Neoplasm - basic of oncology
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This document discusses cancer and tumors from several perspectives. It begins by defining key terms like neoplasm, tumor, and cancer. It then covers the classification of tumors based on tissue of origin and behavior. Benign and malignant tumors are compared in terms of characteristics like growth rate, invasion, and metastasis. The metastatic cascade is described as a multi-step process. The major sites of cancer metastasis are outlined. Risk factors for cancer and models of carcinogenesis on the genetic and molecular level are reviewed.
![Human Oncogenic DNA virus
Human Papillomavirus (HPV) High risk type: HPV-16,18,31,33,35 &51
Ca of cervix, anogenital region mouth and larynx,
Low risk type: HPV-6 & 11 condyloma and squamous
papillomas (warts)
Hepatitis B virus (HBV) Hepatocellular Ca
Epstein-Barr virus (EBV) Burkitt lymphoma
Kaposi sacoma herpes virus (KSHV) also called human
herpesvirus-8 [HHV-8] (association with HIV)
Kaposi sarcoma
B-cell lymphoma
Merkel cell virus - a polyoma virus
Human Oncogenic RNA virus
Hepatitis C virus (HCV) Hepatocellular Ca
Human T-cell leukemia virus type 1 (HTLV-1) adult T-cell leukemia/lymphoma (ATLL), (mostly seen in
Japan)
Bacteria
HELICOBACTER PYLORI Gastric adenocarcinoma and
MALT lymphoma (mucosa-associated lymphoid tissue)
Microbial Agents:](https://image.slidesharecdn.com/neoplasm-210906204414/85/Neoplasm-basic-of-oncology-27-320.jpg)
Neoplasm - basic of oncology
- 1. Dr Kamrun Nahar Classified Specialist Pediatric Oncology
- 2. Neoplasia: aka Neoplasm • Neo + Plasia New + Growth. • Tumour Swelling any swelling* • Clinically tumour = neoplasm (technically incorrect..!) • Willis definition: “A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissue and persists in the same manner after cessation of the stimuli which evoked the change” • “Cell division without control” • Irreversible DNA damage, resulting in autonomous growth of abnormal cells *
- 3. CANCER Cancer – derives from the term Latin ―Crab‖ - Because a cancer adheres to any part that it seizes upon in an obstinate manner like the crab. Cancer can start almost anywhere in human body, which is made up of trillions of cells. Normally, human cells grow and divide to form new cells as the body needs them. When cells grow old or become damaged, they die, and new cells take their place. When cancer develops, however, this orderly process breaks down. As cells become more and more abnormal, old or damaged cells survive when they should die, and new cells form when they are not needed. These extra cells can divide without stopping and may form growths called tumors. NCI-2021
- 4. Classification: Classification on Tissue of origin: Classification on Behavior: Other classification: a. Organ of origin b. Naked-eye appearance c. Histology d. Function e. Aetiology
- 5. Classification on tissue of origin: 1. Composed of one parenchymal cell type a. Tumours of epithelial cells – Epithelial Tumor eg. Papilloma, Adenoma, Carcinoma b. Tumors of mesenchymal cell – Mesenchymal Tumor eg. Benign – ‗oma‘ or Malignant --sarcoma Fibroma-fibrosarcoma, lipoma-liposarcoma, leiomyoma-leiomyosarcoma, rhabdomyoma- rhabdomyosarcoma, synovial sarcoma, hemangioma, osteoma, chondroma, leukemia, lymphoma. 2. Mixed tumors: composed of more than one parenchymal cell type usually derived from same/one germ cell layer eg Pleomorphic adenoma, wilm tumor 3. Tumors of totipotent cells – composed of more than one parenchymal cell type usually derived from more than one germ cell layer eg Teratoma
- 6. Tissue of Origin Benign Malignant COMPOSED OF ONE PARENCHYMAL CELL TYPE Tumors of Mesenchymal Origin Connective tissue and derivatives Fibroblast Fibroma Fibrosarcoma Fat cells Lipoma Liposarcoma Cartilage Chondroma Chondrosarcoma Bone tumor Osteoma Osteogenic sarcoma Endothelial and Related Tissues Blood vessels Hemangioma Angiosarcoma Lymph vessels Lymphangioma Lymphangiosarcoma Synovium Synovial sarcoma Mesothelium Mesothelioma Brain coverings Meningioma Invasive meningioma Blood Cells and Related Cells Hematopoietic cells - Leukemias Lymphoid tissue - Lymphomas Smooth muscle Leiomyoma Leiomyosarcoma Striated muscle Rhabdomyoma Rhabdomyosarcoma Tumors of Epithelial Origin Stratified squamous Squamous cell papilloma Squamous cell carcinoma - Basal cells of skin or adnexa Basal cell carcinoma Epithelial lining of glands or ducts Adenoma Adenocarcinoma Papilloma Papillarycarcinomas Cystadenoma Cystadenocarcinoma Respiratory passages Bronchial adenoma Bronchogenic carcinoma Renal epithelium Renal tubular adenoma Renal cell carcinoma Liver cells Liver cell adenoma Hepatocellular carcinoma Urinary tract epithelium (transitional) Transitional-cell papilloma Transitional-cell carcinoma Placental epithelium Hydatidiform mole Choriocarcinoma Testicular epithelium (germ cells) Seminoma Embryonal carcinoma Tumors of Melanocytes Nevus Malignant melanoma MORE THAN ONE NEOPLASTIC CELL TYPE—MIXED TUMORS, USUALLY DERIVED FROM ONE GERM CELLLAYER Salivary glands Pleomorphic adenoma (mixed tumor of salivary origin) Malignant mixed tumor of salivary gland origin Renal anlage Wilms tumor MORE THAN ONE NEOPLASTIC CELL TYPE DERIVED FROM MORE THAN ONE GERM CELLLAYER—TERATOGENOUS Totipotential cells in gonads or in embryonic rests Mature teratoma,dermoid cysts Immature teratoma, teratocarcinoma
- 7. Classification on Behavior: Benign tumor Malignant tumor
- 8. Malignant tumor (Adenocarcinoma) of the colon. Note that compared with the well-formed and normal looking glands characteristic of a benign tumors, the cancerous glands are irregular in shape and size and do not resemble the normal colonic glands. BENIGN MALIGNANT
- 9. Comparisons Between Benign & Malignant Tumor Differentiation/ anaplasia Well-differentiated; tumor cells/structure may resemble normal cells of tissue of origin Some lack of differentiation with anaplasia; structure is often atypical Rate of growth Usually progressive & slow; may come to a standstill or regress; mitotic figures rare and normal Erratic (may be slow to rapid); mitotic figures may be numerous and abnormal Local invasion Usually cohesive and expansile well demarcated masses that do remain localized; not invade or infiltrate surrounding normal tissues. Locally invasive, infiltrating the surrounding normal tissues; sometimes may be seemingly cohesive and expansile Metastasis Absent Frequently present T elomerase Normal Increased
- 10. Comparisons Between Benign & Malignant Tumors Histology Resembles cell of origin Shows failure of cellular differentiation Few mitoses Many mitoses, some are abnormal forms Normal or slight increase in nuclear/cytoplasmic ratio High nuclear/cytoplasmic ratio (1:1) Cells are uniform throughout the tumor Cellular and nuclear Pleiomorphism (variation in size and shape) Encapsulated Not capsulated Stroma well formed Usually poorly formed stroma Haemorrhage and necrosis less tendency Commonly seen Orientation of neoplastic cells are not disturbed Disturbed
- 11. Neoplasm
- 12. Neoplasm Heritable genetic alterations Passed down from progeny of tumor cells Excessive and unregulated proliferation Becomes independent of physiologic growth stimuli (autonomous growth) PERSISTENCE OF TUMOR Neoplasm
- 13. Sequence of events in the invasion of epithelial basement membranes by tumor cells It is an active process: Follows 4 steps; 1.Loosening of intercellular connections between tumor cells that is Detachment or loosening of malignant cells from each other - due reduced ability of adhesiveness of malignant cells & attract inflammatory cells. Occurs due to inactivation of E-cadherin through a variety of pathways. 2. Local degradation of the basement membrane and interstitial connective tissue that is Enzymatic degradation of ECM components - Proteases secreted from tumor cells and inflammatory cells degrade the basement membrane, leads to formation of passage thorugh basement membrane and interstitial connective tissue. The activity of protease regulated by anti-proteases, which may be reduced. 3. Attachment or Binding of tumor cells to proteolytically generated binding sites (ECM) /Changes in attachment of tumor cells to ECM proteins. 4. Locomotion or tumor cell migration- final step of invasion, propelling tumor cells through the degraded basement membranes and zones of matrix proteolysis. - Occurs by chemotactic activity. A. INVASION OR LOCAL SPREAD IN THE SURROUNDING TISSUE Robin 2018,p222
- 14. The metastatic cascade: Sequential steps involved in the hematogenous spread of a tumor CSBRP-July- 2018 Invasion of ECM 1. Clonal Expansion, detachment of malignant cells 2. Invasion of extracellular matrix 3. Intravasation – attachment to and invasion of bm 4. Formation of tumour cell embolus 5. Extravasation of tumor emboli 6. Metastatic deposit, growth & angiogenesis What chemical mediators are involved? • E-Cadherin, β-catenin • Matrix Metalloproteinases (MMP) • Collagenase (not in benign) • Actin Cytoskeleton, chemokine
- 15. Spread of Malignant Tumors ▹ Invasion or local spread in surrounding tissue / Extra-cellular matrix ▹ Metastasis or distant spread- primary tumor spreads to form secondary or metastatic tumor at a distant sites discontinuous with the primary tumor. Routes or pathways of distant spread: 1. Lymphatic spread 2. Haematogenous or blood spread 3. Seeding of body cavities and surfaces SITES a. Liver & Lungs- most frequent sites b. Bone c. Brain d. Skeletal muscle, Spleen – very rarely e. Peritoneal cavity is mostly seeded, but pleural, pericardial, subarachnoid and joint space may be affected.
- 16. Main sites of blood-borne metastasis. (a) Sites of hematogenous metastasis. (b) Metastasis in bone. (c) Metastasis in brain. (d) Metastasis in liver. (e) Metastasis in adrenals. (f) Metastasis in lungs. P R O P E R T I E S
- 17. E P I D E M I O L O G Y Cancer Incidence • Most common tumors in men: 1. Prostate 2. Lung 3. Colorectal • Most common tumors in women: 1. Breast 2. Lung 3. Colon and rectum • Most common tumors in children: 1. Acute Leukemia mostly ALL 2. CNS tumors (eg. Cerebellar astrocytoma) 3. Lymphoma mostly Burkitt’s lymphoma
- 18. Cancer incidence and mortality by site and sex: CSBRP-July- 2012 Excludes basal cell and squamous cell skin cancers and in situ carcinomas, except urinary bladder
- 19. Aetiology of Tumors: A. Carcinogens ------------------------------------- B. Predisposing factors a. Host Factors i. Genetic or Inherited predisposition to cancer ii. Age iii. Hormonal influences iv. Acquired pre malignant or pre-cancerous disorder v. Immune status b. Environmental Factors i. Diet ii. Cigarette smoking iii. Alcohol consumption iv. Air pollution v. Occupational hazards
- 21. Flowchart depicting a simplified scheme of the molecular basis of cancer. CSBRP-July- 2012 Steps of Carcinogenesis: Genetic & Molecular basis of Cancer Carcinogenesis or Tumorogenesis is the process of development of tumor. Mutation lies at the heart of carcinogenesis. It may be either a. acquired – by the action of carcinogens b. inherited How carcinogens affect tumor cell growth
- 22. General schema of events in chemical carcinogenesis CSBRP-July-2016
- 23. Tumor progression and generation of heterogeneity CSBRP-July- 2012
- 24. CARCINOGENIC AGENTS Carcinogenic agents inflict genetic damage, which lies at the heart of carcinogenesis (Process of development of cancer) Three classes of carcinogenic agents have been identified: (1) Chemicals, (2) Radiant energy, and (3) Microbial products CSBRP-July-2018 ETIOLOGY OF CANCER:
- 25. Chemical Carcinogens: Direct-Acting Agents: - require no metabolic conversion to become carcinogenic. - Typically weak carcinogens - Anti Cancer drugs are in this group. Indirect-Acting Agents - require metabolic conversion to an ultimate carcinogen.
- 26. • Ionizing radiation - causes chromosome breakage, chromosome rearrangements, and, less frequently, point mutations, any of which may affect cancer genes and thereby drive carcinogenesis. • UV rays in sunlight (280-320 nm wave length) - - Induce formation of pyrimidine dimers within DNA, leading to mutations that can give rise to squamous cell carcinomas, basal cell carcinoma & melanomas of skin. - More prevalent in areas close to equator having great deal of sunlight eg Australia. Radiation Carcinogens:
- 27. Human Oncogenic DNA virus Human Papillomavirus (HPV) High risk type: HPV-16,18,31,33,35 &51 Ca of cervix, anogenital region mouth and larynx, Low risk type: HPV-6 & 11 condyloma and squamous papillomas (warts) Hepatitis B virus (HBV) Hepatocellular Ca Epstein-Barr virus (EBV) Burkitt lymphoma Kaposi sacoma herpes virus (KSHV) also called human herpesvirus-8 [HHV-8] (association with HIV) Kaposi sarcoma B-cell lymphoma Merkel cell virus - a polyoma virus Human Oncogenic RNA virus Hepatitis C virus (HCV) Hepatocellular Ca Human T-cell leukemia virus type 1 (HTLV-1) adult T-cell leukemia/lymphoma (ATLL), (mostly seen in Japan) Bacteria HELICOBACTER PYLORI Gastric adenocarcinoma and MALT lymphoma (mucosa-associated lymphoid tissue) Microbial Agents:
- 28. Occupational cancer – occurs mostly among who exposed to radiation eg miners of radioactive elements, radiologists, radiotherapists. Common cancers are Thyroid, breast, lungs and salivary glands.
- 29. Agents or Groups ofAgents Human Cancer Site for Which Reasonable Evidence Is Available Typical Use or Occurrence Arsenic and arsenic compounds Lung, skin, hemangiosarcoma Byproduct of metal smelting; component of alloys, electrical and semiconductor devices, medications and herbicides, fungicides, and animal dips Asbestos Lung, mesothelioma; gastrointestinal tract (esophagus, stomach, large intestine) Formerly used for many applications because of fire, heat, and friction resistance; still found in existing construction as well as fire- resistant textiles, friction materials (i.e., brake linings), underlayment and roofing papers, and floor tiles Benzene Leukemia, Hodgkin lymphoma Principal component of light oil; despite known risk, many applications exist in printing and lithography, paint, rubber, dry cleaning, adhesives and coatings, and detergents; formerly widely used as solvent and fumigant Beryllium and beryllium compounds Lung Missile fuel and space vehicles; hardener for lightweight metal alloys, particularly in aerospace applications and nuclear reactors Cadmium and cadmium compounds Prostate Uses include yellow pigments and phosphors; found in solders; used in batteries and as alloy and in metal platings and coatings Chromium compounds Lung Component of metal alloys, paints, pigments, and preservatives Nickel compounds Nose, lung Nickel plating; component of ferrous alloys, ceramics, and batteries; by- product of stainless-steel arc welding Radon and its decay products Lung From decay of minerals containing uranium; potentially serious hazard in quarries and underground mines Vinyl chloride Angiosarcoma, liver CSBRP Refrigerant; monomer for vinyl polymers; adhesive for plastics; formerly inert aerosol propellant in pressurized -July-2012 containers
- 30. INHERITED CANCER SYNDROMES (AUTOSOMAL DOMINANT) Gene Inherited Predisposition RB Retinoblastoma p53 Li-Fraumeni syndrome (various tumors) p16/INK4A Melanoma APC Familial adenomatous polyposis/colon cancer NF1, NF2 Neurofibromatosis 1 and 2 BRCA1, BRCA2 Breast and ovarian tumors MEN1, RET Multiple endocrine neoplasia 1 and 2 MSH2, MLH1, MSH6 Hereditary nonpolyposis colon cancer PTCH Nevoid basal cell carcinoma syndrome PTEN Cowden syndrome (epithelial cancers) LKB1 Peutz-Jegher syndrome (epithelial cancers) VHL Renal cell carcinomas INHERITED AUTOSOMAL RECESSIVE SYNDROMES OF DEFECTIVE DNA REPAIR Xeroderma pigmentosum Ataxia-telangiectasia Bloom syndrome Fanconi anemia FAMILIAL CANCERS Familial clustering of cases, but role of inherited predisposition not clear for each individual Ca of Lung, Colon, Breast, Ovary, Brain Host Factors- Genetic or Inherited predisposition
- 31. Malignancy Due to - Breast carcinoma Increase exposure of oestogen Endometrial carcinoma (adenocarcinoma) Increase excretion of oestogen Prostatic carcinoma Endocrine changes Host Factors- Age Host Factors- Hormonal influences Incidence increases with age, but childhood cancer is rare 1%
- 32. Chronic Inflammatory States and Cancer Pathologic Condition Associated Neoplasm(s) Etiologic Agent Asbestosis, silicosis Mesothelioma, lung carcinoma Asbestos fibers, silica particles Bronchitis Lung carcinoma Silica, asbestos, smoking (nitrosamines, peroxides) Cystitis, bladder inflammation Bladder carcinoma Chronic indwelling urinary catheters Gingivitis, lichen planus Oral squamous cell carcinoma Inflammatory bowel disease Colorectal carcinoma Lichen sclerosis Vulvar squamous cell carcinoma Chronic pancreatitis Pancreatic carcinoma Alcoholism Hereditary pancreatitis Pancreatic carcinoma Mutation in trypsinogen gene Reflux esophagitis, Barrett esophagus Esophageal carcinoma Gastric acids Sialadenitis Salivary gland carcinoma Sjögren syndrome, Hashimoto thyroiditis MALT lymphoma CANCERS ASSOCIATED WITH INFECTIOUS AGENTS Opisthorchis, cholangitis Cholangiosarcoma, colon carcinoma Liver flukes (Opisthorchis viverrini) Bile acids Chronic cholecystitis Gallbladder cancer Bacteria, gallbladder stones Gastritis/ulcers Gastric adenocarcinoma, MALT Helicobacter pylori Hepatitis Hepatocellular carcinoma Hepatitis B and/or C virus Mononucleosis B-cell non-Hodgkin lymphoma and Hodgkin lymphoma Epstein-Barr virus AIDS Non-Hodgkin lymphoma, squamous cell carcinoma, Kaposi sarcoma Human immunodeficiency virus, human herpesvirus type 8 Osteomyelitis Carcinoma in draining sinuses Bacterial infection Pelvic inflammatory disease, chronic cervicitis Ovrian carcinoma, cervical/anal carcinoma Gonorrhea, chlamydia, human papillomavirus Chronic cystitis Bladder, liver, r e C c S t B a R lP c a - J r u c l i y n - o 2 m 0 1 a 2 Schistosomiasis
- 33. Oncogene ▹ Oncogenes are cancer causing genes, A gene that is a mutated (changed) form of a gene (protooncognes) involved in normal cell growth and differentiation. ▹ Proto-oncogenes are transformed into cellular oncogenes (c-oncs) by point mutations or chormosomal rearrangement (translocations & inversions) ▹ Proto-oncogene: A normal gene which, when altered by mutation, becomes an oncogene that can contribute to cancer. It may provide signals for cell division or regulate programmed cell death (apoptosis). ▹ Oncogenes encode proteins called oncoproteins (abnormal gene products), which contribute to uncontrolled cellullar proliferation of neoplasm. Eg philiadelphia chromosome. ▹ Anti-oncogenes or Tumor suppressor genes: they halt cell proliferation and regulate cell growth. Eg p53 gene, RB gene, BRCA-1 & BRCA-2, APC gene, NF-1&2, WT-1, VHL gene.
- 34. Paraneoplastic Syndromes ▹ A group of symptoms that may develop when substances released by some cancer cells disrupt the normal function of surrounding cells and tissue. (NCI) ▹ Symptom complexes that occur in patients with cancer and that cannot be readily explained by local or distant spread of the tumor or by the elaboration of hormones indigenous to the tissue of origin of the tumor are referred to as paraneoplastic syndromes. (Robin, 2018) ▹ They appear in 10% to 15% of patients with cancer. ▹ Importance: 1. may represent the earliest manifestation of an occult neoplasm. 2. associated with significant clinical illness and may even be lethal. 3. may mimic metastatic disease Paraneoplastic syndromes also may manifest as hypercoagulability, leading to venous thrombosis and nonbacterial thrombotic endocarditis
- 36. Staging of cancer Primary tumor (T) - T refers to size and extent of main tumor. Regional lymph nodes (N) - N refers to number of nearby lymph nodes that have cancer. Distant metastasis (M) -M refers to whether cancer has metastasized ; cancer has spread from primary tumor to other parts of body. TX: Main tumor cannot be measured. T0: Main tumor cannot be found. T1, T2, T3, T4: Refers to the size and/or extent of the main tumor. The higher the number after the T, the larger the tumor or the more it has grown into nearby tissues. T's may be further divided to provide more detail, such as T3a and T3b. NX: Cancer in nearby lymph nodes cannot be measured. N0: No cancer in nearby lymph nodes. N1, N2, N3: Refers to the number and location of lymph nodes that contain cancer. The higher the number after the N, the more lymph nodes that contain cancer. MX: Metastasis cannot be measured. M0: Cancer has not spread to other parts of the body. M1: Cancer has spread to other parts of the body. A cancer describe in TNM system as- T1N0MX or T3N1M0. It determines the severity of the lesion and is of clinical significance. The staging of solid cancers is based on the size of the primary lesion, its extent of spread to regional lymph nodes, and the presence or absence of blood borne metastases. Major staging system currently in use is the American Joint Committee on Cancer Staging (AJCC). This system uses a classification called the TNM system— o T for primary tumor, T1 to T4 o N for regional lymph node involvement, and o M for metastases.
- 37. Stage What it means Stage 0 Abnormal cells are present but have not spread to nearby tissue. Also called carcinoma in situ, or CIS. CIS is not cancer, but it may become cancer. Stage I, Stage II, and Stage III Cancer is present. The higher the number, the larger the cancer tumor and the more it has spread into nearby tissues. Stage IV The cancer has spread to distant parts of the body. five main categories: •In situ—Abnormal cells are present but have not spread to nearby tissue. •Localized—Cancer is limited to the place where it started, with no sign that it has spread. •Regional—Cancer has spread to nearby lymph nodes, tissues, or organs. •Distant—Cancer has spread to distant parts of the body. •Unknown—There is not enough information to figure out the stage. Staging method 2: NCI- 2021
- 38. Neoplasia TNM: Staging of tumor: Lung Ca Stage - Features T0 In-situ T1 Primary site T2 Sec. Anat. site T3 Tertiary site T4 Adjacent region N0 No LN mets. N1 Primary LN N2 Seondary LN N3 Tertiary LN M0 No metastases M1 Metastases + Based on - ANATOMY & LYMPHATICS T1 T4
- 39. Staging of cancer: Prostate cancer
- 40. Tumor grade is the description of a tumor based on how abnormal it look under a microscope. It based on the degree of differentiation of the tumor cells and, in some cancers, the number of mitoses and the presence of certain architectural features. It is an indicator of how quickly a tumor is likely to grow and spread. Grading schemes have evolved for each type of malignancy, their criteria can vary between different types of cancer. Some have specific grading system (eg Prostate, Breast Cancer) In general, a lower grade indicates a slower- growing cancer and a higher grade indicates a faster-growing one. GX: Grade cannot be assessed (undetermined grade) G1: Well differentiated (low grade) cancer cells that resemble normal cells and grow and spread at slower rate G2: Moderately differentiated (intermediate grade) cancer cells that does not look like normal cells and are growing faster than normal cells G3: Poorly differentiated (high grade) abnormal looking cells, may lack normal tissue structure and may grow or spread more aggressively G4: Undifferentiated or poorly differentiated,‖ (high grade) Cancer Research UK &NCI The grading system that's usually used is as follows: Grading Classification of cancer
- 41. Neoplasia Stage & Grade of Cancer: Staging: Progression or spread in the body. Grading: Cell differentiation & Rate of growth – Microscopy. Well differentiated (low grade) Adenocarcinoma Grade Undiff. (high grade)
- 42. Neoplasia Prostate Ca : Gleason Grading: 22 Low Grade High Grade
- 43. Clinical effects of Tumor Benign tumor Local effects: Discomfort, mechanical difficulties, pressure on adjacent tissues, obstruction, intussusception, torsion, ulceration, secondary bacterial infection & haemorrhage from surface tumor. Hormonal effects: ▹ Thyroid tumor thyrotoxicosis ▹ Primary adenoma gigantism, acromegaly, cushing syndrome Malignant transformation: Eg. Villous adenoma of colon may transform to adenocarcinoma Malignant tumor Local effects: as like benign + invasion & destruction of surrounding tissues including vital structures, Pain Hematological changes: anemia, neutrophilic leukocytosis, eosinophilia Starvation, Cachexia – action of TNF, IL-1, IFN-γ Hormone production: rare Effects of metastasis- depends on site Impairment of immune response Paraneoplasic syndrome
- 44. How to Diagnose? History Physical examination Laboratory investigation: o Cytology ( i. exfoliative cytology, FNAC) o Histopathology – H&E stain o Tumor markers – biochemical indicators o Immunocytochemistry - specific antibodies use for identify tumor cell antigen o Molecular diagnosis – gene analysis (FISH, ISH etc) o Flow cytometry – measure cell characteristics such as membrane antigens & DNA content of tumour cells.
- 45. Neoplasia When we made a Cancer Diagnosis: e.g. Lung Cancer. We describe it as -- • Mitotic rate – grade. ▹ – Low, Intermediate, high • Maturation of cells ▹ – Well – Mod – Poor – Un diff. • Rate of growth • Differentiation • Local Invasion • Metastasis • Cell of origin • Bronchial Epith. • Tumour Stage.. 1,2,3,4. • Distant Spread.. DIAGNOSIS: (Lung cancer) Bronchogenic Squamous cell Carcinoma, high grade, Stage T2, N1, M1, Liver+ LN++ Grade Stage
- 46. How to treat? Chemotherapy Radiotherapy Surgery Immmunotherapy Targeted therapy Hormone therapy Stem cell transplantation Precision medicine – treating genetic changes How to treat?
- 47. Adenoma – derived from glands but not necessarily reproducing glandular patterns Cystadenoma – form large cystic masses Papilloma – produce papillary patterns that protrude into cystic spaces Polyp – macroscopically visible projection above a mucosal surface N O M E N C L A T U R E 2. Carcinoma – epithelial cell origin 1. Sarcoma - mesenchymal tissue; with little connective tissue stroma fleshy Benign Tumors Malignant Tumors
- 48. LATENT CANCER ‗সুপ্ত‘ A tumor is clinically silent but has the histologic features of carcinoma and does not metastasize. Example: Carcinoma of prostate in elderly. DORMANT CANCER ‗সুপ্ত‘ Dormancy is a stage in cancer progression where the cells cease dividing but survive in a quiescent state while waiting for appropriate environmental conditions to begin proliferation again. Quiescence is the state where cells are not dividing but at arrest in cell cycle in G0-G1. After surgical removal and or chemotherapy there may be no clinically detectable tumor remaining in a patient. In such case, malignant cells may remain occult or dormant at a distant site even for several years and then grow causing signs and symptoms.
- 49. Teratomas: Tumors that are - • Usually benign • Arise from totipotent cells • Tumors that derive from more than one germ cell layer contain tissue derived from ectoderm, endoderm, and mesoderm • Sites: ovaries, testes, anterior mediastinum, pineal gland A, Gross appearance of an opened cystic teratoma of the ovary. Note the presence of hair, sebaceous material, and tooth. B, A microscopic view of a similar tumor shows skin, sebaceous glands, fat cells, and a tract of neural tissue (arrow).