Lecture 39 - Neoplasia V
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Neoplasia By Prof. J.T. Anim Department of Pathology
Lecture V
Topics
Effect of neoplasm on host Effect of host on neoplasm
Tumour immunity Spontaneous regression of malignant tumours
Effect of Neoplasm on Host
Local effects
Mechanical pressure Destruction of tissue (pressure/aggressive invasion) Haemorrhage +/- ulceration Infection
Systemic effects
Fever - TNFα, IL-1 (tumour cells, macrophages) Cachexia (anorexia, malabsorption, anaerobic metabolism of neoplasm, cytokines eg. TNFα = cachexin, IL-6) Effect on immune system (immunosuppression due to tumour itself or treatment; autoimmunity – non-organ specific)
Effect of Neoplasm on Host
Systemic effects Contd.
Haematological effects
Anaemia – iron deficiency, nutritional, excess Rbc destruction (AIHA)(HD, lymphomas, thymoma), MAHA (ca stomach, pancreas, colon, lung, breast), decreased erythropoietin, sideroblastic, red cell aplasia (thymoma) Increased red cell production – ectopic EPO (renal cell carcinoma, cerebellar haemangioblastoma, uterine fibroleiomyoma, liver carcinoma, ovarian carcinoma, lung carcinoma) Effects on platelets and clotting – thrombocytopaenia (immune-mediated destruction); intravascular coagulation (prostate, bronchus, stomach, breast), migratory thrombophlebitis (carcinoma of bronchus, pancreas, stomach, female genitalia, breast – mucin producing tumours)
Effect of Neoplasm on Host
Systemic effects contd
Cutaneous manifestations
Acanthosis nigricans – 75% adenocarcinoma Dermatomyositis – 15% malignancy Exfoliative dermatitis – lymphomas & leukaemias Erythema gyratum repens – carcinoma of bronchus Pigmentation – carcinomatosis Pruritis – lymphomas & some carcinomas Herpes zoster – Hodgkin’s and other lymphomas Acquired ichthyosis – lymphomas Necrolytic migratory erythema - glucagonoma
Effect of Neoplasm on Host
Neuromuscular effects
Myopathy – carcinomas & lymphomas Myasthenic syndrome – oat cell carcinoma of bronchus, thymoma Mixed neuropathy (sensory and motor)
Ca bronchus, stomach, breast, lymphoma, myeloma
Sensory neuropathy – carcinoma of bronchus Autonomic neuropathy Dementia or psychosis Cerebellar degeneration – ca bronchus, ovary, lymphoma Brain stem degeneration PMLE (papova virus) – rarely, lymphoma
Effect of Neoplasm on Host
Systemic effects contd
Endocrine effects
Appropriate hormone production Ectopic/inappropriate hormone production
Non-metastatic osseous and soft tissue changes (clubbing)
Effect of Neoplasm on Host
Inappropriate hormone production by tumour cells
Cushing’s syndrome (ACTH production)
Hyponatremia (ADH-like substance)
Oat cell carcinoma of bronchus Thymoma Carcinoid tumours Medullary carcinoma of thyroid Oat cell carcinoma of bronchus
Hypoglycaemia (insulin-like substance)
Mesothelioma Liver cell carcinoma Adrenal cortical carcinoma
Effect of Neoplasm on Host
Inappropriate hormone production by tumour cells
Hypercalcaemia (prostaglandins, parathormone)
Polycythaemia (haemopoietin production)
Squamous cell carcinoma of bronchus, cervix Renal cell carcinoma Lymphomas Breast carcinoma Renal carcionma Uterine leiomyoma Liver carcinoma Cerebellar haemangioblastoma Nephroblastoma (Wilm’s tumour)
Carcinoid syndrome (5 H-T)
Oat cell carcinoma of bronchus Medullary carcinoma of thyroid
Effect of Neoplasm on Host
Inappropriate hormone production by tumour cells
Gynaecomastia (HCG or human placental lactogen)
Hypertension (excess renin production)
Nephroblastoma
Hyperthyroidism (TSH-like substance)
Anaplastic/squamous cell carcinoma of bronchus Testicular tumours Hepatocellular carcinoma
Hydatidiform mole, choriocarcinoma Orchioblastoma Malignant teratoma of testis
Pigmentation (melanin stimulating hormone - MSH)
Oat cell carcinoma of bronchus
Effect of Host on Neoplasm
Mainly through interaction with host immune system Tumour regression – neuroblastoma, malignant melanoma, regression of metastases after removal of primary Evidence of immunological reaction
Histology – infiltration by lymphocytes, plasma cells, macrophages (correlation with prognosis), granulomas in draining lymph nodes Immune deficiency states and malignancy – Ataxia telangiectasia, Wiskott-Aldrich, Chediak-Higashi and Iatrogenic immunosuppression – lymphomas. ?Provides indirect evidence for cancer immunosurveillance.
Effect of Host on Neoplasm
Evidence of immunological reaction contd.
Rejection of tumour by animal hosts (animal models show CMI controls tumour growth) Tumour associated transplantation antigens (separate from histocompatibility antigens)
Especially irradiation and chemical-induced tumours Virally induced tumours produce TATAs – different from viral structural proteins Spontaneous tumours (animal/human) – less antigens Some neoplasms elicit CMI eg. malignant melanoma, renal carcinoma, astrocytoma
Possible mechanisms of immune tumour cytotoxicity in animal models
Spontaneous Regression
Shrinkage of a neoplasm that may or may not lead to total disappearance.
May be temporary May occur without therapy - spontaneous Has been observed in medical practice and in laboratory
Spontaneous Regression
Series of 176 regressions published between 1900 and 1966
Renal cell carcinoma, neuroblastoma, melanoma, choriocarcinoma, carcinoma of bladder In 41 cases metastases regressed after resection of primary tumour
Spontaneous Regression
Neuroblastoma in infants – can change from malignant to benign
Neuroblastoma - ganglioneuroma
Melanoma – regression suggests an immunological mechanism Haemangiomas – spontaneous regression
Lecture V
Topics
Effect of neoplasm on host Effect of host on neoplasm
Tumour immunity Spontaneous regression of malignant tumours
Effect of Neoplasm on Host
Local effects
Mechanical pressure Destruction of tissue (pressure/aggressive invasion) Haemorrhage +/- ulceration Infection
Systemic effects
Fever - TNFα, IL-1 (tumour cells, macrophages) Cachexia (anorexia, malabsorption, anaerobic metabolism of neoplasm, cytokines eg. TNFα = cachexin, IL-6) Effect on immune system (immunosuppression due to tumour itself or treatment; autoimmunity – non-organ specific)
Effect of Neoplasm on Host
Systemic effects Contd.
Haematological effects
Anaemia – iron deficiency, nutritional, excess Rbc destruction (AIHA)(HD, lymphomas, thymoma), MAHA (ca stomach, pancreas, colon, lung, breast), decreased erythropoietin, sideroblastic, red cell aplasia (thymoma) Increased red cell production – ectopic EPO (renal cell carcinoma, cerebellar haemangioblastoma, uterine fibroleiomyoma, liver carcinoma, ovarian carcinoma, lung carcinoma) Effects on platelets and clotting – thrombocytopaenia (immune-mediated destruction); intravascular coagulation (prostate, bronchus, stomach, breast), migratory thrombophlebitis (carcinoma of bronchus, pancreas, stomach, female genitalia, breast – mucin producing tumours)
Effect of Neoplasm on Host
Systemic effects contd
Cutaneous manifestations
Acanthosis nigricans – 75% adenocarcinoma Dermatomyositis – 15% malignancy Exfoliative dermatitis – lymphomas & leukaemias Erythema gyratum repens – carcinoma of bronchus Pigmentation – carcinomatosis Pruritis – lymphomas & some carcinomas Herpes zoster – Hodgkin’s and other lymphomas Acquired ichthyosis – lymphomas Necrolytic migratory erythema - glucagonoma
Effect of Neoplasm on Host
Neuromuscular effects
Myopathy – carcinomas & lymphomas Myasthenic syndrome – oat cell carcinoma of bronchus, thymoma Mixed neuropathy (sensory and motor)
Ca bronchus, stomach, breast, lymphoma, myeloma
Sensory neuropathy – carcinoma of bronchus Autonomic neuropathy Dementia or psychosis Cerebellar degeneration – ca bronchus, ovary, lymphoma Brain stem degeneration PMLE (papova virus) – rarely, lymphoma
Effect of Neoplasm on Host
Systemic effects contd
Endocrine effects
Appropriate hormone production Ectopic/inappropriate hormone production
Non-metastatic osseous and soft tissue changes (clubbing)
Effect of Neoplasm on Host
Inappropriate hormone production by tumour cells
Cushing’s syndrome (ACTH production)
Hyponatremia (ADH-like substance)
Oat cell carcinoma of bronchus Thymoma Carcinoid tumours Medullary carcinoma of thyroid Oat cell carcinoma of bronchus
Hypoglycaemia (insulin-like substance)
Mesothelioma Liver cell carcinoma Adrenal cortical carcinoma
Effect of Neoplasm on Host
Inappropriate hormone production by tumour cells
Hypercalcaemia (prostaglandins, parathormone)
Polycythaemia (haemopoietin production)
Squamous cell carcinoma of bronchus, cervix Renal cell carcinoma Lymphomas Breast carcinoma Renal carcionma Uterine leiomyoma Liver carcinoma Cerebellar haemangioblastoma Nephroblastoma (Wilm’s tumour)
Carcinoid syndrome (5 H-T)
Oat cell carcinoma of bronchus Medullary carcinoma of thyroid
Effect of Neoplasm on Host
Inappropriate hormone production by tumour cells
Gynaecomastia (HCG or human placental lactogen)
Hypertension (excess renin production)
Nephroblastoma
Hyperthyroidism (TSH-like substance)
Anaplastic/squamous cell carcinoma of bronchus Testicular tumours Hepatocellular carcinoma
Hydatidiform mole, choriocarcinoma Orchioblastoma Malignant teratoma of testis
Pigmentation (melanin stimulating hormone - MSH)
Oat cell carcinoma of bronchus
Effect of Host on Neoplasm
Mainly through interaction with host immune system Tumour regression – neuroblastoma, malignant melanoma, regression of metastases after removal of primary Evidence of immunological reaction
Histology – infiltration by lymphocytes, plasma cells, macrophages (correlation with prognosis), granulomas in draining lymph nodes Immune deficiency states and malignancy – Ataxia telangiectasia, Wiskott-Aldrich, Chediak-Higashi and Iatrogenic immunosuppression – lymphomas. ?Provides indirect evidence for cancer immunosurveillance.
Effect of Host on Neoplasm
Evidence of immunological reaction contd.
Rejection of tumour by animal hosts (animal models show CMI controls tumour growth) Tumour associated transplantation antigens (separate from histocompatibility antigens)
Especially irradiation and chemical-induced tumours Virally induced tumours produce TATAs – different from viral structural proteins Spontaneous tumours (animal/human) – less antigens Some neoplasms elicit CMI eg. malignant melanoma, renal carcinoma, astrocytoma
Possible mechanisms of immune tumour cytotoxicity in animal models
Spontaneous Regression
Shrinkage of a neoplasm that may or may not lead to total disappearance.
May be temporary May occur without therapy - spontaneous Has been observed in medical practice and in laboratory
Spontaneous Regression
Series of 176 regressions published between 1900 and 1966
Renal cell carcinoma, neuroblastoma, melanoma, choriocarcinoma, carcinoma of bladder In 41 cases metastases regressed after resection of primary tumour
Spontaneous Regression
Neuroblastoma in infants – can change from malignant to benign
Neuroblastoma - ganglioneuroma
Melanoma – regression suggests an immunological mechanism Haemangiomas – spontaneous regression
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