symptoms of adrenal cortex disease, it's essential to seek medical attention from a qualified healthcare provider for proper diagnosis and treatment.
There are several risk factors for developing HCC, including:
* Cirrhosis, which can be caused by heavy alcohol consumption, viral hepatitis (such as hepatitis B and C), or fatty liver disease
* Family history of liver disease
* Chronic obstructive pulmonary disease (COPD)
* Diabetes
* Obesity
HCC can be challenging to diagnose, as the symptoms are non-specific and can be similar to those of other conditions. However, some common symptoms of HCC include:
* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Loss of appetite
* Abdominal pain or discomfort
* Weight loss
If HCC is suspected, a doctor may perform several tests to confirm the diagnosis, including:
* Imaging tests, such as ultrasound, CT scan, or MRI, to look for tumors in the liver
* Blood tests to check for liver function and detect certain substances that are produced by the liver
* Biopsy, which involves removing a small sample of tissue from the liver to examine under a microscope
Once HCC is diagnosed, treatment options will depend on several factors, including the stage and location of the cancer, the patient's overall health, and their personal preferences. Treatment options may include:
* Surgery to remove the tumor or parts of the liver
* Ablation, which involves destroying the cancer cells using heat or cold
* Chemoembolization, which involves injecting chemotherapy drugs into the hepatic artery to reach the cancer cells
* Targeted therapy, which uses drugs or other substances to target specific molecules that are involved in the growth and spread of the cancer
Overall, the prognosis for HCC is poor, with a 5-year survival rate of approximately 20%. However, early detection and treatment can improve outcomes. It is important for individuals at high risk for HCC to be monitored regularly by a healthcare provider, and to seek medical attention if they experience any symptoms.
Adenomas are caused by genetic mutations that occur in the DNA of the affected cells. These mutations can be inherited or acquired through exposure to environmental factors such as tobacco smoke, radiation, or certain chemicals.
The symptoms of an adenoma can vary depending on its location and size. In general, they may include abdominal pain, bleeding, or changes in bowel movements. If the adenoma becomes large enough, it can obstruct the normal functioning of the affected organ or cause a blockage that can lead to severe health complications.
Adenomas are usually diagnosed through endoscopy, which involves inserting a flexible tube with a camera into the affected organ to visualize the inside. Biopsies may also be taken to confirm the presence of cancerous cells.
Treatment for adenomas depends on their size, location, and severity. Small, non-pedunculated adenomas can often be removed during endoscopy through a procedure called endoscopic mucosal resection (EMR). Larger adenomas may require surgical resection, and in some cases, chemotherapy or radiation therapy may also be necessary.
In summary, adenoma is a type of benign tumor that can occur in glandular tissue throughout the body. While they are not cancerous, they have the potential to become malignant over time if left untreated. Therefore, it is important to seek medical attention if symptoms persist or worsen over time. Early detection and treatment can help prevent complications and improve outcomes for patients with adenomas.
In the medical field, the term is often used to describe various conditions that affect gender development or sexual differentiation in individuals with variations in sex chromosomes, hormones, or genitalia. Feminization can occur in individuals assigned male at birth but who exhibit female physical characteristics, such as those with congenital adrenal hyperplasia (CAH) or other intersex traits.
The term is also used to describe the effects of estrogen on the male body, particularly during puberty. For example, boys taking estrogen medication for hormone therapy may experience feminization of their physical features, such as breast tissue growth and a softer voice.
It's important to note that the term feminization is sometimes used in medical contexts to describe a process or outcome that is perceived as negative or undesirable, particularly when it comes to gender identity or expression. However, it's essential to recognize that all individuals, regardless of their gender identity or expression, deserve respect and support in their healthcare needs.
In summary, feminization within the medical field refers to a process or condition whereby male characteristics are acquired by an individual or group, often as a result of hormonal or genetic factors. The term is used to describe various conditions affecting gender development or sexual differentiation and the effects of estrogen on the male body. However, it's important to recognize that the term can be perceived as negative, and healthcare providers should approach patients with respect and sensitivity regardless of their gender identity or expression.
Adrenocortical hyperfunction can be caused by a variety of factors, including:
1. Cushing's syndrome: This is a rare hormonal disorder caused by excessive production of cortisol by the adrenal glands. It can be caused by a benign tumor in the pituitary gland or an adrenal gland, or by taking too much corticosteroid medication.
2. Adrenocortical carcinoma: This is a rare and aggressive type of cancer that affects the adrenal glands. It can cause excessive production of cortisol and other hormones.
3. Familial Cushing's syndrome: This is a genetic disorder that causes excessive production of cortisol by the adrenal glands.
4. Glucocorticoid-remediable aldosteronism (GRA): This is a rare genetic disorder that affects the production of hormones by the adrenal glands, leading to excessive production of cortisol and aldosterone.
5. Licorice ingestion: Consuming large amounts of licorice can cause an increase in the production of cortisol and other hormones by the adrenal glands.
6. Primary aldosteronism (PA): This is a group of rare genetic disorders that affect the production of hormones by the adrenal glands, leading to excessive production of aldosterone and cortisol.
7. Secondary adrenocortical hyperfunction: This can occur due to various conditions such as thyroid disorders, pituitary tumors, or other endocrine disorders that affect the regulation of hormone production by the adrenal glands.
Symptoms of adrenocortical hyperfunction may include:
1. Weight gain and central obesity
2. Increased appetite and food cravings
3. Fatigue and weakness
4. Mood changes, such as anxiety or depression
5. Insomnia and sleep disturbances
6. High blood pressure and cardiovascular risk factors
7. Easy bruising and poor wound healing
8. Muscle weakness and fatigue
9. Thinning of the skin and bones (osteoporosis)
10. Increased risk of infections and decreased immune function.
If you suspect that you or someone you know may have adrenocortical hyperfunction, it is essential to consult with a healthcare professional for proper diagnosis and treatment. A doctor may perform several tests, including:
1. Blood tests to measure hormone levels in the body, such as cortisol and aldosterone.
2. Saliva tests to measure cortisol levels throughout the day.
3. Urine tests to measure cortisol levels over a 24-hour period.
4. Imaging tests, such as CT scans or MRI scans, to examine the adrenal glands and look for any signs of tumors or other abnormalities.
5. Other tests to assess the body's response to stress, such as a corticotropin (ACTH) stimulation test.
Treatment options for adrenocortical hyperfunction depend on the underlying cause of the condition and may include:
1. Medications to reduce hormone production in the adrenal glands, such as metyrapone or ketoconazole.
2. Surgery to remove any tumors or cysts in the adrenal glands.
3. Radiation therapy to shrink tumors and reduce hormone production.
4. Lifestyle changes, such as weight loss, stress management techniques, and regular exercise.
5. Monitoring of hormone levels and other health markers to ensure that the condition is under control.
People with LFS have a high risk of developing cancer at an early age, often before the age of 40. The syndrome is usually diagnosed in individuals who have a family history of breast cancer, ovarian cancer, or soft tissue sarcomas.
The signs and symptoms of LFS can vary depending on the type of cancer that develops, but may include:
* Breast cancer: A lump or thickening in the breast, change in the size or shape of the breast, or nipple discharge
* Ovarian cancer: Abdominal pain, bloating, or swelling, difficulty eating or feeling full quickly
* Soft tissue sarcomas: A soft tissue mass or lump, often in the arm or leg
There is no cure for LFS, but regular monitoring and screening can help to detect cancer early, when it is most treatable. Treatment for cancer in LFS typically involves surgery, chemotherapy, and/or radiation therapy.
The prognosis for individuals with LFS varies depending on the type of cancer that develops and the age at which it is diagnosed. In general, the earlier cancer is detected and treated, the better the prognosis. However, the syndrome can be challenging to diagnose, as the symptoms can be nonspecific and may not appear until late in the disease process.
There is currently no cure for Li-Fraumeni Syndrome, but researchers are working to develop new treatments and improve early detection methods. Individuals with a family history of LFS or breast cancer should speak with their healthcare provider about genetic testing and counseling to determine if they may be at risk for the syndrome.
Also known as CIS.
Retroperitoneal neoplasms can occur in various locations, including the kidney, adrenal gland, pancreas, liver, spleen, and small intestine. These tumors can cause a variety of symptoms, such as abdominal pain, weight loss, fever, and difficulty urinating or passing stool.
The diagnosis of retroperitoneal neoplasms is based on a combination of imaging studies, such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and positron emission tomography (PET) scans, and a biopsy, which involves removing a small sample of tissue from the suspected tumor and examining it under a microscope.
Treatment options for retroperitoneal neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment, and may involve removing the tumor and any affected surrounding tissue or organs. Radiation therapy and chemotherapy may also be used to shrink the tumor before surgery or to kill any remaining cancer cells after surgery.
Some common types of retroperitoneal neoplasms include:
1. Renal cell carcinoma (RCC): a type of kidney cancer that originates in the cells that line the renal tubules.
2. Adrenocortical carcinoma: a type of cancer that arises in the adrenal gland.
3. Pancreatic neuroendocrine tumors: tumors that arise in the pancreas and produce excess hormones.
4. Liver cancer (hepatocellular carcinoma): a type of cancer that originates in the liver cells.
5. Gastrointestinal stromal tumors (GISTs): tumors that arise in the digestive system, usually in the stomach or small intestine.
6. Soft tissue sarcomas: tumors that arise in the soft tissues of the body, such as the muscles, fat, and connective tissue.
7. Retroperitoneal fibrosis: a condition where the tissue in the retroperitoneum becomes scarred and thickened.
8. Metastatic tumors: tumors that have spread to the retroperitoneum from another part of the body, such as the lung, breast, or colon.
It is important to note that this is not an exhaustive list and there may be other types of retroperitoneal neoplasms not mentioned here. If you suspect you may have a retroperitoneal neoplasm, it is important to consult with a qualified medical professional for proper diagnosis and treatment.
Symptoms of hyperaldosteronism may include high blood pressure, low potassium levels, muscle weakness, and heart arrhythmias. Treatment options vary depending on the underlying cause but may include medications to reduce aldosterone production, dietary modifications, and in some cases, surgery or radiation therapy.
It is important for individuals with hyperaldosteronism to receive regular monitoring and treatment from a healthcare provider to manage their condition effectively and prevent complications such as heart disease and stroke.
Adrenocortical carcinoma
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Adrenocortical carcinoma: MedlinePlus Medical Encyclopedia
Adrenal Surgery: Practice Essentials, Background, History of the Procedure
Adrenocortical Carcinoma With Cushing's Syndrome and Extensive Tumor Thrombosis of the Inferior Vena Cava in a 30-Year-Old...
IMSEAR at SEARO: The rhabdoid variant of adrenocortical carcinoma-Report of three cases and literature review
Endocrine, Parathyroid, and Thyroid Surgery | Johns Hopkins Medicine in Baltimore, MD
Can Physiologic FDG Uptake by the Bowel Be Reduced?
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The genome of the pygmy right whale illuminates the evolution of rorquals | BMC Biology | Full TextExpression in adrenocortical carcinoma1
- Indoleamine 2,3-Dioxygenase-1 Expression in Adrenocortical Carcinoma. (uchicago.edu)
Tumors7
- Key learning points Adrenocortical tumors comprise frequent benign adenomas and rare aggressive carcinomas (ACC). (endocrine-abstracts.org)
- Introduction: Adrenocortical tumors consist in frequent benign adenomas (ACA) and rare highly malignant carcinomas (ACC). (endocrine-abstracts.org)
- In this study, we investigated the prevalence of circulating anti-FATE1 antibodies in pediatric and adult patients with adrenocortical tumors using three different methods (immunofluorescence, ELISA and Western blot). (uni-wuerzburg.de)
- Immunohistochemical staining designed to detect a specific R132H mutation to IDH1 showed expression in the normal adrenal cortex, raising interest to study the potential role of IDH1 in the pathogenesis of adrenocortical tumors. (endocrine.org)
- The objective of this work is to study the role of IDH1 and its mutations in adrenocortical tumors. (endocrine.org)
- IDH1 R132H immunohistological staining was performed on a cohort of 197 adrenocortical tumors. (endocrine.org)
- We were unable to identify IDH1 mutations among our adrenocortical tumors using a targeted next-generation sequencing panel or via exon sequencing. (endocrine.org)
Adrenalectomy1
- Minimally Invasive Adrenalectomy for Adrenocortical Carcinoma: Five-Year Trends and Predictors of Conversion. (uchicago.edu)
H295R2
- 2009). Cytotoxicity and gene expression profiling of two hydroxylated polybrominated diphenyl ethers in human H295R adrenocortical carcinoma cells . (up.pt)
- Carboxy derivatives of isoflavones that exhibit oestrogenic/anti-oestrogenic properties were used as carriers for affinity drug targeting to H295R adrenocortical carcinoma cells that express transcripts of oestrogen receptor (ER) alpha and beta. (bioscientifica.com)
Hepatocellular carcinoma1
- Autoantibodies directed against FATE1 were previously detected in patients with hepatocellular carcinoma. (uni-wuerzburg.de)
Adrenal incidentalomas2
- In most cases, adrenal incidentalomas are nonfunctioning adrenocortical adenomas, but may also represent conditions requiring therapeutic intervention (e.g. adrenocorti. (bvsalud.org)
- Reduced serum levels of dehydroepiandrosterone sulfate in adrenal incidentalomas : a marker of adrenocortical tumor. (who.int)
Malignant2
- Adrenocortical carcinoma (ACC) is a malignant tumor with poor prognosis and no established therapy in advanced stage. (endocrine-abstracts.org)
- Positive IDH1 R132H immunohistochemical staining correlated with a better prognosis among patients with a malignant adrenocortical tumor. (endocrine.org)
Tumor2
- Adrenocortical Carcinoma With Cushing's Syndrome and Extensive Tumor Thrombosis of the Inferior Vena Cava in a 30-Year-Old Filipino Female. (bvsalud.org)
- Adrenocortical carcinoma (ACC) is a rare and in most cases steroid hormone-producing tumor with variable prognosis. (bvsalud.org)
Cushing1
- The common major pathologic entities of the adrenal gland that require surgical intervention are primary hyperaldosteronism (ie, Conn syndrome , see the second image below), Cushing syndrome , pheochromocytoma , neuroblastoma , and adrenocortical carcinoma . (medscape.com)
Recurrent1
- The combination of insulin-like growth factor receptor 1 (IGF1R) antibody cixutumumab and mitotane as a first-line therapy for patients with recurrent/metastatic adrenocortical carcinoma: a multi-institutional NCI-sponsored trial. (uchicago.edu)
Chemotherapy1
- The SF-1 transcription factor target gene FATE1 encodes a cancer-testis antigen that has an important role in regulating apoptosis and response to chemotherapy in adrenocortical carcinoma (ACC) cells. (uni-wuerzburg.de)
Neoplasm2
- Adrenocortical carcinoma (ACC) is a rare and aggressive neoplasm with poor prognosis . (bvsalud.org)
- We reviewed the clinicopathological features of nine cases of adrenocortical neoplasm. (who.int)
Adenomas1
- In a previous study we found mutations in the main catalytic subunit of protein kinase A (PKA Cα) to be responsible for cortisol-secreting adrenocortical adenomas (ACAs). (endocrine-abstracts.org)
Resection2
- Development of Ipsilateral Adrenocortical Carcinoma Sixteen Years after Resection of an Adrenal Tumour Causing. (annals.edu.sg)
- Risk factors associated with positive resection margins in patients with adrenocortical carcinoma. (tuftsmedicalcenter.org)
Endocrine1
- Adrenocortical carcinoma (ACC) is one of the most aggressive endocrine malignancies. (endocrine-abstracts.org)
Cancer3
- Adrenocortical carcinoma (ACC) is a cancer of the adrenal glands . (medlineplus.gov)
- Trovagene believes the combination of its targeted PLK-1 inhibitor, PCM-075, with other compounds has the potential for improved clinical efficacy in Acute Myeloid Leukemia (AML), Castration-Resistant Prostate Cancer ( CRPC ), Non-Hodgkin Lymphoma (NHL), Triple Negative Breast Cancer (TNBC) and Adrenocortical Carcinoma (ACC). (salesandmarketingnetwork.com)
- Expression of programmed death ligand 1 and 2 in adrenocortical cancer tissues: An exploratory study. (uchicago.edu)
Marker1
- Thus, IDH1 R132H immunohistochemical staining could serve as a prognostic or as a potential predictive marker in adrenocortical carcinomas. (endocrine.org)
Prognosis1
- Among adrenocortical carcinomas, IDH1 R132H immunopositivity correlated with a better prognosis. (endocrine.org)
Adult1
- Adrenocortical carcinoma treatment (Adult) (PDQ) - health professional version. (medlineplus.gov)
Patients1
- Determine the safety and possible effectiveness of antineoplastons A10 and AS2-1 in patients with stage IV adrenal gland carcinoma. (knowcancer.com)
Aggressive2
- Adrenocortical carcinoma (ACC) is a rare and aggressive malignancy. (who.int)
- Ad Adrenocortical carcinoma (ACC) is an aggressive tumour and treatment remains unsatisfactory in advanced disease. (endocrine-abstracts.org)
Study1
- The aim of our study was to evaluate the expression of BIRC7 in normal adrenals and adrenocortical tu. (endocrine-abstracts.org)
Status1
- Treatment Differences for Adrenocortical Carcinoma by Race and Insurance Status. (uchicago.edu)
Article1
- No article was found for Adrenocortical Carcinoma and GSK3B[original query] . (cdc.gov)
Treatment4
- Background: Standard treatment for advanced adrenocortical carcinoma (ACC) is mitotane in monotherapy or combined with etoposide, doxorubicin and cisplatin (EDP), yet biomarkers predictive of treatment response are lacking. (endocrine-abstracts.org)
- Tierney JF, Chivukula SV, Poirier J, Pappas SG, Schadde E, Hertl M, Kebebew E, Keutgen X. National Treatment Practice for Adrenocortical Carcinoma: Have They Changed and Have We Made Any Progress? (tuftsmedicalcenter.org)
- Treatment differences at high volume centers and low volume centers IN NON -metastatic and metastatic adrenocortical carcinoma. (uchicago.edu)
- National Treatment Practice for Adrenocortical Carcinoma: Have They Changed and Have We Made Any Progress? (uchicago.edu)
Cases1
- Ayyanar P, Sable MN, Adhya AK, Das MK, Kar M, Mishra P.. The rhabdoid variant of adrenocortical carcinoma-Report of three cases and literature review. (who.int)
