A sarcoma of the deep layers of the skin. The tumors are locally aggressive tends to recur but rarely metastatic. It can be classified into variants depending on the cell type tumors are derived from or by its characteristics: Pigmented variant from MELANIN-containing DERMAL DENDRITIC CELLS; Myxoid variant, myxoid STROMAL CELLS; Giant cell variant characterized by GIANT CELLS in the tumors; and Fibrosarcomatous variant chracterized by tumor areas histologically indistinguishable from FIBROSARCOMA.
Retrovirus-associated DNA sequences (v-sis) originally isolated from the simian sarcoma virus (SSV). The proto-oncogene c-sis codes for a growth factor which is the B chain of PLATELET-DERIVED GROWTH FACTOR. v-sis or overexpression of c-sis causes tumorigenesis. The human sis gene is located at 22q12.3-13.1 on the long arm of chromosome 22.
A benign tumor composed, wholly or in part, of cells with the morphologic characteristics of HISTIOCYTES and with various fibroblastic components. Fibrous histiocytomas can occur anywhere in the body. When they occur in the skin, they are called dermatofibromas or sclerosing hemangiomas. (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 5th ed, p1747)
A surgical technique used primarily in the treatment of skin neoplasms, especially basal cell or squamous cell carcinoma of the skin. This procedure is a microscopically controlled excision of cutaneous tumors either after fixation in vivo or after freezing the tissue. Serial examinations of fresh tissue specimens are most frequently done.
Tumors or cancer of the SKIN.
The outer covering of the calvaria. It is composed of several layers: SKIN; subcutaneous connective tissue; the occipitofrontal muscle which includes the tendinous galea aponeurotica; loose connective tissue; and the pericranium (the PERIOSTEUM of the SKULL).
Activated form of FACTOR XIII, a transglutaminase, which stabilizes the formation of the fibrin polymer (clot) culminating the blood coagulation cascade.
The GENETIC RECOMBINATION of the parts of two or more GENES, including an ONCOGENE as at least one of the fusion partners. Such gene fusions are often detected in neoplastic cells and are transcribed into ONCOGENE FUSION PROTEINS.
Tumors of bone tissue or synovial or other soft tissue characterized by the presence of giant cells. The most common are giant cell tumor of tendon sheath and GIANT CELL TUMOR OF BONE.
The GENETIC TRANSLATION products of the fusion between an ONCOGENE and another gene. The latter may be of viral or cellular origin.
A specific pair of GROUP G CHROMOSOMES of the human chromosome classification.
Neoplasms of whatever cell type or origin, occurring in the extraskeletal connective tissue framework of the body including the organs of locomotion and their various component structures, such as nerves, blood vessels, lymphatics, etc.
BENZOIC ACID amides.
Thinly cut sections of frozen tissue specimens prepared with a cryostat or freezing microtome.
Operative procedures performed on the SKIN.
A malignant skin neoplasm that seldom metastasizes but has potentialities for local invasion and destruction. Clinically it is divided into types: nodular, cicatricial, morphaic, and erythematoid (pagetoid). They develop on hair-bearing skin, most commonly on sun-exposed areas. Approximately 85% are found on the head and neck area and the remaining 15% on the trunk and limbs. (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1471)
'Skin diseases' is a broad term for various conditions affecting the skin, including inflammatory disorders, infections, benign and malignant tumors, congenital abnormalities, and degenerative diseases, which can cause symptoms such as rashes, discoloration, eruptions, lesions, itching, or pain.

The dermatofibrosarcoma protuberans-associated collagen type Ialpha1/platelet-derived growth factor (PDGF) B-chain fusion gene generates a transforming protein that is processed to functional PDGF-BB. (1/56)

Dermatofibrosarcoma protuberans (DFSP) displays chromosomal rearrangements involving chromosome 17 and 22, which fuse the collagen type Ialpha1 (COLIA1) gene to the platelet-derived growth factor (PDGF) B-chain (PDGFB) gene. To characterize the functional and structural properties of the COLIA1/PDGFB fusion protein, we generated a stable NIH3T3 cell line that contained a tumor-derived chimeric gene resulting from a COIA1 intron 7-PDGFB intron 1 fusion. Expression of the fusion protein led to morphological transformation and increased growth rate of these cells. The PDGF receptor kinase inhibitor CGP57148B reversed the transformed phenotype and reduced the growth rate of COLIA1/PDGFB-expressing cells but had no effects on control cells. The presence of dimeric COLIA1/PDGFB precursors was demonstrated through PDGFB immunoprecipitations of metabolically labeled cells and also by PDGFB immunoprecipitations followed by immunoblotting with COLIA1 antibodies. Pulse-chase studies demonstrated that the COLIA1/PDGFB precursor was processed to an end product that was indistinguishable from wild-type PDGF-BB. Finally, COLIA1/PDGFB-expressing cells generated tumors after s.c. injection into nude mice, and tumor growth was reduced by treatment with CGP57148B. We conclude that the COLIA1/PDGFB fusion associated with DFSP contributes to tumor development through ectopic production of PDGF-BB and the formation of an autocrine loop. Our findings, thus, suggest that PDGF receptors could be a target for pharmacological treatment of DFSP and giant cell fibroblastoma, e.g., through the use of PDGF receptor kinase inhibitors such as CGP57148B.  (+info)

Overexpression of the hepatocyte growth factor (HGF) receptor (Met) and presence of a truncated and activated intracellular HGF receptor fragment in locally aggressive/malignant human musculoskeletal tumors. (2/56)

Enhanced hepatocyte growth factor (HGF) receptor (Met) signaling has been suggested to play an important role in the development and progression of various epithelial and nonepithelial tumors. N-terminally truncated forms of the HGF receptor have been shown to be constitutively activated and tumorigenic in animal experiments. In the present study, 102 benign and malignant human musculoskeletal tumors were examined for expression of the HGF receptor by Western blotting and/or immunohistochemistry. A clear predominance of HGF receptor expression was seen in malignant as compared to benign tumors (Western blotting, P < 0.001; immunohistochemistry, P < 0.02). For the first time we show HGF receptor expression in the following four tumor types: dermatofibrosarcoma protuberans, clear cell sarcoma of tendons, malignant primitive neuroectodermal tumor, and benign fibrous histiocytoma. In three cases of sarcoma with high HGF receptor expression by Western blotting, we found indications of a short 85-kd N-terminally truncated HGF receptor that was tyrosine phosphorylated and located in the cytoplasm. Although fragments of this length were seen in 18 of 65 tumors, most were not tyrosine-phosphorylated. Northern blotting revealed only the 7.5-kb full-length HGF receptor transcript, suggesting that the 85-kd fragment is generated by an alternative initiation of translation or by proteolytic cleavage. Southern blotting detected no amplification of the Hgfr/Met gene in the 35 tumors examined, in contrast to our recent report of Hgfr/Met gene amplification in 7, 12-dimethylbenz(a)anthracene (DMBA)-induced rat sarcomas. The present data suggest that the locally aggressive and malignant properties of human mesenchymal tumors maybe related, in part, to high levels of full-length HGF receptors, and in some cases to the occurrence of N-terminally truncated HGF receptors, activated independently of HGF.  (+info)

COL1A1-PDGFB fusion transcripts in fibrosarcomatous areas of six dermatofibrosarcomas protuberans. (3/56)

The fibrosarcomatous transformation of dermatofibrosarcoma protuberans (DFSP) has been considered for some time to be associated with an adverse clinical outcome. However, the molecular and cellular mechanism underlying the tumor progression remains undetermined. As the chimeric gene, COL1A1-PDGFB, has been proposed to play an important role in the histogenesis of DFSP, we conducted a reverse transcription-polymerase chain reaction assay to ascertain whether the COL1A1-PDGFB fusion transcripts can be detected in both conventional DFSP and fibrosarcomatous components of DFSP with fibrosarcomatous areas (DFSP-FS), using a simple method of microdissection on sections of archival formalin-fixed, paraffin-embedded tumor specimens from six DFSP-FS cases. The COL1A1-PDGFB fusion transcripts could be detected in FS areas in five of the six cases, whereas conventional DFSP areas of all cases expressed the chimeric mRNA. A subsequent sequence analysis of the polymerase chain reaction products confirmed that the detected messages were derived from identical gene fusions in the two different components of each of the five cases. Our results verify that the COL1A1-PDGFB fusion transcripts are preserved in the FS areas of most DFSP-FSs. The expression of the fusion transcripts in both conventional DFSP and FS areas of DFSP-FS supports a common histogenesis of the two components.  (+info)

Dermatofibrosarcoma protuberans of scalp : a case report. (4/56)

A case of dermatofibrosarcoma protuberans of scalp involving the underlying bone, operated after recurrence by taking safety margin of 3 cm and skin deficit covered by transposition flap, is being reported. Modality of treatment has been discussed.  (+info)

Structural and functional analysis of a chimeric protein COL1A1-PDGFB generated by the translocation t(17;22)(q22;q13.1) in Dermatofibrosarcoma protuberans (DP). (5/56)

Dermatofibrosarcoma protuberans (DP), an infiltrative skin tumour of intermediate malignancy, presents specific cytogenetic features such as reciprocal translocations t(17;22)(q22;q13.1) or supernumerary ring chromosomes derived from t(17;22). We have previously shown that both rings and translocated chromosomes derived from t(17;22) presented the same molecular rearrangement with fusion of the COL1A1 gene on chromosome 17 to the PDGFB gene on chromosome 22. To study the structure and function of the COL1A1-PDGFB chimeric protein, we used a tumour-derived chimeric COL1A1-PDGFB cDNA to perform stable and transient transfections in the Chinese hamster lung fibroblastic cell line PS200 and the human epithelial cell line HEK293. We demonstrated that the stably transfected clones that expressed the COL1A1-PDGFB chimeric protein became growth factors independent and tumorigenic in nude mice. In addition, COL1A1-PDGFB transfected cell supernatants significantly stimulated fibroblastic cell growth, through the activation of the PDGFB receptor pathway. By using anti-PDGFB and specific anti-COL1A1-PDGFB antibodies, we showed that, similar to PDGFB, the COL1A1-PDGFB chimeric proteins are processed in transfected cells into mature PDGFB dimers. These results strongly suggest that the COL1A1-PDGFB chimeric gene expression associated with DP, induces tumours formation through production of mature PDGFB, in an autocrine or paracrine way. Strikingly, mutagenesis experiments indicated that uncleaved COL1A1-PDGFB forms are mitogenic and therefore could contribute, as well as mature PDGFB, to the establishment of a transformed phenotype.  (+info)

Growth inhibition of dermatofibrosarcoma protuberans tumors by the platelet-derived growth factor receptor antagonist STI571 through induction of apoptosis. (6/56)

Dermatofibrosarcoma protuberans (DFSP) and giant cell fibroblastoma (GCF) are recurrent, infiltrative skin tumors that presently are treated with surgery. DFSP and GCF tumors are genetically characterized by chromosomal rearrangements fusing the collagen type Ialpha1 (COLIA1) gene to the platelet-derived growth factor B-chain (PDGFB) gene. It has been shown that the resulting COL1A1/PDGF-B fusion protein is processed to mature PDGF-BB. Autocrine PDGF receptor stimulation has therefore been predicted to contribute to DFSP and GCF tumor development and growth. Here we demonstrate presence of activated PDGF receptors in primary cultures derived from six different DFSP and GCF tumors. Three of the primary cultures were further characterized; their in vitro growth displayed an increased sensitivity to treatment with the PDGF receptor tyrosine kinase inhibitor STI571, as compared with normal fibroblasts. Transplantable tumors, displaying a DFSP-like histology, were established from one of the DFSP primary cultures. Treatment of tumor-bearing severe combined immunodeficient mice with STI571 reduced tumor growth. The growth-inhibitory effects in vitro and in vivo occurred predominantly through induction of tumor cell apoptosis. Our study demonstrates growth-inhibitory effects of PDGF receptor antagonists on human DFSP- and GCF-derived tumor cells and demonstrates that autocrine PDGF receptor stimulation provides antiapoptotic signals contributing to the growth of these cells. These findings suggest targeting of PDGF receptors as a novel treatment strategy for DFSP and GCF.  (+info)

Dermatofibrosarcoma protuberans metastasizing to cavernous sinuses and lungs: a case report. (7/56)

Dermatofibrosarcoma protuberans (DFSP) is a locally aggressive tumor with a low potential for distant metastases. We report a 22-year-old female patient with a typical cutaneous DFSP who developed five local recurrences followed by left cavernous sinus metastasis at the eighth year and right cavernous sinus and lung metastases at the ninth year. In each local recurrence the tumor showed histological signs of progression as being more cellular, having higher mitotic index and being aggressively invasive through the underlying soft tissues. The histopathological evaluation of the metastatic tumor resected from the left cavernous sinus revealed dedifferentiation from low-grade DFSP to higher grade fibrosarcomatous morphology. Immunohistochemical studies of the primary tumor and also the recurrent and metastatic tumors showed diffuse CD34 positivity in all specimens and p53 positivity was detected in the metastatic tumor resected from left cavernous sinus.  (+info)

Molecular targeting of platelet-derived growth factor B by imatinib mesylate in a patient with metastatic dermatofibrosarcoma protuberans. (8/56)

PURPOSE: Dermatofibrosarcoma protuberans is caused by activation of the platelet-derived growth factor B (PDGFB) receptor, a transmembrane tyrosine kinase. We investigated the response of dermatofibrosarcoma protuberans to the tyrosine kinase inhibitor imatinib mesylate. PATIENTS AND METHODS: A patient with unresectable, metastatic dermatofibrosarcoma protuberans received imatinib mesylate (400 mg bid). Response to therapy was assessed by [18F]fluorodeoxyglucose (FDG) positron emission tomography, magnetic resonance imaging, and histopathologic and immunohistochemical evaluation. RESULTS: The patient was treated for 4 months with imatinib mesylate. The hypermetabolic uptake of FDG fell to background levels within 2 weeks of treatment, and the tumor volume shrank by over 75% during the 4 months of therapy, allowing for resection of the mass. There was no residual viable tumor in the resected specimen, indicating a complete histologic response to treatment with imatinib mesylate. CONCLUSION: Imatinib mesylate is highly active in dermatofibrosarcoma protuberans. The dramatic response seen in this patient demonstrates that inhibition of PDGFB receptor tyrosine kinase activity can significantly impact viability of at least one type of solid tumor.  (+info)

Dermatofibrosarcoma protuberans (DFSP) is a rare type of skin cancer that begins in the middle layer of the skin known as the dermis. It often appears as a scar or bruise that does not go away and may grow slowly over time, sometimes spreading to deeper tissues and other parts of the body. DFSP can be difficult to treat if it has spread, but when caught early, it is usually curable with surgery.

DFSP is characterized by the growth of abnormal fibroblasts, which are cells that produce collagen, a protein that helps make up connective tissues in the body. The exact cause of DFSP is not known, but it has been linked to genetic mutations and previous injuries or surgeries to the skin.

Treatment for DFSP typically involves surgical removal of the tumor, along with a margin of healthy tissue around it. In some cases, radiation therapy or targeted therapy may also be used to help ensure that all cancer cells have been removed. Regular follow-up care is important to monitor for any signs of recurrence or spread of the disease.

Hello! I'd be happy to explain that in simple terms.

Genes are the basic units of heredity in living organisms. They are made up of DNA (deoxyribonucleic acid), a long molecule that contains the instructions an organism needs to develop, live, and reproduce. These instructions include things like eye color, hair color, height, and other traits.

Each gene provides specific instructions for the production of a particular protein, which plays a critical role in the structure and function of every cell in the body. Think of genes as the "blueprint" for building and maintaining our bodies.

I hope this helps! Let me know if you have any other questions.

Benign fibrous histiocytoma (BFH) is a common benign tumor of the skin and superficial soft tissues. It primarily affects middle-aged adults and is more prevalent in men than women. The exact cause of BFH is unknown, but it's thought to arise from dermal fibroblasts or histiocytes.

Medical Definition: Benign Fibrous Histiocytoma (BFH) is a benign, slowly growing, solitary cutaneous or subcutaneous nodular tumor predominantly composed of a mixture of fibroblastic and histiocytic-like cells. The tumor typically presents as a well-circumscribed, firm, dome-shaped papule or nodule, ranging in size from a few millimeters to several centimeters. Histologically, BFH is characterized by the proliferation of spindle-shaped fibroblasts and histiocytes arranged in a storiform pattern, along with variable amounts of collagen deposition, multinucleated giant cells, and hemosiderin deposits. The lesion usually has a pushing border with no invasion into the surrounding tissues. BFH generally follows a benign clinical course, with local recurrence being uncommon following complete surgical excision.

Mohs surgery, also known as Mohs micrographic surgery, is a precise surgical technique used to treat common types of skin cancer. It's primarily used for basal cell carcinomas and squamous cell carcinomas that have recurred, are large, aggressive, or in critical areas where preservation of healthy tissue is important, such as the face.

The procedure involves removing the visible tumor along with a thin layer of surrounding tissue. This layer is then processed and examined under a microscope while the patient waits. If cancer cells are found in the margin of the removed tissue, another layer of tissue is taken from that specific area and examined. This process continues until no cancer cells are found in the margins, ensuring complete removal of the tumor while minimizing the removal of healthy tissue.

The main advantage of Mohs surgery is its ability to accurately assess the depth and extent of the cancer, leading to high cure rates and improved cosmetic outcomes. However, it's a specialized procedure that requires extensive training and should be performed by a fellowship-trained Mohs surgeon.

Skin neoplasms refer to abnormal growths or tumors in the skin that can be benign (non-cancerous) or malignant (cancerous). They result from uncontrolled multiplication of skin cells, which can form various types of lesions. These growths may appear as lumps, bumps, sores, patches, or discolored areas on the skin.

Benign skin neoplasms include conditions such as moles, warts, and seborrheic keratoses, while malignant skin neoplasms are primarily classified into melanoma, squamous cell carcinoma, and basal cell carcinoma. These three types of cancerous skin growths are collectively known as non-melanoma skin cancers (NMSCs). Melanoma is the most aggressive and dangerous form of skin cancer, while NMSCs tend to be less invasive but more common.

It's essential to monitor any changes in existing skin lesions or the appearance of new growths and consult a healthcare professional for proper evaluation and treatment if needed.

The scalp is the anatomical region located at the upper part of the human head, covering the skull except for the face and the ears. It is made up of several layers: the skin, the connective tissue, the galea aponeurotica (a strong, flat, tendinous sheet), loose areolar tissue, and the periosteum (the highly vascularized innermost layer that attaches directly to the skull bones). The scalp has a rich blood supply and is home to numerous sensory receptors, including those for touch, pain, and temperature. It also contains hair follicles, sebaceous glands, and sweat glands.

Factor XIIIa is a protein involved in the blood clotting process. It is a activated form of Factor XIII, which is a protransglutaminase enzyme that plays a role in stabilizing blood clots. Factor XIIIa cross-links fibrin molecules in the clot to form a more stable and insoluble clot. This action helps prevent further bleeding from the site of injury.

Factor XIIIa is formed when thrombin, another protein involved in blood clotting, cleaves and activates Factor XIII. Once activated, Factor XIIIa catalyzes the formation of covalent bonds between fibrin molecules, creating a mesh-like structure that strengthens the clot.

Deficiencies or dysfunctions in Factor XIIIa can lead to bleeding disorders, including factor XIII deficiency, which is a rare but serious condition characterized by prolonged bleeding and an increased risk of spontaneous hemorrhage.

An oncogene fusion, also known as oncogenic fusion or chimeric oncogene, is a result of a genetic rearrangement where parts of two different genes combine to form a hybrid gene. This fusion can lead to the production of an abnormal protein that contributes to cancer development and progression. In many cases, one of the fused genes is a proto-oncogene, a normal gene that regulates cell growth and division. When this gene is altered through fusion, it can acquire increased activity or new functions, promoting uncontrolled cell growth and eventually leading to tumor formation. Oncogene fusions are often associated with specific types of cancer and can be used as diagnostic markers or therapeutic targets for cancer treatment.

Giant cell tumors (GCTs) are a type of benign or rarely malignant bone tumor that is characterized by the presence of multinucleated giant cells. These tumors typically affect adults between the ages of 20 and 40, and they can occur in any bone, but they most commonly involve the long bones near the knee joint.

GCTs are composed of three types of cells: mononuclear stromal cells, which produce the matrix of the tumor; multinucleated osteoclast-like giant cells, which resemble the bone-resorbing cells found in normal bone; and macrophages, which are part of the body's immune system.

The mononuclear stromal cells produce a variety of growth factors that stimulate the formation and activity of the osteoclast-like giant cells, leading to localized bone destruction. The tumor may cause pain, swelling, and limited mobility in the affected area.

While GCTs are typically benign, they can be aggressive and locally destructive, with a tendency to recur after surgical removal. In some cases, GCTs may undergo malignant transformation, leading to the development of sarcomas. Treatment options for GCTs include curettage (scraping out) of the tumor, followed by bone grafting or the use of a cement spacer to fill the defect, and/or adjuvant therapy with radiation or chemotherapy.

An oncogene protein fusion is a result of a genetic alteration in which parts of two different genes combine to create a hybrid gene that can contribute to the development of cancer. This fusion can lead to the production of an abnormal protein that promotes uncontrolled cell growth and division, ultimately resulting in a malignant tumor. Oncogene protein fusions are often caused by chromosomal rearrangements such as translocations, inversions, or deletions and are commonly found in various types of cancer, including leukemia and sarcoma. These genetic alterations can serve as potential targets for cancer diagnosis and therapy.

Human chromosome pair 22 consists of two rod-shaped structures present in the nucleus of each cell in the human body. Each chromosome is made up of DNA tightly coiled around histone proteins, forming a complex structure called a chromatin.

Chromosome pair 22 is one of the 22 autosomal pairs of human chromosomes, meaning they are not sex chromosomes (X or Y). Chromosome 22 is the second smallest human chromosome, with each arm of the chromosome designated as p and q. The short arm is labeled "p," and the long arm is labeled "q."

Chromosome 22 contains several genes that are associated with various genetic disorders, including DiGeorge syndrome, velocardiofacial syndrome, and cat-eye syndrome, which result from deletions or duplications of specific regions on the chromosome. Additionally, chromosome 22 is the location of the NRXN1 gene, which has been associated with an increased risk for autism spectrum disorder (ASD) and schizophrenia when deleted or disrupted.

Understanding the genetic makeup of human chromosome pair 22 can provide valuable insights into human genetics, evolution, and disease susceptibility, as well as inform medical diagnoses, treatments, and research.

Soft tissue neoplasms refer to abnormal growths or tumors that develop in the soft tissues of the body. Soft tissues include muscles, tendons, ligaments, fascia, nerves, blood vessels, fat, and synovial membranes (the thin layer of cells that line joints and tendons). Neoplasms can be benign (non-cancerous) or malignant (cancerous), and their behavior and potential for spread depend on the specific type of neoplasm.

Benign soft tissue neoplasms are typically slow-growing, well-circumscribed, and rarely spread to other parts of the body. They can often be removed surgically with a low risk of recurrence. Examples of benign soft tissue neoplasms include lipomas (fat tumors), schwannomas (nerve sheath tumors), and hemangiomas (blood vessel tumors).

Malignant soft tissue neoplasms, on the other hand, can grow rapidly, invade surrounding tissues, and may metastasize (spread) to distant parts of the body. They are often more difficult to treat than benign neoplasms and require a multidisciplinary approach, including surgery, radiation therapy, and chemotherapy. Examples of malignant soft tissue neoplasms include sarcomas, such as rhabdomyosarcoma (arising from skeletal muscle), leiomyosarcoma (arising from smooth muscle), and angiosarcoma (arising from blood vessels).

It is important to note that soft tissue neoplasms can occur in any part of the body, and their diagnosis and treatment require a thorough evaluation by a healthcare professional with expertise in this area.

Benzamides are a class of organic compounds that consist of a benzene ring (a aromatic hydrocarbon) attached to an amide functional group. The amide group can be bound to various substituents, leading to a variety of benzamide derivatives with different biological activities.

In a medical context, some benzamides have been developed as drugs for the treatment of various conditions. For example, danzol (a benzamide derivative) is used as a hormonal therapy for endometriosis and breast cancer. Additionally, other benzamides such as sulpiride and amisulpride are used as antipsychotic medications for the treatment of schizophrenia and related disorders.

It's important to note that while some benzamides have therapeutic uses, others may be toxic or have adverse effects, so they should only be used under the supervision of a medical professional.

"Frozen sections" is a medical term that refers to the process of quickly preparing and examining a small piece of tissue during surgery. This procedure is typically performed by a pathologist in order to provide immediate diagnostic information to the surgeon, who can then make informed decisions about the course of the operation.

To create a frozen section, the surgical team first removes a small sample of tissue from the patient's body. This sample is then quickly frozen, typically using a special machine that can freeze the tissue in just a few seconds. Once the tissue is frozen, it can be cut into thin slices and stained with dyes to help highlight its cellular structures.

The stained slides are then examined under a microscope by a pathologist, who looks for any abnormalities or signs of disease. The results of this examination are typically available within 10-30 minutes, allowing the surgeon to make real-time decisions about whether to remove more tissue, change the surgical approach, or take other actions based on the findings.

Frozen sections are often used in cancer surgery to help ensure that all of the cancerous tissue has been removed, and to guide decisions about whether additional treatments such as radiation therapy or chemotherapy are necessary. They can also be used in other types of surgeries to help diagnose conditions and make treatment decisions during the procedure.

Dermatologic surgical procedures refer to various types of surgeries performed by dermatologists, which are aimed at treating and managing conditions related to the skin, hair, nails, and mucous membranes. These procedures can be divided into several categories, including:

1. Excisional surgery: This involves removing a lesion or growth by cutting it out with a scalpel. The resulting wound is then closed with stitches, sutures, or left to heal on its own.
2. Incisional biopsy: This is a type of excisional surgery where only a portion of the lesion is removed for diagnostic purposes.
3. Cryosurgery: This involves using extreme cold (usually liquid nitrogen) to destroy abnormal tissue, such as warts or precancerous growths.
4. Electrosurgical procedures: These use heat generated by an electric current to remove or destroy skin lesions. Examples include electrodessication and curettage (ED&C), which involves scraping away the affected tissue with a sharp instrument and then applying heat to seal the wound.
5. Laser surgery: Dermatologic surgeons use various types of lasers to treat a wide range of conditions, such as removing tattoos, reducing wrinkles, or treating vascular lesions.
6. Mohs micrographic surgery: This is a specialized surgical technique used to treat certain types of skin cancer, particularly basal cell carcinomas and squamous cell carcinomas. It involves removing the tumor in thin layers and examining each layer under a microscope until no cancer cells remain.
7. Scar revision surgery: Dermatologic surgeons can perform procedures to improve the appearance of scars, such as excising the scar and reclosing the wound or using laser therapy to minimize redness and thickness.
8. Hair transplantation: This involves removing hair follicles from one area of the body (usually the back of the head) and transplanting them to another area where hair is thinning or absent, such as the scalp or eyebrows.
9. Flap surgery: In this procedure, a piece of tissue with its own blood supply is moved from one part of the body to another and then reattached. This can be used for reconstructive purposes after skin cancer removal or trauma.
10. Liposuction: Dermatologic surgeons may perform liposuction to remove excess fat from various areas of the body, such as the abdomen, thighs, or chin.

Carcinoma, basal cell is a type of skin cancer that arises from the basal cells, which are located in the lower part of the epidermis (the outermost layer of the skin). It is also known as basal cell carcinoma (BCC) and is the most common form of skin cancer.

BCC typically appears as a small, shiny, pearly bump or nodule on the skin, often in sun-exposed areas such as the face, ears, neck, hands, and arms. It may also appear as a scar-like area that is white, yellow, or waxy. BCCs are usually slow growing and rarely spread (metastasize) to other parts of the body. However, they can be locally invasive and destroy surrounding tissue if left untreated.

The exact cause of BCC is not known, but it is thought to be related to a combination of genetic and environmental factors, including exposure to ultraviolet (UV) radiation from the sun or tanning beds. People with fair skin, light hair, and blue or green eyes are at increased risk of developing BCC.

Treatment for BCC typically involves surgical removal of the tumor, along with a margin of healthy tissue. Other treatment options may include radiation therapy, topical chemotherapy, or photodynamic therapy. Prevention measures include protecting your skin from UV radiation by wearing protective clothing, using sunscreen, and avoiding tanning beds.

Skin diseases, also known as dermatological conditions, refer to any medical condition that affects the skin, which is the largest organ of the human body. These diseases can affect the skin's function, appearance, or overall health. They can be caused by various factors, including genetics, infections, allergies, environmental factors, and aging.

Skin diseases can present in many different forms, such as rashes, blisters, sores, discolorations, growths, or changes in texture. Some common examples of skin diseases include acne, eczema, psoriasis, dermatitis, fungal infections, viral infections, bacterial infections, and skin cancer.

The symptoms and severity of skin diseases can vary widely depending on the specific condition and individual factors. Some skin diseases are mild and can be treated with over-the-counter medications or topical creams, while others may require more intensive treatments such as prescription medications, light therapy, or even surgery.

It is important to seek medical attention if you experience any unusual or persistent changes in your skin, as some skin diseases can be serious or indicative of other underlying health conditions. A dermatologist is a medical doctor who specializes in the diagnosis and treatment of skin diseases.

February 2008). "Dermatofibrosarcoma protuberans COL1A1-PDGFB fusion is identified in virtually all dermatofibrosarcoma ... "Dermatofibrosarcoma protuberans (DFSP)". www.pathologyoutlines.com. Retrieved 2020-06-09. Dermatofibrosarcoma protuberans in ... also termed dermatofibrosarcoma protuberans, fibro sarcomatous) of the dermatofibrosarcoma protuberans as a specific form of ... pigmented dermatofibrosarcoma protuberans ICD-0: 8834/1 - giant cell fibroblastoma Fibrosarcomatous dermatofibrosarcoma ...
... (DFSP-FS), also termed fibrosarcomatous dermatofibrosarcoma protuberans, is a ... a more aggressive form of the dermatofibrosarcoma protuberans (DFSP) tumors because they have areas that resemble and tend to ...
Smola MG, Soyer HP, Scharnagl E (October 1991). "Surgical treatment of dermatofibrosarcoma protuberans. A retrospective study ...
GCF tumors are closely related to dermatofibrosarcoma protuberans (DFSP) and dermatofibrosarcoma protuberans, fibrosarcomatous ... Hao X, Billings SD, Wu F, Stultz TW, Procop GW, Mirkin G, Vidimos AT (June 2020). "Dermatofibrosarcoma Protuberans: Update on ... Braswell DS, Ayoubi N, Motaparthi K, Walker A (April 2020). "Dermatofibrosarcoma protuberans with features of giant cell ... "Dermatofibrosarcoma protuberans, giant cell fibroblastoma, and hybrid lesions in children: clinicopathologic comparative ...
... distinctive CD34-positive lesions that may mimic dermatofibrosarcoma protuberans". Journal of Cutaneous Pathology. 32 (6): 413- ...
... a novel marker for dermatofibrosarcoma protuberans". The American Journal of Surgical Pathology. 28 (8): 1063-9. doi:10.1097/01 ...
The FDA granted approval for the treatment of dermatofibrosarcoma protuberans (DFSP) patients in 2006. Specifically adult ... In 2006 the FDA expanded approved use to include dermatofibrosarcoma protuberans (DFSP), myelodysplastic/myeloproliferative ... and dermatofibrosarcoma protuberans. Imatinib was invented in the late 1990s by scientists at Ciba-Geigy (which merged with ... recurrent and/or metastatic dermatofibrosarcoma protuberans. On 25 January 2013, Gleevec was approved for use in children with ...
Dean Turner died on 21 August 2009 of dermatofibrosarcoma protuberans, a rare form of tissue cancer. He was 37 years old. ... Turner died in August 2009 of dermatofibrosarcoma protuberans (a soft tissue cancer). From 2010 to November 2018, the band were ... Dean battled an extremely rare form of soft tissue cancer called dermatofibrosarcoma protuberans (DFSP). This cancer became ...
... distinctive CD34-positive lesions that may mimic dermatofibrosarcoma protuberans". Journal of Cutaneous Pathology. 32 (6): 413- ...
... mimicking pigmented dermatofibrosarcoma protuberans". Journal of Cutaneous Pathology. 48 (2): 290-294. doi:10.1111/cup.13772. ...
Among other CD34-positive tumours, GRIA2 is also expressed in dermatofibrosarcoma protuberans (DFSP); however, clinical and ...
June 2000). "Dermatofibrosarcoma protuberans: A clinicopathologic analysis of patients treated and followed at a single ...
Early clinical trials indicate that imatinib may be effective in treatment of dermatofibrosarcoma protuberans. Gefitinib ( ...
Benign fibrous histiocytoma Dermatofibrosarcoma protuberans Fibrous connective tissue Fibroma Malignant fibrous histiocytoma ...
Dermatofibrosarcoma protuberans, NOS M8833/3 Pigmented dermatofibrosarcoma protuberans Bednar tumor M8834/1 Giant-cell ... hemangioma Cutaneous histiocytoma Subepidermal nodular fibrosis Dermatofibroma lenticulare M8832/3 Dermatofibrosarcoma, NOS ( ...
FMTs Dermatofibrosarcoma protuberans, fibrosarcomatous, also termed fibrosarcomatous dermatofibrosarcoma protuberans (or ... Giant cell fibroblastoma Dermatofibrosarcoma protuberans Fibrous hamartoma of infancy Intermediate (rarely metastasizing) ... "Risk factors related to postoperative recurrence of dermatofibrosarcoma protuberans: A retrospective study and literature ... fibrosarcomatous DFSP), is a more aggressive tumor than dermatofibrosarcoma protuberans tumors). Solitary fibrous tumour, also ...
Dean battled an extremely rare form of soft tissue cancer called dermatofibrosarcoma protuberans or (DFSP)... This cancer ...
Furthermore, PDGFB translocation to the COL1A1 gene locus has been identified to be responsible for dermatofibrosarcoma ...
"Stromelysin-3 expression in the differential diagnosis of dermatofibroma and dermatofibrosarcoma protuberans: Comparison with ... from rare malignant fibrohistocytic tumours like dermatofibrosarcoma protuberans. Dermatofibromas typically have a positive ...
Dermatofibrosarcoma protuberans often is associated with a chromosomal translocation in which the COL1A1 gene becomes fused to ... Dermatofibrosarcoma protuberans, fibrosarcomatous Giant cell fibroblastoma Malignant solitary fibrous tumor Inflammatory ... and myxoid pleomorphic liposarcoma Atypical lipomatous tumor Dermatofibrosarcoma protuberans (includes pigmented varieties) ...
Turner died on 21 August 2009 of dermatofibrosarcoma protuberans, a rare form of tissue cancer, and work on the album ceased. ...
NF may resemble and therefore be misdiagnosed as dermatofibrosarcoma protuberans, fibrosarcoma, malignant fibrous histiocytoma ...
Mohs surgery is also used for squamous-cell carcinoma, melanoma, atypical fibroxanthoma, dermatofibrosarcoma protuberans, ...
The other diseases were a follicular keratosis (Darier-White syndrome), dermatofibrosarcoma (Darier-Ferrand disease), erythema ...
... dermatofibrosarcoma protuberans, gastrointestinal stromal tumors, giant cell fibroblastoma, granulocytic sarcoma, Kaposi's ...
Dermatofibrosarcoma protuberans Desmoid tumor Diffuse cutaneous mastocytosis Diffuse infantile fibromatosis Dupuytren's ...
Leiomyosarcoma Fibrous histiocytoma Proximal epithelioid sarcoma Alveolar soft part sarcoma Liposarcoma Dermatofibrosarcoma ...
She shared her story about being diagnosed with Dermatofibrosarcoma protuberans in 2012 and the subsequent two years of life- ...
... dermatofibrosarcoma MeSH C04.557.450.565.590.350.590 - neurofibrosarcoma MeSH C04.557.450.565.590.425 - histiocytoma MeSH ... dermatofibrosarcoma MeSH C04.557.450.795.350.590 - neurofibrosarcoma MeSH C04.557.450.795.390 - hemangiosarcoma MeSH C04.557. ...
... dermatofibrosarcoma protuberans, and dermatofibrosarcoma protuberans, sarcomatous. Two splice variants have been identified for ...

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