SOLID TUMORS PPX PRESENTATION.pptx for education

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1. SOLID TUMORS Presenter : barnabas

2. Solid tumors are abnormal masses of tissue that result from the uncontrolled growth of cells. Solid tumors are classified as: malignant tumors premalignant tumors benign tumors

3. Malignant Tumors Develops when abnormal cells divide without control and can invade nearby tissues. Classification carcinomas —malignancies of epithelial origin or cancerous tumors of the internal or external lining of the body. It can begin in the skin or in tissues that line or cover internal organs. There are different subtypes, including adenocarcinoma, basal cell carcinoma, squamous cell carcinoma, transitional cell carcinoma, and ductal carcinoma. Sarcomas —arise from connective or supporting tissues and can transform into soft or synovial sarcoma. Beginning sites: bone, cartilage, fat, muscle, or blood vessels ( angiosarcoma , bone sarcoma, fibroblastic sarcoma, and rhabdomyosarcomas) Lymphomas —affects the cells of the immune system called lymphocytes; cancer begins in infection-fighting lymphocytes found in lymph nodes and spleen, e.g., Hodgkin’s disease and non-Hodgkin’s lymphomas.

4. Blastoma , brain, and spinal cord cancers — blastoma develops mainly in pediatric populations. The rest of the solid tumors arise in the brain, central nervous system, or in the eye. Melanoma —skin malignancy. It can also form in the eyes, and, rarely, in internal organs. Germ cell tumors —usually arise in the ovaries and testes, but can also occur in the brain, abdomen, or chest. Carcinosarcoma —rare malignant solid tumors that arise in different organs and are formed by two types of cancerous cells that have the potential to metastasize: carcinoma

5. Pre-malignant tumors D escribe a condition that may (or is likely to) become cancer. Also called precancerous. Strict monitoring of pre-malignant tumors is important because they have the potential to change into a cancerous tumor. A consequence of the pre-malignant initiation is the production of higher quantities of matrix remodeling proteases and the release of pro- angiogenic , proliferation, and survival factors within the tumor’s microenvironment.

6. Examples of premalignant tumors are Paget's disease. Chronic osteomyelitis. Osteochondroma . Multiple enchondromas . Synovial chondromatosis

7. Benign tumors Benign tumors are a normal, controlled category of non-cancerous solid tumor that can form anywhere in the body. They have almost the same cellular features as the malignant ones, but they do not have the ability to travel elsewhere in the body to form metastatic sites. Even so, a benign tumor can produce damage if it compresses nearby tissue, vital organs, or blood circulation. In rare cases, such as adenoma or colon polyps, this kind of tumor has the capacity to transition to a malignant state.

8. Benign tumors can be classified by: The type of extracellular matrix production. The type of cells. Fibrous and connective tissue of any organ. Localization on the blood vessels.

9. Grading of solid tumors

10. Grading of cancer is denoted by the letter “G . ” It describes a tumor in terms of how abnormal the tumor cells are when compared to the normal cells . Unlike grading, staging is a process of determining the extent to which cancer has grown and spread. Cancer grade is mostly based on factors like the degree of differentiation, mitosis, or architectural features. Each factor is given a score and that score determines the grade of the tumor.  Cancer grading helps to predict how rapidly it will grow and spread .

11. Various methods are there to assign a cancer grade. For instance, the Bloom- Scarff -Richardson grading scheme is most widely used to grade invasive ductal carcinoma of the breast (Carcinoma of No Special Type), The Gleason scoring scheme is used to grade prostate cancer . Generally, there are 3 grades in a cancer grading system, but some types of cancer have their grading systems Low-grade tumors grow and spread slowly, possess a better prognosis than high-grade tumors .

12. Grading of cancer Identifying features Grade 1 The cancer cells look very similar to normal cells and are growing slowly, is assigned for a total score of 3 to 5. This is also called a well-differentiated or low grade. Grade 2 The cells don’t look like normal cells and are growing more quickly than normal, is assigned for a total score of 6 to 7. This is also called a moderately differentiated or intermediate grade. Grade 3 The cancer cells look very abnormal and are growing quickly, is assigned for a total score of 8 to 9. This is called poorly differentiated or high grade. GX Doctors can’t assess the grade. It is also called undetermined grade.a

13. Gleason score prostate cancer grades were described according to the  Gleason Score , a system named for the pathologist who developed it in the 1960s . Dr. Donald Gleason realized that cancerous cells fall into 5 distinct patterns as they change from normal cells to tumor cells . The cells are graded on a scale of 1 to 5.  Grade 1 cells resemble normal prostate tissue. Cells closest to 5 are considered “high-grade” and have mutated so much that they barely resemble normal cells .

14. The pathologist looking at the biopsy sample will assign one Gleason grade to the most predominant pattern in your biopsy and a second Gleason grade to the second most predominant pattern . For example: 3 + 4. The two grades will then be added together to determine your Gleason score .   Theoretically , Gleason scores range from 2-10.  However, since Dr. Gleason’s original classification, pathologists almost never assign scores 2-5, and Gleason scores assigned will range from 6 to 10, with 6 being the lowest grade cancer.

15. What Does it Mean ? A Gleason score of 6 is low grade, 7 is intermediate grade, and a score of 8 to 10 is high grade cancer. Get More Information It’s also important to know whether any cells rated at Gleason grade 5 are present, even in just a small amount, and most pathologists will report this. Having any Gleason grade 5 in your biopsy or prostate puts you at a higher risk of recurrence. But because many prostate cancer cases are extremely slow-growing, the Gleason system didn’t necessarily do a good job of communicating the risks for these cases. Patients with scores of 6 and 7 didn’t have a clear picture of the nature of their particular cancer.

16. How is the Gleason Score Derived? In 2014, the International Society of Urological Pathology released supplementary guidance and a revised prostate cancer grading system, called the Grade Groups. The Grade Group system is simpler, with just five grades, 1 through 5.

17. Grading of Breast cancer

18. There are different "scoring systems" available for determining the grade of a breast cancer. One of these systems is the Nottingham Histologic Score system (also termed “ the Elston -Ellis modification of Scarff -Bloom-Richardson grading system”). In this scoring system, there are three factors that the pathologists take into consideration : the amount of gland formation (the cell “differentiation,” or how well the tumor cells are trying to recreate normal glands) the nuclear features (the degree of " pleomorphism " or how "ugly" the tumor cells look) the mitotic activity (how much the tumor cells are dividing, or proliferating )

19. Each of these features is scored from 1-3, and then the scores is added to give a final total score ranging from 3-9. The final total score is used to determine the grade in the following way: Grade I  tumors have a total score of 3-5 Grade II  tumors have a total score of 6-7 Grade III  tumors have a total score of 8-9

20. Main Routes of Spread of tumors ' Direct spread Lymphatics Vascular spread Transcoelomic spread Perineural spread

21. Direct invasion Growth of cancers is accompanied by progressive infiltration, invasion and destruction by the surrounding tissue. In general they are poorly demarcate by surrounding normal tissue and well defined cleavage plane is lacking .

22. Mechanism of tumour cell invasion and metastasis Factors increasing cell mobility Decreased adhererance of tumour cells Increased growth factor secretion Increased secretion of autocrine motility factor

23. Failure to synthesise basement membrane Factors for facilitation of movement through stroma Secretion of collagenase, cathepsin B, gelatinase Stimulation of stromal cells to secrete stromelysin & alternative extracellular matrix Factors improving tumor cell survival and spread

24. Metastasis is mainly by Lymphatic spread Haematogenous spread Transcoelomic spread

25. Lymphatic spread Carcinomas generally spreads via lymphatics first But sarcomas can use this route too. The pattern of lymph node involvement follows the natural routes of drainage. Carcinoma of breast (upper outer quadrant) spread to axillary lymph nodes, the inner quadrant drain through the nodes along the internal mammaryartery . Later supraclavicular and infraclavicular nodes may become involved.

26. Skip metastasis Local lymph nodes may be bypassed due to venous lymphatic anastomosis or because the inflammation or radiation has obliterated the channels.

27. Regional nodes act as a barrier to further spread of the tumour , at least for a time. The cells, after arrest within the node, may be destroyed. Drainage of tumour cell debris or tumour cell antigens , or both can induce reactive changes . The enlargement of the nodes may be due to 1. Spread of the cancer cells 2. Reactive hyperplasia

28. Vascular spread Haematogenous spread is typical of sarcomas but is seen in carcinoma too. Tumour emboli Permeation

29. Via blood stream spread As tumor emboli Osteosarcomas metastasizing to the lungs Gastrointestinal malignancies metastasizing to the liver

30. Permeation Cords of cells grow along the blood vessels Eg . In renal cell carcinoma the malignant cell cords grow along the vessel walls, renal vein and IVC

31. Haematogenous spread Typical for sarcomas but also used by the carcinomas . Arteries: due to thicker walls are less readily penetrated. But is seen when a tumour pass through pulmonary capillary beds or pulmonary arterio -venous shunts or when pulmonary metastasis give rise to tumour emboli. Venous invasion follow venous flow draining the site of neoplasm . Eg . Liver and lung.( all portal drainage to the liver and all caval blood flows to the lungs) Cancers arising in close proximity to the vertebral column often embolise through the paravertebral plexus . Eg : thyroid and prostate carcinomas

32. Certain cancers have a propensity for venous invasion . Renal cell carcinoma invades branches of renal vein then renal vein and grow along the IVC in a snake like fashion some times reaching the right side of the heart . Hepatocellular carcinoma often penetrate the portal vein Such IV growth may not be accompanied by widespread dissemination .

33. Secondary carcinoma of lung Metastases to the lungs are more common even than primary lung neoplasms simply because so many other primary tumors can metastasize to the lungs .

34. Certain types of tumors have a characteristic patterns of spread. Eg . Prostatic ca is often spread to bone It is thought that the malignant cells and the target organ must express mutually compatible receptors and cell surface adhesion molecules which facilitate cellular anchorage and growth promotion. Hepatic metastasis: portal circulation Pulmonary metastasis: from systemic circulation

35. Transcoelomic spread Peritoneal cavity Pleural cavity Pericardial cavity Subarachnoid cavity Joint space

36. Breast and lung tumors commonly involve pleural space and cause pleural effusion Ovarian and gastric tumors are responsible for peritoneal involvement and cause malignant ascites. There is commonly an inflammatory response in the lining with the accumulation of protein rich fluid and inflammatory cells, proliferation of mesothelial cells and hemorrhage

37. Transcoelomic spread Tumor cells may remain confined to the surface of the abdominal viscera without penetrating into the substance. Some times the mucous secreting tumors of the ovarian or appendiceal carcinoma fill the peritoneal cavity with gelatinous neoplastic mass referred to as pseudomyxoma peritonei .

38. Krukenberg tumour Gastric carcinoma with secondary deposits in the ovary and pouch of Douglas Colonic carcinoma with secondary deposits in the ovary and pouch of Douglas