Which of the following is an oncogene?
Which of the following has tumor promoting effect?
Which chromosomal translocation is associated with follicular thyroid carcinoma?
Calcified pulmonary metastasis is seen in which carcinoma?
Which of the following is commonly associated with osteolytic metastasis?
Which of the following is a premalignant lesion for carcinoma of the rectum?
The most common subtype of Non-Hodgkin's lymphoma in India is:
What is a hamartoma?
All are growth promoting oncogenes except ?
Flexner-Wintersteiner rosette is seen in-
Explanation: ***RAS*** - RAS is an **oncogene**, not a tumor suppressor gene; it promotes cell proliferation and survival [1]. - Mutations in RAS lead to uncontrolled cell division, contributing to various cancers. *p53* - p53 is a crucial **tumor suppressor gene** responsible for regulating the cell cycle and preventing tumor formation [1,2]. - It functions by inducing apoptosis in cells with damaged DNA, preventing their proliferation [2]. *WT-1* - WT-1 is a **tumor suppressor gene** associated with Wilms' tumor and regulates kidney and gonadal development. - It plays a role in cell growth and differentiation, preventing tumorigenesis when functioning correctly. *Rb* - The Rb gene encodes the **retinoblastoma protein**, a key tumor suppressor that regulates the cell cycle by inhibiting cell division [1,2]. - Loss of Rb function is primarily associated with retinoblastoma and other cancers, indicating its critical role in tumor suppression [1,2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-301. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 227-228.
Explanation: ***MYC*** - **MYC** is a well-known **oncogene** that promotes cell growth and proliferation, thus contributing to tumorigenesis [1,2,5]. - Its expression is often **dysregulated** in various tumors, leading to increased **cellular metabolism** and survival, facilitating cancer progression [1,4]. *BRAC* - Refers to **BRCA1 and BRCA2** genes, which are primarily associated with **tumor suppression** and repair of DNA double-strand breaks. - Mutations in these genes lead to a higher risk of cancers but do not directly promote tumor growth. *RB* - The **RB gene** encodes a protein that functions as a tumor suppressor by inhibiting cell cycle progression from G1 to S phase. - Its loss leads to **uncontrolled cell division**, but it does not promote tumors directly; rather, it prevents their formation. *p16* - **p16** is a cyclin-dependent kinase inhibitor that plays a critical role in regulating the cell cycle, thereby acting as a **tumor suppressor**. - Its loss or dysfunction is often implicated in cell cycle dysregulation but does not promote tumors itself. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 296-297. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 292. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 228-229. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 229-230. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 292-293.
Explanation: ***PAX8 - PPARγ*** - The **PAX8-PPARγ fusion oncogene** is a well-established molecular marker directly associated with **follicular thyroid carcinoma (FTC)**. - This translocation leads to the expression of a fusion protein that contributes to **thyroid cell proliferation** and **tumorigenesis**. *ALK - NPM1* - The **ALK-NPM1 fusion** is primarily observed in some types of **anaplastic large cell lymphoma**, not thyroid cancers. - This translocation typically results in an **activated anaplastic lymphoma kinase (ALK)**, driving lymphoproliferation. *ETV6 - NTRK3* - The **ETV6-NTRK3 rearrangement** is characteristic of **secretory carcinoma** (formerly mammary analogue secretory carcinoma), often affecting salivary glands, and is not a common finding in thyroid malignancies. - This fusion leads to the activation of the **NTRK3 receptor tyrosine kinase**, involved in cell growth and survival. *RET - PTC1* - The **RET-PTC1 rearrangement (RET/papillary thyroid carcinoma 1)** is specifically associated with **papillary thyroid carcinoma (PTC)**, which is histologically distinct from follicular thyroid carcinoma. - This fusion activates the **RET proto-oncogene**, promoting cell proliferation and survival in papillary thyroid cancer.
Explanation: ***Thyroid carcinoma*** - **Papillary** and **medullary thyroid carcinomas** can produce **calcified pulmonary metastases**. - In **papillary thyroid cancer**, calcification occurs due to **psammoma bodies** (concentrically laminated calcified structures). - In **medullary thyroid cancer**, calcification can occur through **dystrophic calcification** within the tumor tissue. - Other common causes of calcified lung metastases include **osteosarcoma** and **chondrosarcoma**. *Pancreatic carcinoma* - Pancreatic carcinoma rarely causes **calcified pulmonary metastases**; metastatic lesions are typically **non-calcified**. - Metastases are more commonly found in the **liver** and **peritoneum**. - Primary pancreatic tumors may show calcification, but metastases usually do not. *Endometrial carcinoma* - Endometrial carcinoma metastases to the lungs are usually **non-calcified** and appear as **soft tissue nodules**. - While it can metastasize to the lungs, **calcification** is not a typical feature of its pulmonary spread. *None of the options* - This option is incorrect because **thyroid carcinoma** (particularly papillary type) is a well-recognized cause of **calcified pulmonary metastases**. - Among epithelial malignancies, thyroid carcinoma is one of the classic causes of this finding.
Explanation: ### Breast cancer - **Breast cancer** is the **most common** primary malignancy causing osteolytic bone metastases in clinical practice due to its **high prevalence** and frequent bone tropism [1]. - Breast cancer metastases stimulate **osteoclast activity** leading to bone destruction and **purely lytic lesions** in approximately 80% of cases. - The high incidence of breast cancer makes it the **leading cause** of osteolytic metastases overall. *Renal cell carcinoma* - **Renal cell carcinoma (RCC)** characteristically produces **highly osteolytic, aggressive, and vascular** bone metastases [1]. - While RCC metastases are predominantly lytic, they are **less common** than breast cancer metastases due to lower disease prevalence. - RCC bone metastases often present with **expansile lesions** and high risk of pathological fractures. *Thyroid cancer* - **Thyroid cancer** (especially follicular subtype) produces predominantly **osteolytic metastases** that are often vascular [1]. - However, bone metastases from thyroid cancer are **relatively uncommon** compared to breast cancer due to the rarity of metastatic thyroid disease. *Lung cancer* - Lung cancer bone metastases are typically **mixed osteolytic-osteoblastic lesions** rather than purely lytic. - While common, lung cancer is **less characteristically associated with pure osteolytic lesions** compared to breast, renal, or thyroid cancers [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 671-672.
Explanation: ***Familial polyposis*** - Familial adenomatous polyposis (FAP) is characterized by numerous **adenomatous polyps** in the colon and rectum, which have a high risk of progressing to colorectal cancer [1]. - Individuals with FAP are at significant risk for developing **carcinoma rectum** at a young age if the condition is not managed properly [1]. *Juvenile polyp* - Juvenile polyps are generally **benign** and occur in children, with a very low risk of malignancy. - They do not contribute significantly to the risk of **carcinoma rectum** like adenomatous polyps do. *Adenomatous polyp* - While adenomatous polyps are indeed premalignant [1], the term **Familial polyposis** indicates a hereditary condition that specifically has a higher and more defined risk for rectal carcinoma. - Adenomatous polyps can occur sporadically and do not imply a genetic syndrome like familial polyposis. *FAP* - FAP refers specifically to **familial adenomatous polyposis** [1], which is the same concept as familial polyposis but less encompassed in terms of broad assessment in this context. - It is important to note that **familial polyposis** is a broader term that includes conditions like FAP and indicates a significant risk factor for rectal cancer [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 817, 821-822.
Explanation: ***Diffuse large B cell lymphoma*** - It is the most common subtype of **Non-Hodgkin's lymphoma** observed in India, reflecting a higher prevalence in the population. - Characterized by **aggressive clinical behavior** [1] and typically presents as a rapidly enlarging mass, often involving lymph nodes or extranodal sites. *Burkitt's lymphoma* - This subtype is known for its **high proliferation rate** and is more common in specific demographics, such as children and immunocompromised individuals. - It typically presents with **jaw lesions** or abdominal masses, which is not typical in the broader Indian population. *Diffuse small cell lymphocytic lymphoma* - More accurately classified as **chronic lymphocytic leukemia** (CLL), it is not the most common subtype of Non-Hodgkin's lymphoma. - Characterized by a **milder clinical course** and presents with lymphocytosis in peripheral blood, lacking aggressive features. *Follicular lymphoma* - This is usually a **low-grade lymphoma** associated with **indolent behavior** and may not be the most commonly diagnosed subtype in India. - It typically involves multiple lymph nodes and is characterized by **nodular patterns on histology**, making it less prevalent than diffuse large B cell lymphoma. Follicular lymphoma is rare in Asian populations [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 563-564. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 602-604.
Explanation: ***Development malformation*** - A **hamartoma** is a type of **benign tumor** that consists of an overgrowth of mature cells, representing a **developmental malformation** [1]. - It is formed from tissues that are normally present in the affected organ but are disorganized, leading to a characteristic appearance. *Malignant tumor* - Hamartomas are classified as **benign tumors** [1], not malignant, as they do not invade surrounding tissues or metastasize. - Despite being a growth, they do not exhibit the aggressive characteristics of malignant tumors. *Hemorrhage in vessel* - Hemorrhage refers to bleeding within a vessel and is unrelated to the definition or nature of a **hamartoma**. - Hamartomas do not consist of blood or bleeding; instead, they involve disorganized tissue growth. *Metastatic tissue* - Metastatic tissue refers to cancerous cells that have spread from their original site, which contrasts with the **non-cancerous** nature of hamartomas [1]. - Hamartomas do not involve the spread of cancer cells, but rather a **local abnormality** in tissue arrangement. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 481-482.
Explanation: ***TGF-p*** - **TGF-p (Transforming Growth Factor beta)** is primarily known as a **growth inhibitory** factor rather than a promoting oncogene. - It plays a crucial role in **cell differentiation**, **apoptosis**, and inhibits cell proliferation, counteracting the effects of other oncogenes. *TGF-a* - **TGF-a (Transforming Growth Factor alpha)** is a **growth factor** that stimulates cell proliferation and is involved in various cancers [1][2]. - It binds to the **EGF receptor**, promoting growth and tumor development. *PDGF* - **PDGF (Platelet-Derived Growth Factor)** acts as a potent **mitogen** for connective tissue cells and is involved in wound healing and tumor growth [2][4]. - It plays a central role in promoting cell proliferation and migration, contributing to cancer progression [4]. *FGF* - **FGF (Fibroblast Growth Factor)** promotes mitosis and is crucial in **angiogenesis**, wound healing, and several developmental processes [2]. - Its overexpression is linked to various tumors, making it a significant oncogenic growth promoter [2][3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 30-31. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 292. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 292-293. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 31-32.
Explanation: ***Retinoblastoma*** - Flexner-Wintersteiner rosettes are **characteristic histological features** seen in retinoblastoma, indicating retinal differentiation [1]. - These rosettes reflect the **presence of photoreceptor-like structures**, which are specific to this type of tumor [1]. *Hepatoblastoma* - Histologically, hepatoblastoma shows **primitive epithelial cells** and **mixed patterns**, not Flexner-Wintersteiner rosettes. - It is primarily associated with **liver** and does not present with retinal differentiation. *Nephroblastoma* - Nephroblastoma, or Wilms tumor, typically exhibits **triphasic histology** (epithelial, stromal, and blastemal components) without rosette formation. - It primarily affects the **kidney** and does not involve the retina. *Neuroblastoma* - Neuroblastoma is characterized by **small round blue cells** and **neuroid differentiation** but lacks Flexner-Wintersteiner rosettes. - This tumor usually arises in the **adrenal glands** or sympathetic nervous system, not in retinal tissue. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Eye, p. 1342.
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