Sarcoma
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Sarcoma represents 1% of all malignant tumors and includes soft tissue sarcomas (STS), bone sarcomas, and visceral sarcomas. STS are more common than bone sarcomas by a ratio of 4:1. Risk factors for sarcoma include genetic syndromes, radiation exposure, and certain chemical exposures. Diagnosis involves imaging such as MRI or CT along with pathological confirmation. Treatment depends on the location and stage of disease, and may involve surgery, radiation therapy, chemotherapy, or targeted therapy. The goal is curative treatment for localized disease and palliation for metastatic disease.
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Follicular dendritic cell sarcoma is a rare cancer that arises from follicular dendritic cells in lymph nodes or extranodal sites. It is classified as a dendritic cell neoplasm. Most cases occur in cervical or axillary lymph nodes, but extranodal cases can arise in organs like the spleen, gastrointestinal tract, liver, or lungs. Complete surgical resection is the primary treatment, but recurrence rates are high without adjuvant therapy. Prognosis is related to factors like tumor size and location, with intra-abdominal and larger tumors associated with poorer outcomes.
THYROID MALIGNANCIES
This document discusses various types of thyroid malignancies. It begins with an introduction to the epidemiology and classification of thyroid cancers. It then focuses on specific types including papillary thyroid carcinoma, follicular thyroid carcinoma, and the Hürthle cell variant. For each type, it covers characteristic features, diagnosis, staging, surgical management including the role of thyroidectomy and neck dissection, as well as prognosis. The document provides an overview of the clinical approach and management considerations for the main thyroid cancer subtypes.
Thyroid tumors varun
This document discusses thyroid cancer, the most common endocrine malignancy. It accounts for about 3% of cancers and is six times more common in women. The prognosis is excellent for most patients, with an overall 10-year survival rate of 85%. Differentiated thyroid cancers including papillary, follicular, and Hurthle cell carcinomas comprise over 90% of cases and have very favorable outcomes. Despite their generally good prognosis, local recurrence occurs in up to 20% of patients and distant metastases in about 10% at 10 years. Initial management involves surgical removal of the thyroid gland followed by radioactive iodine in most cases.
Thyroid cancer
Thyroid cancers are the most common endocrine malignancies, with papillary carcinoma being the most frequent type at 60% of cases. Papillary carcinoma commonly presents in younger females and has a good prognosis with a 95% 20-year survival rate. Medullary carcinoma is a rare but aggressive type associated with genetic syndromes. Anaplastic carcinoma is the most lethal type with median survival of only 4-5 months. Treatment options depend on tumor size and extent, and may include thyroid lobectomy, total thyroidectomy, radioactive iodine, chemotherapy, or external beam radiation.
Cancer basics
This document provides an overview of cancer basics including epidemiology, common cancers, pathophysiology, symptoms, diagnosis, staging, treatment, prevention and screening. Cancer is characterized by uncontrolled growth of abnormal cells that can invade locally or metastasize. It is one of the leading causes of death worldwide and risk increases with age. Both genetic and environmental factors can contribute to cancer development.
The connection between germline risk variants and somatic mutation patterns i...
Platform session presentation at the 2016 American Society of Human Genetics Conference in Vancouver by Dr. David Goode, Peter MacCallum Cancer Centre, Melbourne, Australia.
Etiology of Cancer
Cancer is caused by various genetic, environmental, and lifestyle factors. The document discusses the major etiological factors of cancer such as tobacco use (25-30% of cancers), certain viral infections, chronic inflammation, chemical and physical carcinogens, dietary components, and obesity. It provides details on how each of these factors can damage DNA and promote uncontrolled cell growth and tumor development. The key message is that lifestyle modifications like quitting tobacco, eating healthy, and staying physically active can prevent up to 65% of cancers.
Sumit testicular tumors
This document provides an overview of testicular cancer, including:
1. Testicular cancer most commonly affects men aged 20-40 and is the most common cancer in that age group. It has very good survival rates due to effective diagnostic techniques, tumor markers, and multimodal treatments.
2. Risk factors include cryptorchidism, Klinefelter syndrome, trauma, and genetic factors. Cryptorchidism increases risk by 14-48 times.
3. Types include seminomas, embryonal carcinomas, teratomas, and others. Seminomas and non-seminomas are treated differently.
4. Diagnosis involves physical exam, ultrasound, tumor markers like AFP and H
MCC 2011 - Slide 4
This document summarizes several genetic syndromes associated with an increased risk of colorectal cancer, including Lynch syndrome, familial adenomatous polyposis (FAP), MYH-associated polyposis, Peutz-Jeghers syndrome, and juvenile polyposis syndrome. It describes the characteristic features, inheritance patterns, cancer risks, and genes involved for each syndrome. Technological advances in genetic sequencing methods are making the identification of causal gene mutations more efficient.
Ewing Sarcoma
This document provides an outline on Ewing sarcoma. It discusses that Ewing sarcoma is a morphologically varied tumor characterized by chromosomal translocations. It most commonly affects children and young adults aged 5-20. The pathology involves a lobulated mass invading the bone marrow and destroying bone. Genetics involve a translocation of the EWS gene with FLI1 transcription factor genes. Diagnosis involves imaging and biopsy to identify the characteristic translocation. Treatment typically involves chemotherapy and surgery or radiation.
Genetic Testing (Eastern Biotech & Life Sciences)
The document discusses various genetic diagnostic tests including cytogenetic tests, molecular tests, and molecular diagnostics for infectious diseases and genetic identification. It describes tests for genetic diseases including somatic rearrangements in cancer, genetic risk factors, pharmacogenetics, and mutations in monogenic diseases. Specific tests and diseases are discussed, along with factors that impact diagnosis such as disease mutations, technology, cost, and organization.
Rare Solid Cancers: An Introduction - Slide 10 - V. Kataja - Rare urological ...
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This document summarizes rare and unusual types of urological cancers. It discusses rare subtypes of renal cell carcinoma defined by their histology and genetic abnormalities. It also describes rare histological variants of bladder cancer and non-urothelial cancers of the bladder such as squamous cell carcinoma, adenocarcinoma, small cell carcinoma, and lymphomas. Finally, it briefly outlines other rare non-urothelial cancers including sarcomas, carcinoid tumors, and other even less common malignancies of the bladder.Similar to Sarcoma (20)
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More from Mohammed Fathy
Thyroid cancer
Thyroid cancer is the most common cancer of the endocrine system. The three main types are papillary, follicular, and medullary thyroid carcinoma. Risk factors include radiation exposure, family history, and genetic conditions. Symptoms may include a neck mass, lymph node swelling, difficulty swallowing or breathing, and diarrhea. Diagnosis involves thyroid imaging tests, biopsy, and genetic testing. Treatment depends on cancer type and stage but commonly includes surgery, radioactive iodine therapy, and medication for differentiated cancers, and surgery plus other therapies for medullary and anaplastic thyroid cancers.
H & N cancer
Head and neck cancer is the 6th most common cancer worldwide. The incidence increases with age, with most cases being diagnosed after age 60. It is also more common in men. Risk factors include cigarette smoking, HPV or EBV infection, alcohol intake, and prior history of head and neck cancer or radiation exposure. The most common type is squamous cell carcinoma. Symptoms depend on the location but may include masses, ulcers, pain, swallowing difficulties, voice changes, and sinus problems. Diagnosis involves endoscopy, imaging tests, and biopsy. Staging depends on tumor size and spread. Treatment options include surgery, radiation therapy, chemotherapy, and biological therapies depending on cancer type and stage.
Testicular cancer
Testicular tumors are the most common cancer in men aged 20-40. They make up about 1% of all cancers in men. Risk factors include family history, undescended testes, infertility, and genetic conditions. The majority are germ cell tumors which are divided into seminomas and non-seminomas. Common symptoms are a painless mass in the scrotum or painful enlargement of the testis. Diagnosis involves blood tests, ultrasound, and CT scans. Staging determines the appropriate treatment which may include surgery, radiation therapy, chemotherapy, or active surveillance depending on the stage and type of tumor.
Bladder cancer
Bladder cancer is the 4th most common cancer in men worldwide, with a peak incidence around age 65. Risk factors include smoking, occupational exposure, and certain infections. Symptoms depend on whether the cancer is non-metastatic or metastatic, and may include blood in the urine, bladder irritability, and pelvic or flank pain. Diagnosis involves cystoscopy, imaging tests, and urine cytology. Treatment depends on the stage, and includes surgery, chemotherapy, and immunotherapy.
DNA repair
DNA repair systems help maintain the integrity of genetic material by correcting damage from mutagens. There are several types of DNA repair mechanisms, including direct damage reversal, mismatch repair, base excision repair, nucleotide excision repair, and recombination repair. Key DNA repair proteins like p53 play an important role in recognizing DNA damage and initiating cell cycle arrest to allow time for repair or inducing apoptosis if damage is irreparable. Double strand breaks are the most difficult to repair and can lead to chromosomal rearrangements if unrepaired.
Apoptosis
Apoptosis is a genetically programmed cell death process that eliminates unwanted cells through activation of caspases. There are two main pathways that activate caspases - the extrinsic death receptor pathway where ligands bind to cell surface receptors, and the intrinsic mitochondrial pathway where increased permeability of mitochondria releases proteins that activate caspase. The Bcl-2 family of proteins regulate apoptosis by integrating both pro-apoptotic and anti-apoptotic signals to determine if a cell should undergo programmed cell death.
Cancer genes
Cancer genes can be divided into two main classes: oncogenes and tumor suppressor genes. Oncogenes promote cell growth and proliferation when activated by mutations, while tumor suppressor genes normally inhibit cell growth and their inactivation allows for unchecked cell division. Dysfunction of multiple cancer genes is typically required for malignant transformation, as an imbalance between oncogene and tumor suppressor gene activity leads to cancer development. Common oncogenes include ras, myc, and HER2, while tumor suppressor genes include RB, p53, and APC. Mutations in DNA repair genes can also contribute to cancer by allowing genetic errors to persist.
Cell cycle
The document discusses the cell cycle and its control. It describes the cell cycle as consisting of interphase (which includes G1, S, and G2 phases) and mitosis (M phase). Interphase involves cell growth and DNA replication, while mitosis involves the division of the cell into two daughter cells. Transition between phases is regulated by cyclins and cyclin-dependent kinases (Cdks). Key checkpoints ensure replication and division occur accurately. The centromere and chromatids are also described along with their behavior in the different mitotic phases.
Cancer metastasis
1) Cancer metastasis is a multi-step process involving invasion of surrounding tissue, transportation through the bloodstream, and formation of tumors in distant organs.
2) Key steps include degradation of the extracellular matrix, entry and survival in the circulation, arrest and extravasation at distant sites, and induction of angiogenesis to establish blood supply for growing tumors.
3) Factors such as matrix metalloproteinases, integrins, and angiogenic growth factors regulate these steps by promoting degradation of barriers, cell adhesion, and new blood vessel formation to enable metastatic tumors to grow.
Hallmarks of cancer
Cancer cells exhibit six hallmarks that allow tumor growth and metastasis. They are: self-sufficiency in growth signals, insensitivity to anti-growth signals, evading apoptosis, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Cancer cells achieve these hallmarks through genetic and epigenetic alterations that disrupt normal cell signaling pathways.
Carcinogenesis
1) Carcinogenesis is a multistep process involving initiation, promotion, and progression. Initiation involves genetic mutations from environmental factors like smoking. Promotion involves clonal expansion driven by growth factors in a reversible stage. Progression results in irreversible aneuploidy and cellular anaplasia.
2) The multihit hypothesis proposes cancer develops through accumulation of multiple genetic mutations in oncogenes and tumor suppressor genes, requiring 4-5 mutations for malignancy.
3) Cancers arise from a single cell of origin (monoclonal) that accumulates mutations over time, leading to intratumor heterogeneity as subclones evolve. Evidence for monoclonal origin includes single enzyme/immunoglob
Diagnostic tools in oncology
This document discusses various diagnostic tools used in oncology, including tumor markers, immunohistochemistry, immunocytology, cytogenetics, molecular diagnosis, and gene expression analysis. It provides details on tumor markers including their definition, classification, factors that affect serum levels, and indications for use. It also discusses immunohistochemistry in detail, covering tumor antigens, immunoreactivity, clinical applications for diagnosis, predicting therapy response and prognosis, and specific carcinoma markers like cytokeratins, CEA, and hormone receptors.
Classification of tumors
There are 9 main classes of cancer: carcinomas, neuroectodermal tumors, sarcomas, hemolymphoid tumors, germ cell tumors, blastemal tumors, embryonal vestigal remnants tumors, uncertain histogenesis tumors, and undifferentiated tumors. Carcinomas are the most common type, arising from epithelial cells. Sarcomas arise from mesenchymal cells and grow more rapidly than carcinomas. Neuroectodermal tumors include tumors of neural, neuroendocrine, and primitive neuroectodermal origin. Hemolymphoid malignancies include lymphomas and leukemias. Other classes are defined by their origin from germ cells, embryonic rests, vestigial remnants
Neoplasia
Neoplasia refers to abnormal tumor growth. There are two main types of tumors: benign tumors, which remain localized and do not recur after removal, and malignant tumors, which invade surrounding tissues and can metastasize to distant sites. Benign tumors are well-defined masses that grow slowly by expansion, while malignant tumors are poorly defined masses that grow rapidly by infiltration. Microscopically, benign tumor cells resemble normal cells and have few blood vessels and mitoses, whereas malignant tumor cells are poorly differentiated with irregular nuclei, frequent mitoses, and necrosis. Malignant tumors can recur after removal and are always a health risk.
Etiology of cancer
This document discusses the etiology of cancer. It classifies etiological factors into extrinsic (chemical, physical, biological) and intrinsic (genetic, hormonal, immune) factors. Extrinsic factors predominate in causing adult cancers while intrinsic factors are more common in pediatric cancers. Major extrinsic factors include chemicals, radiation, infections, and tobacco. Chemicals can directly or indirectly damage DNA. Radiation can directly or indirectly ionize DNA. Certain viruses and bacteria are associated with specific cancer types. The interaction between multiple genetic and environmental factors usually leads to cancer development.
Disorders of Growth
This document discusses various disorders of growth including hypertrophy, hyperplasia, metaplasia, dysplasia, carcinoma in situ, and precancerous lesions.
Hypertrophy is an increase in size of cells and organelles leading to organ enlargement. Hyperplasia is an increase in cell number, often with some hypertrophy. Metaplasia is a reversible change where one adult cell type replaces another of the same category. Dysplasia is a disorder of growth seen as abnormal cell maturation and arrangement. Carcinoma in situ represents severe dysplasia involving the entire epithelium but no invasion. Precancerous lesions are non-malignant conditions that may undergo malignant transformation.
Targeted therapy
Targeted therapies such as tyrosine kinase inhibitors (TKIs), monoclonal antibodies (MABs), and other small molecules are used to treat various cancers. TKIs like gefitinib, erlotinib, sorafenib, sunitinib, and imatinib are indicated for lung cancer, gastrointestinal stromal tumor, kidney cancer, and chronic myeloid leukemia. They can cause diarrhea, rash, hypertension, and myelosuppression. MABs including trastuzumab, rituximab, cetuximab, and bevacizumab are used for breast cancer, lymphoma, colorectal cancer, and lung cancer. Potential toxicities are cardiomyopathy, hypersensitivity
Hormonal treatment
This document summarizes hormonal treatments for breast cancer and prostate cancer. It discusses how hormonal treatments work by interfering with hormone production or action in hormone-dependent cancers. It then provides details on indications, toxicity, and trade names for LHRH agonists, antiestrogens, aromatase inhibitors, and antiandrogens which are commonly used as hormonal treatments for breast cancer, prostate cancer, or both.
Mitotic spindle agents
Mitotic spindle agents such as vinca alkaloids and taxanes inhibit microtubule function during cell division. Vinca alkaloids like vinblastine and vincristine bind to microtubules and inhibit polymerization, while taxanes such as paclitaxel and docetaxel inhibit depolymerization. These agents are used to treat various cancers including lymphomas, breast cancer, lung cancer, and ovarian cancer. Common toxicities include myelosuppression, neuropathy, and alopecia. Proper administration and premedication are important to minimize risks.
Topoisomerase inhibitors
This document discusses topoisomerase inhibitors, which are chemotherapy drugs that work by inhibiting topoisomerase enzymes. It describes several topoisomerase inhibitors including irinotecan, etoposide, and camptothecin. Irinotecan is indicated for non-small cell lung cancer and colorectal cancer. Common toxicities include myelosuppression and diarrhea. Etoposide is used for lung cancer, testicular carcinoma, and lymphoma. It can cause myelosuppression and hypotension if rapidly infused. Guidelines are provided for administering and storing irinotecan and etoposide.
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Cell Therapy Expansion and Challenges in Autoimmune Disease
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In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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The Nervous and Chemical Regulation of Respiration
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Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
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5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
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Sarcoma
- 1. Sarcoma Mohammed Fathy Bayomy, MSc, MD Lecturer of Clinical Oncology Clinical Oncology & Nuclear Medicine Department Faculty of Medicine Zagazig University
- 2. STS represents 1% of all malignant tumors Median age 40-60 Slightly common in males STS outnumber bone sarcomas by ratio of 4:1
- 3. Radiation Chromosomal aberrations Chemical exposure Other risks Phenoxy herbicides Vinyl chloride monomer Dioxin Cyclophosphamide Melphalan Nitrosoureas Anthracyclines Stewart–Treves syndrome HHV8 HIV Paget’s disease of bone Radiation-induced sarcomas
- 4. Hereditary Neurofibro- matosis type I Familial retinoblastoma Osteosarcoma Rb1 gene Chr.13 Gardner’s syndrome Desmoids APC gene Chr. 5 Li–Fraumeni syndrome MPNST NF1 gene Chr.17 Osteosarcoma p53 gene Chr.17 Tuberous sclerosis Gorlin’s syndrome Rhabdo- myosarcoma TSC1 gene Chr.9 Rhabdo- myosarcoma PTCH1 gene Chr.9
- 5. SoftTissueSarcomas(STSs) Alveolar soft part sarcoma Pleomorphic sarcoma (NOS) Fibrosarcoma Liposarcoma Synovial sarcoma Clear cell sarcoma Epithelioid sarcoma Solitary fibrous tumor Hemangio- sarcoma Lymphangio- sarcoma Kaposi sarcoma Rhabdo- myosarcoma Schwannoma MPNST
- 6. Bonesarcomas Visceral Sarcomas Chondro- sarcoma Adamantinoma Osteogenic sarcoma Fibrosarcoma of bone MFH of bone Ewing sarcoma Parosteal sarcoma Giant cell tumor of bone Chordoma Rhabdo- myosarcoma Leiomyo- sarcoma GIST Tumours Hemangio- sarcoma Lymphangio- sarcoma
- 8. Extremities STSs Painless soft tissue swelling H & N STSs Proptosis Masses Neurologic abnormalities GIST tumours Bleeding Haematemesis Blood in faecesAnaemiaUterine sarcoma Vaginal bleeding Lower abdominal pain Retroperitoneal Sarcomas Back pain Lower limb edema Abdominal masses Bone sarcomas Localised soft tissue swelling Localised pain Pathologic fractures Joint effusions Limited & painful adjacent joints movement Constitutional symptoms
- 9. MRI Chest Imaging Pathological confirmation Laboratory Extremities STSs Visceral & Retroperitoneal Sarcomas CT &/or MRI
- 10. Bone Sarcoma Plain X-ray of bone Codman triangle Sun-ray spiculation Onion-skin appearance MRI Bone scan Pathological confirmation Laboratory Bone marrow aspirate and biopsy
- 11. Non-metastatic STSs Surgery Limb-sparing surgery (WLE) Limb amputation Adjuvant Radiotherapy High- grade > 5cm +ve margin Adjuvant Chemotherapy Five cycles of ifosfamide + epirubicin Neoadjuvant Radiotherapy Borderline resectable Definitive Radiotherapy Unresectable Medically inoperable EBRT Brachytherapy &/or Chemotherapy ± Metastatic STSs Surgery Metastasectomy Chemotherapy High-dose ifosfamide Doxorubicin + ifosfamide AD (Adriamycin, Dacrabazine) MAID (Mesna, Adriamycin, Ifosfamide, Dacrabazine) Gemcitabine + Docetaxel Limited number of pulmonary metastases
- 12. Resectable Surgery WLE Radical surgery Adjuvant Radiotherapy High-grade +ve margin Neoadjuvant RT Unresectable Locally Advanced Radiotherapy Palliative Surgery Chemotherapy Retroperitoneal/VisceralSarcomas Gastrointestinalstromaltissuetumours Resectable Surgery Radical surgery Marginally Resectable Adjuvant Targeted Therapy (TKI) Imatinib Neoadjuvant Targeted Therapy (TKI) Imatinib (3- 6months) Surgery Radical surgery Adjuvant Targeted Therapy (TKI) Imatinib Unresectable/Metastatic Targeted Therapy (TKI) Imatinib Sunitinib Regorafenib
- 13. Non-metastaticOsteosarcomaofBone Neodjuvant Chemotherapy High-dose MTX + leucovorin rescue Doxorubicin + Cisplatin Surgery Limb-sparing surgery Limb salvage surgery Osteoarticular resection Adjuvant Chemotherapy Whole bone resection Amputation Definitive Radiotherapy Refuse amputation Metastatic Surgery Metastasectomy Chemotherapy Palliative Radiotherapy Ewing’s Sarcoma Combined-modality approach Induction chemotherapy VAC/IEVACA Local radiotherapy &/or Surgery Consolidation chemotherapy VAC/IEVACA