Neoplasia Practice Questions

Q: A biopsy from a breast lump shows small, uniform cells that are estrogen receptor positive. This finding is most consistent with which type of breast cancer?

Lobular carcinoma. ***Lobular carcinoma*** - Characterized by **small, uniform cells** that are often estrogen receptor positive, aligning with the biopsy findings [1]. - Typically, **invasive lobular carcinoma** may present with subtle features and often leads to bilateral involvement. *Triple-negative breast cancer* - Defined by the absence of **estrogen receptors**, **progesterone receptors**, and **HER2/neu**, which contradicts the positive estrogen receptor finding. - Often associated with **high histological grade** and a more aggressive behavior compared to other types. *Ductal carcinoma in situ* - Although it can show **positive estrogen receptors**, it is primarily characterized by **ductal involvement** without invasion into surrounding tissue. - Typically presents with **calcifications** on mammography rather than the solid tumor appearance noted in this biopsy. *Inflammatory breast cancer* - Features **cutaneous changes** and **lymphedema** rather than small, uniform cells; it causes a more aggressive and diffuse breast distortion. - Rarely presents with estrogen receptor positivity, particularly when compared to lobular carcinoma's characteristics. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1068-1069.

Q: A biopsy shows tumor cells with an increased nuclear-to-cytoplasmic ratio, individual cell keratinization, and intercellular bridges. What is this characteristic of?

Squamous cell carcinoma. ***Squamous cell carcinoma*** - **Increased nuclear-to-cytoplasmic ratio**, **individual cell keratinization (dyskeratosis)**, and **intercellular bridges** are pathognomonic histological features of squamous cell carcinoma [1]. - These findings indicate **squamous differentiation** with cellular atypia and loss of normal maturation, characteristic of this malignancy [2]. - Keratin pearl formation may also be present in well-differentiated tumors [1]. *Lymphoma* - Lymphoma typically presents with a proliferation of **monomorphic lymphoid cells**, often forming diffuse sheets or nodules. - While it can show an increased nuclear-to-cytoplasmic ratio, it lacks squamous differentiation features like keratinization and intercellular bridges. *Basal cell carcinoma* - Characterized by nests of **basaloid cells** with **peripheral palisading** and retraction artifact [3]. - It arises from the basal layer of the epidermis and does **not show squamous differentiation** such as keratinization or intercellular bridges [3]. *Melanoma* - Melanoma cells are typically large with prominent nuclei and nucleoli, often containing abundant cytoplasm and **melanin pigmentation**. - It represents a proliferation of melanocytes and does not exhibit squamous features like keratinization or intercellular bridges. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 643-645. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 723. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 643-644.

Q: How does a nucleotide excision repair (NER) defect lead to an increased risk of skin cancer?

Inability to repair UV-induced DNA damage. ***Inability to repair UV-induced DNA damage.*** - Nucleotide excision repair (NER) is the primary pathway for removing **bulky DNA adducts**, such as **pyrimidine dimers** caused by ultraviolet (UV) radiation [1]. - A defect in NER means these **mutagenic lesions** accumulate, leading to **genomic instability** and an increased likelihood of oncogenic mutations in skin cells [1]. *Increased oxidative damage* - While oxidative damage can contribute to cancer, it is primarily repaired by **base excision repair (BER)**, not nucleotide excision repair (NER). - NER plays a minor role in addressing **oxidative DNA lesions**, which are typically smaller than the bulky adducts targeted by NER. *Impaired mismatch repair* - Mismatch repair (MMR) is a correction system that fixes errors made during **DNA replication**, such as incorrect base pairing or small insertions/deletions. - Defects in MMR are associated with hereditary nonpolyposis colorectal cancer (HNPCC), rather than the increased skin cancer risk seen with NER defects. *Defective base excision repair* - Base excision repair (BER) is responsible for removing **small, non-bulky DNA lesions**, such as modified bases, abasic sites, and single-strand breaks. - While critical for genome integrity, its defect does not directly explain the heightened **UV-induced skin cancer risk**, which is characteristic of NER impairment. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-333.

Q: A woman presents with massive pulmonary thromboembolism. Which of the following, based on findings from a subsequent liver autopsy, is the most likely underlying cause of the pulmonary embolism?

Colonic adenocarcinoma with metastasis. ***Colonic adenocarcinoma with metastasis*** - The presentation of massive pulmonary thromboembolism can be associated with **malignancy** [3], particularly from **colonic sources**. - This diagnosis is consistent with **liver metastasis** [1][2], which often results in **pulmonary emboli** due to increased risk of thrombosis. *Locally invaded hepatocellular carcinoma* - Hepatocellular carcinoma usually presents with **liver dysfunction** and **weight loss**, not specifically massive PE. - While it can invade surrounding tissues, it does not typically lead to **pulmonary embolism** from liver pathology. *Metastasis from PE* - This option is misleading as **pulmonary embolism** itself does not cause **metastatic disease**; it often results from existing malignancies. - The concept of metastasis is associated with bloodstream transport of cancer cells [2], not the origin of PE. *Angiosarcoma* - Angiosarcoma is a rare vascular tumor that typically causes **massive bleeding** rather than thromboembolic events. - Its clinical presentation is distinct and not typically linked to **colonic malignancies** or massive PE. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 398-399. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 282. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 705.

Q: What is the primary molecular defect in xeroderma pigmentosa?

DNA repair defect. ***DNA repair defect*** - Xeroderma pigmentosum is characterized by a hereditary defect in **DNA repair mechanisms**, specifically **nucleotide excision repair (NER)** [1]. - This defect prevents the proper removal of **pyrimidine dimers** and other DNA damage caused by **ultraviolet (UV) light**, leading to an accumulation of mutations [1]. *Autosomal recessive* - While xeroderma pigmentosum is indeed inherited in an **autosomal recessive** pattern, this describes its inheritance rather than the fundamental molecular defect [1]. - The core pathophysiological issue is the inability to repair damaged DNA, which then manifests due to this recessive genetic trait. *Poor long term prognosis* - Patients with xeroderma pigmentosum do have a **poor long-term prognosis** due to a significantly increased risk of developing various cancers, especially **skin cancers** and potentially internal malignancies. - However, this is a consequence of the underlying molecular defect (DNA repair) rather than the primary mechanism itself. *Pyrimidine dimers* - **Pyrimidine dimers** (specifically **thymine dimers**) are indeed a key type of DNA damage that accumulates in xeroderma pigmentosum due to the defective repair mechanism [1]. - While their presence is central to the disease's pathology, the direct cause is the **failure to repair them**, which points to the underlying DNA repair defect. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-323, 332-333.

Q: Retinoblastomas are characterized by which of the following features?

Flexner-Wintersteiner rosettes and Fleurettes. ***None*** - Retinoblastomas exhibit **various histopathological features** including necrosis, small round cells, and pseudorosettes. - The statement "all of the following" implies the other options are present, hence "none" fits as the correct answer because it negates the presence of any aberrant features. *Necrosis* - Retinoblastomas typically show areas of **necrosis** due to rapid cell proliferation outpacing blood supply [1]. - The presence of necrosis is a common association in many cancer types, including retinoblastoma. *Small round cells* - The tumor is characterized by **small round blue cells** on histological examination, which is a hallmark feature of retinoblastomas. - This cytological appearance helps differentiate retinoblastoma from other retinal tumors. *Pseudorosettes and Fleurettes* - Pseudorosettes and **fleurettes** are indicative of **certain neuroectodermal tumors** but are not diagnostic features of retinoblastoma. - These structures are more associated with other tumors like medulloblastoma rather than retinoblastoma. Retinoblastomas characteristically show Flexner-Wintersteiner rosettes instead [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Eye, p. 1342.

Q: Which of the following statements about VEGF is false?

Inhibits angiogenesis. ***Inhibits angiogenesis*** - **Incorrect statement**, as VEGF (Vascular Endothelial Growth Factor) actually **promotes angiogenesis**, fostering the development of new blood vessels. - It plays a crucial role in **vascular permeability** and is vital for **tumor growth and survival** [1]. *Highly specific for endothelium* - VEGF is indeed **specific for endothelial cells**, acting primarily on these cells to stimulate their proliferation and migration. - This specificity is central to its role in **angiogenesis**, targeting the endothelial cells of blood vessels [1]. *Hypoxia potentiates its expression* - Contrary to the statement, **hypoxia** (low oxygen levels) actually increases VEGF expression as part of the body's mechanism to enhance oxygen delivery through new vessel formation [1]. - This response is critical in **tumor biology** where rapid cell growth often leads to low oxygen environments. *Helps in tumor metastasis* - VEGF contributes to **tumor progression** by aiding in angiogenesis, but it does not directly cause tumor metastasis. - Metastasis is more related to **cellular adhesion** and **migratory** properties rather than just vascular growth. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 313-314.

Q: Immunohistochemical marker for sentinel node biopsy in breast carcinoma?

Cytokeratin. ***Cytokeratin*** - **Cytokeratin** is a specific marker for **epithelial cells**, including those of breast carcinoma, making it ideal for detecting micrometastases in lymph nodes. - Immunohistochemistry with cytokeratin antibodies can identify even small clusters of tumor cells not visible on routine hematoxylin and eosin (H&E) staining. *Vimentin* - **Vimentin** is a filament protein characteristic of **mesenchymal cells**, such as fibroblasts and endothelial cells, not epithelial carcinoma cells. - While some carcinomas can exhibit **epithelial-mesenchymal transition (EMT)** and express vimentin, it is not the primary or most specific marker for detecting breast carcinoma cells in lymph nodes. *Calretinin* - **Calretinin** is a marker typically used to identify **mesothelial cells** and is often employed in the diagnosis of **mesothelioma**. - It is not expressed by breast carcinoma cells and would not be useful for detecting metastatic disease in sentinel lymph nodes. *CD45* - **CD45** (Leukocyte Common Antigen) is a specific marker for **hematopoietic cells**, including lymphocytes, macrophages, and other immune cells. - It is used to identify and distinguish lymphoid infiltrates but is not expressed by breast carcinoma cells, making it unsuitable for this purpose.

Q: What is the most common tumor suppressor gene involved in carcinogenesis?

p53. ***p53*** [1][2] - The **p53 gene** is widely recognized as the most common tumor suppressor gene associated with various cancers, particularly due to its role in apoptosis and cell cycle regulation [1][2]. - Mutations in **p53** are found in over **50%** of human tumors, highlighting its critical role in cancer genesis [2]. *Rb* - While the **Rb gene** is significant in preventing retinoblastoma and other cancers, it is less commonly mutated overall compared to p53 [1]. - Rb primarily regulates the **cell cycle**, particularly the transition from G1 to S phase, but its involvement in cancer is more limited in scope [2]. *p16* - **p16** acts as an inhibitor of cyclin-dependent kinases but is primarily associated with specific cancers such as melanoma, not broadly across all cancers. - It serves as a cell cycle checkpoint but is not as ubiquitous a tumor suppressor as p53. *p73* - Although **p73** shares structural similarities with p53 and has roles in apoptosis, it is not as frequently implicated in cancer development. - Its functions are more related to developmental processes and it does not have the same high mutation rates seen in tumors as p53. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-298, 302-304. [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.

Question 1

A biopsy from a breast lump shows small, uniform cells that are estrogen receptor positive. This finding is most consistent with which type of breast cancer?

Accepted Answer

Lobular carcinoma

Answer

Ductal carcinoma in situ

Answer

Inflammatory breast cancer

Answer

Triple-negative breast cancer

Question 2

A biopsy shows tumor cells with an increased nuclear-to-cytoplasmic ratio, individual cell keratinization, and intercellular bridges. What is this characteristic of?

Accepted Answer

Squamous cell carcinoma

Answer

Lymphoma

Answer

Basal cell carcinoma

Answer

Melanoma

Question 3

How does a nucleotide excision repair (NER) defect lead to an increased risk of skin cancer?

Accepted Answer

Inability to repair UV-induced DNA damage

Answer

Increased oxidative damage

Answer

Impaired mismatch repair

Answer

Defective base excision repair

Question 4

What is the consequence of defects in DNA repair enzymes on genomic stability in cancer development?

Accepted Answer

Increased mutation rate due to genomic instability.

Answer

Enhanced DNA repair mechanisms.

Answer

Increased cell survival.

Answer

Increased cellular differentiation.

Question 5

A woman presents with massive pulmonary thromboembolism. Which of the following, based on findings from a subsequent liver autopsy, is the most likely underlying cause of the pulmonary embolism?

Accepted Answer

Colonic adenocarcinoma with metastasis

Answer

Locally invaded hepatocellular carcinoma

Answer

Angiosarcoma

Answer

Hepatic metastasis from primary lung adenocarcinoma

Question 6

What is the primary molecular defect in xeroderma pigmentosa?

Accepted Answer

DNA repair defect

Answer

Autosomal recessive

Answer

Poor long term prognosis

Answer

Pyrimidine dimers

Question 7

Retinoblastomas are characterized by which of the following features?

Accepted Answer

Flexner-Wintersteiner rosettes and Fleurettes

Answer

Necrosis

Answer

Small round cells

Answer

Retinal detachment

Question 8

Which of the following statements about VEGF is false?

Accepted Answer

Inhibits angiogenesis

Answer

Hypoxia potentiates its expression

Answer

Helps in tumor metastasis

Answer

Highly specific for endothelium

Question 9

Immunohistochemical marker for sentinel node biopsy in breast carcinoma?

Accepted Answer

Cytokeratin

Answer

Vimentin

Answer

Calretinin

Answer

CD45

Question 10

What is the most common tumor suppressor gene involved in carcinogenesis?

Accepted Answer

p53

Answer

Retinoblastoma (Rb)

Answer

Tumor protein p73 (p73)

Answer

Cyclin-dependent kinase inhibitor 2A (p16)

Neoplasia — MCQs

Neoplasia — MCQs

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