Carcinogenesis models US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Carcinogenesis models. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Carcinogenesis models US Medical PG Question 1: A scientist is researching the long term effects of the hepatitis viruses on hepatic tissue. She finds that certain strains are oncogenic and increase the risk of hepatocellular carcinoma. However, they appear to do so via different mechanisms. Which of the following answer choices correctly pairs the hepatitis virus with the correct oncogenic process?
- A. Hepatitis A virus - chronic inflammation
- B. Hepatitis C virus - chronic inflammation
- C. Hepatitis E virus - integration of viral DNA into host hepatocyte genome
- D. Hepatitis B virus - integration of viral DNA into host hepatocyte genome (Correct Answer)
- E. Hepatitis A virus - integration of viral DNA into host hepatocyte genome
Carcinogenesis models Explanation: ***Hepatitis B virus - integration of viral DNA into host hepatocyte genome***
- **Hepatitis B virus (HBV)** is a **DNA virus** that can integrate its genetic material into the host hepatocyte genome, leading to genomic instability and promoting oncogenesis.
- This integration, along with chronic inflammation and the production of viral regulatory proteins, contributes significantly to the development of **hepatocellular carcinoma (HCC)**.
*Hepatitis A virus - chronic inflammation*
- **Hepatitis A virus (HAV)** is an **RNA virus** that causes **acute hepatitis** but does not lead to chronic infection or chronic inflammation.
- Due to its acute and self-limiting nature, HAV is **not associated with hepatocellular carcinoma**.
*Hepatitis C virus - integration of viral DNA into host hepatocyte genome*
- **Hepatitis C virus (HCV)** is an **RNA virus** and therefore does not integrate its DNA into the host genome (as it has no DNA phase).
- HCV causes HCC primarily through **chronic inflammation**, **fibrosis**, and **cirrhosis**, not DNA integration.
*Hepatitis E virus - integration of viral DNA into host hepatocyte genome*
- **Hepatitis E virus (HEV)** is an **RNA virus** that typically causes acute, self-limiting hepatitis and does not integrate its genetic material into the host genome.
- While HEV can cause chronic infection in immunocompromised individuals, it is **not generally recognized as an oncogenic virus** leading to HCC.
*Hepatitis A virus - integration of viral DNA into host hepatocyte genome*
- **Hepatitis A virus (HAV)** is an **RNA virus**, meaning it does not have a DNA stage and therefore cannot integrate DNA into the host genome.
- HAV causes **acute, self-limiting infections** and is definitively **not associated with hepatocellular carcinoma**.
Carcinogenesis models US Medical PG Question 2: A 55-year old man living in Midwest USA comes in complaining of painless hematuria for the past week. He denies dysuria but complains of fatigue and lethargy at work. He has lost about 9.0 kg (20.0 lb) in the past 6 months. He drinks 1–2 beers on the weekends over the past 10 years but denies smoking. He has worked at a plastic chemical plant for the past 30 years and has never been out of the country. His father died of a heart attack at age 62 and his mother is still alive and well. There is a distant history of pancreatic cancer, but he can not remember the specifics. His vitals are stable and his physical exam is unremarkable. Urinary analysis is positive for RBCs. A cystoscopy is performed and finds a pedunculated mass projecting into the bladder lumen. A biopsy shows malignant cells. Which of the following is the most concerning risk factor for this patient’s condition?
- A. Aromatic amine exposure (Correct Answer)
- B. Alcohol
- C. Vinyl chloride exposure
- D. Genetic predisposition
- E. Schistosoma haematobium infection
Carcinogenesis models Explanation: ***Aromatic amine exposure***
- The patient's 30-year employment at a **plastic chemical plant** is a significant risk factor, as many chemicals used in such industries contain **aromatic amines**.
- Exposure to **aromatic amines** is a well-established cause of **transitional cell carcinoma** of the bladder, which is consistent with the painless hematuria and the finding of a malignant bladder mass.
*Alcohol*
- While heavy alcohol consumption can contribute to various health issues, it is **not considered a direct or strong risk factor** for bladder cancer.
- The patient's reported consumption of "1-2 beers on the weekends" over 10 years is relatively moderate and unlikely to be the primary cause of his severe presentation.
*Vinyl chloride exposure*
- **Vinyl chloride** exposure is primarily associated with **hepatic angiosarcoma** and, to a lesser extent, lung cancer and brain tumors.
- It is **not a significant risk factor** for bladder cancer, differentiating it from the patient's presentation of a bladder mass.
*Genetic predisposition*
- While there can be a genetic component to some cancers, the familial history mentioned (father died of heart attack, distant history of pancreatic cancer) does **not specifically point to a strong genetic predisposition** for bladder cancer.
- The powerful occupational exposure to chemicals is a much more direct and concerning risk factor in this case.
*Schistosoma haematobium infection*
- **Schistosoma haematobium** infection is a known cause of **squamous cell carcinoma** of the bladder, especially in endemic regions like parts of Africa and the Middle East.
- The patient has **never been out of the country** and lives in the Midwest USA, making this infection highly unlikely.
Carcinogenesis models US Medical PG Question 3: A research group wants to assess the safety and toxicity profile of a new drug. A clinical trial is conducted with 20 volunteers to estimate the maximum tolerated dose and monitor the apparent toxicity of the drug. The study design is best described as which of the following phases of a clinical trial?
- A. Phase 0
- B. Phase III
- C. Phase V
- D. Phase II
- E. Phase I (Correct Answer)
Carcinogenesis models Explanation: ***Phase I***
- **Phase I clinical trials** involve a small group of healthy volunteers (typically 20-100) to primarily assess **drug safety**, determine a safe dosage range, and identify side effects.
- The main goal is to establish the **maximum tolerated dose (MTD)** and evaluate the drug's pharmacokinetic and pharmacodynamic profiles.
*Phase 0*
- **Phase 0 trials** are exploratory studies conducted in a very small number of subjects (10-15) to gather preliminary data on a drug's **pharmacodynamics and pharmacokinetics** in humans.
- They involve microdoses, not intended to have therapeutic effects, and thus cannot determine toxicity or MTD.
*Phase III*
- **Phase III trials** are large-scale studies involving hundreds to thousands of patients to confirm the drug's **efficacy**, monitor side effects, compare it to standard treatments, and collect information that will allow the drug to be used safely.
- These trials are conducted after safety and initial efficacy have been established in earlier phases.
*Phase V*
- "Phase V" is not a standard, recognized phase in the traditional clinical trial classification (Phase 0, I, II, III, IV).
- This term might be used in some non-standard research contexts or for post-marketing studies that go beyond Phase IV surveillance, but it is not a formal phase for initial drug development.
*Phase II*
- **Phase II trials** involve several hundred patients with the condition the drug is intended to treat, focusing on **drug efficacy** and further evaluating safety.
- While safety is still monitored, the primary objective shifts to determining if the drug works for its intended purpose and at what dose.
Carcinogenesis models US Medical PG Question 4: A 28-year-old male with a history of HIV infection is found to have a CD4+ T lymphocyte count of 68 cells per microliter. As a consequence of his HIV infection, this patient is at increased risk of malignancy due to which of the following?
- A. Pneumocystis jiroveci
- B. Actinomyces israelii
- C. Helicobacter pylori
- D. HHV-6
- E. Epstein-Barr Virus (EBV) (Correct Answer)
Carcinogenesis models Explanation: ***Epstein-Barr Virus (EBV)***
- **EBV** is a major cause of **AIDS-related malignancies**, particularly **B-cell lymphomas** including **non-Hodgkin lymphoma (NHL)** and **primary CNS lymphoma**, which are common in patients with CD4 counts below 100 cells/µL.
- The severe immunosuppression in **HIV/AIDS** allows for unchecked **EBV-driven lymphoproliferative disorders** due to impaired T-cell surveillance of EBV-infected B cells.
- Among the options listed, **EBV** is the only **oncogenic virus** and represents a significant cause of morbidity in advanced AIDS patients.
- **Note:** While HHV-8 (KSHV) causing Kaposi's sarcoma is also a major AIDS-related malignancy, it is not among the listed options.
*Pneumocystis jiroveci*
- **Pneumocystis jiroveci pneumonia (PCP)** is a common opportunistic **fungal infection** in HIV patients with CD4 < 200 cells/µL, causing severe respiratory illness.
- **PCP** is not oncogenic and does not increase malignancy risk; it causes acute infection, not cellular transformation.
*Actinomyces israelii*
- **Actinomyces israelii** is a gram-positive **bacterium** causing **actinomycosis**, a chronic suppurative infection with abscess formation and sinus tracts.
- While it can cause opportunistic infections in immunocompromised patients, it is **not oncogenic** and not associated with malignancy risk.
*Helicobacter pylori*
- **H. pylori** is a bacterium associated with **gastric adenocarcinoma** and **gastric MALT lymphoma** in the general population through chronic gastric inflammation.
- However, in the context of advanced HIV/AIDS with CD4 < 100, the predominant malignancy risk is from **oncogenic viruses** (EBV, HHV-8), not gastric pathology from **H. pylori**.
- **H. pylori** is not typically considered an AIDS-defining or AIDS-related malignancy.
*HHV-6*
- **Human Herpesvirus 6 (HHV-6)** causes roseola infantum in children and can reactivate in immunocompromised patients, potentially causing encephalitis or pneumonitis.
- **HHV-6** is **not established as oncogenic** and lacks strong evidence linking it to malignancy in HIV patients, unlike **EBV** (lymphomas) or **HHV-8** (Kaposi's sarcoma).
Carcinogenesis models US Medical PG Question 5: A 47-year-old man comes to the physician for a routine health maintenance examination. He has no complaints and has no history of serious illness. He works as a forklift operator in a factory. His brother died of malignant melanoma. He smokes occasionally and drinks a glass of wine once a week. His pulse is 79/min and blood pressure is 129/84 mm Hg. Which of the following causes of death is this patient most at risk for over the next 15 years?
- A. Industrial accident
- B. Coronary artery disease (Correct Answer)
- C. Prostate cancer
- D. Malignant melanoma
- E. Lung cancer
Carcinogenesis models Explanation: ***Coronary artery disease***
- **Coronary artery disease (CAD)** is the **leading cause of death** in middle-aged men in the United States, making it the statistically most likely cause of death for this patient over the next 15 years.
- This patient has multiple modifiable risk factors including male sex, smoking (even occasional), and blood pressure of 129/84 mm Hg (elevated blood pressure/stage 1 hypertension by current guidelines).
- Even with relatively modest risk factors, the cumulative 15-year risk of cardiovascular mortality substantially exceeds other causes of death in this demographic group.
*Industrial accident*
- While working as a forklift operator carries some occupational risk, **industrial accidents** account for a very small proportion of deaths compared to chronic diseases in this age group.
- There is no indication of high-risk working conditions or safety concerns that would elevate this above cardiovascular disease as a cause of death.
*Prostate cancer*
- At age 47, the patient is relatively young for **prostate cancer** mortality. Most prostate cancer deaths occur in men over 65.
- While prostate cancer is common in older men, it typically has a long natural history, and mortality within 15 years would be less likely than cardiovascular disease in this age group.
- No specific high-risk features (family history, African-American ethnicity) are mentioned.
*Malignant melanoma*
- Although his brother died of **malignant melanoma**, family history alone does not make this the most likely cause of death over cardiovascular disease.
- The patient has no described personal risk factors (numerous nevi, history of severe sunburns, fair skin) or current lesions of concern.
- Melanoma mortality rates are substantially lower than cardiovascular disease mortality in middle-aged men.
*Lung cancer*
- The patient smokes **occasionally**, which confers some increased risk, but this is not described as heavy or chronic smoking.
- **Lung cancer** typically requires more substantial cumulative tobacco exposure (pack-years) to become a leading cause of mortality.
- Even in smokers, cardiovascular disease often causes death before lung cancer in this age group, particularly with modest smoking history.
Carcinogenesis models US Medical PG Question 6: A 17-year-old man is brought by his mother to his pediatrician in order to complete medical clearance forms prior to attending college. During the visit, his mother asks about what health risks he should be aware of in college. Specifically, she recently saw on the news that some college students were killed by a fatal car crash. She therefore asks about causes of death in this population. Which of the following is true about the causes of death in college age individuals?
- A. More of them die from homicide than suicide
- B. More of them die from suicide than injuries
- C. More of them die from cancer than suicide
- D. More of them die from homicide than injuries
- E. More of them die from homicide than cancer (Correct Answer)
Carcinogenesis models Explanation: ***More of them die from homicide than cancer***
- While relatively rare, **homicide rates** for college-aged individuals (18-24 years) are generally higher than their rates of death due to **cancer**.
- **Cancer** is a leading cause of death in older populations but is much less common in young adults.
*More of them die from homicide than suicide*
- **Suicide** is a significantly more common cause of death than homicide among college-aged individuals.
- Data consistently shows that **suicide** ranks as one of the top causes of death in this demographic, often second only to unintentional injuries.
*More of them die from suicide than injuries*
- **Unintentional injuries** (including motor vehicle accidents, accidental poisoning, and falls) are the leading cause of death in the 18-24 age group.
- **Suicide** is typically the second leading cause, meaning more individuals die from injuries than from suicide.
*More of them die from cancer than suicide*
- As mentioned, **suicide** is a much more prevalent cause of death in young adults than cancer.
- **Cancer deaths** are relatively uncommon in this age group compared to other causes like injuries and suicide.
*More of them die from homicide than injuries*
- **Unintentional injuries** are the leading cause of death among college-aged individuals.
- **Homicide rates** are considerably lower than injury rates in this population.
Carcinogenesis models US Medical PG Question 7: A 38-year-old man presents to his primary care practitioner for 2 months of rectal bleeding. He also reports occasional diarrhea and abdominal pain. His family history is relevant for his father and uncle, who died from complications of colorectal cancer. Colonoscopy shows more than 10 colorectal adenomas. Which of the following genes is most likely affected in this patient?
- A. RAS
- B. TP53
- C. hMLH1
- D. PPAR
- E. APC (Correct Answer)
Carcinogenesis models Explanation: ***APC***
- This patient's presentation with **numerous colorectal adenomas** (over 10), early-onset symptoms (38 years old), and a strong **family history of colorectal cancer** (father and uncle) is highly characteristic of **Familial Adenomatous Polyposis (FAP)**.
- FAP is an **autosomal dominant** condition caused by a germline mutation in the **APC tumor suppressor gene**, leading to the development of hundreds to thousands of adenomatous polyps in the colon, which inevitably progress to colorectal cancer if untreated.
*RAS*
- **RAS mutations** are commonly found in sporadic colorectal cancers and play a role in tumor growth and progression, but they are not typically associated with the **hereditary syndrome of multiple adenomas** seen in this patient.
- RAS activation leads to an increase in **cell proliferation** and can contribute to the development of many cancers, but not as the primary genetic defect in a polyposis syndrome.
*TP53*
- **TP53** is a well-known tumor suppressor gene, and mutations are involved in various cancers, including colorectal cancer (often in its later stages). However, germline mutations in TP53 are associated with **Li-Fraumeni syndrome**, which involves a broad spectrum of early-onset cancers and is not primarily characterized by numerous colonic adenomas.
- TP53 mutations are generally hallmarks of **genomic instability** and are more often seen in the progression of sporadic cancers rather than initiating a polyposis syndrome.
*hMLH1*
- **hMLH1** is a gene involved in **DNA mismatch repair**. Germline mutations in this gene, along with other mismatch repair genes (e.g., MSH2, MSH6, PMS2), are responsible for **Lynch syndrome (hereditary non-polyposis colorectal cancer - HNPCC)**.
- While Lynch syndrome is an important cause of hereditary colorectal cancer, it is characterized by fewer polyps (typically <10) that progress rapidly to cancer, and an increased risk of other cancers (e.g., endometrial), which differs from the presentation of **hundreds of adenomas** seen in FAP.
*PPAR*
- **PPARs (Peroxisome Proliferator-Activated Receptors)** are a group of nuclear receptor proteins that play roles in metabolism, cell differentiation, and inflammation.
- While PPAR pathways have been investigated for their potential role in cancer development and as therapeutic targets, **mutations in PPAR genes are not directly linked** to a common hereditary colorectal cancer syndrome characterized by numerous adenomas like FAP.
Carcinogenesis models US Medical PG Question 8: A researcher has identified a chemical compound that she expects may contribute to the development of colorectal cancer. She designs an experiment where she exposes 70 mice to a diet containing this compound with another 50 mice in a control group that was fed a regular diet. After 9 months, the mice were evaluated for tumor development at necropsy. In total, 14 mice in the experimental group developed colorectal tumor burden, and 1 mouse in the control group developed tumors. Based on this experiment, what risk of colorectal cancer can be attributable to this chemical compound?
- A. 22.0%
- B. 2.0%
- C. 12.5%
- D. 18.0% (Correct Answer)
- E. 20.0%
Carcinogenesis models Explanation: ***18.0%***
- The **attributable risk (AR)** is calculated as the **incidence in the exposed group (Ie)** minus the **incidence in the unexposed group (Iu)**.
- In this case, **Ie = 14/70 = 0.20** and **Iu = 1/50 = 0.02**. Therefore, **AR = 0.20 - 0.02 = 0.18**, or **18.0%**.
*22.0%*
- This value might result from an incorrect calculation or misinterpretation of the attributable risk formula.
- It does not correctly represent the difference in risk between the exposed and unexposed groups.
*2.0%*
- This represents the **incidence of colorectal tumors in the control group (Iu)**, not the attributable risk.
- The attributable risk accounts for the excess risk specifically due to the exposure.
*12.5%*
- This value is not derived from the standard formula for attributable risk using the provided data.
- It might represent a misunderstanding of how to calculate risk difference from incidence rates.
*20.0%*
- This represents the **incidence of colorectal tumors in the experimental group (Ie)**, not the attributable risk.
- The attributable risk needs to subtract the background risk observed in the unexposed group.
Carcinogenesis models US Medical PG Question 9: A 28-year-old male presents to his primary care physician with complaints of intermittent abdominal pain and alternating bouts of constipation and diarrhea. His medical chart is not significant for any past medical problems or prior surgeries. He is not prescribed any current medications. Which of the following questions would be the most useful next question in eliciting further history from this patient?
- A. "Does the diarrhea typically precede the constipation, or vice-versa?"
- B. "Is the diarrhea foul-smelling?"
- C. "Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life"
- D. "Are the symptoms worse in the morning or at night?"
- E. "Can you tell me more about the symptoms you have been experiencing?" (Correct Answer)
Carcinogenesis models Explanation: ***Can you tell me more about the symptoms you have been experiencing?***
- This **open-ended question** encourages the patient to provide a **comprehensive narrative** of their symptoms, including details about onset, frequency, duration, alleviating/aggravating factors, and associated symptoms, which is crucial for diagnosis.
- In a patient presenting with vague, intermittent symptoms like alternating constipation and diarrhea, allowing them to elaborate freely can reveal important clues that might not be captured by more targeted questions.
*Does the diarrhea typically precede the constipation, or vice-versa?*
- While knowing the sequence of symptoms can be helpful in understanding the **pattern of bowel dysfunction**, it is a very specific question that might overlook other important aspects of the patient's experience.
- It prematurely narrows the focus without first obtaining a broad understanding of the patient's overall symptomatic picture.
*Is the diarrhea foul-smelling?*
- Foul-smelling diarrhea can indicate **malabsorption** or **bacterial overgrowth**, which are important to consider in some gastrointestinal conditions.
- However, this is a **specific symptom inquiry** that should follow a more general exploration of the patient's symptoms, as it may not be relevant if other crucial details are missed.
*Please rate your abdominal pain on a scale of 1-10, with 10 being the worst pain of your life*
- Quantifying pain intensity is useful for assessing the **severity of discomfort** and monitoring changes over time.
- However, for a patient with intermittent rather than acute, severe pain, understanding the **character, location, and triggers** of the pain is often more diagnostically valuable than just a numerical rating initially.
*Are the symptoms worse in the morning or at night?*
- Diurnal variation can be relevant in certain conditions, such as inflammatory bowel diseases where nocturnal symptoms might be more concerning, or functional disorders whose symptoms might be stress-related.
- This is another **specific question** that should come after gathering a more complete initial picture of the patient's symptoms to ensure no key information is overlooked.
Carcinogenesis models US Medical PG Question 10: A 67-year-old man comes to the physician because of a 4-month history of fatigue and weight loss. Physical examination shows jaundice. The liver is palpated 3 cm below the right costal margin. Serum studies show an elevated alpha-fetoprotein and a prolonged prothrombin time. Genetic analysis of a liver biopsy specimen shows a G:C to T:A transversion in codon 249 of the gene coding for the TP53 protein in affected cells. Which of the following risk factors is most specific to the patient's condition?
- A. Dietary aflatoxin exposure (Correct Answer)
- B. Alcoholism
- C. Schistosomiasis
- D. Hemochromatosis
- E. Hepatitis C infection
Carcinogenesis models Explanation: ***Dietary aflatoxin exposure***
- The **TP53 mutation** (G:C to T:A transversion at codon 249) is a **signature mutation** strongly associated with **aflatoxin B1 exposure**, particularly in hepatocellular carcinoma.
- Aflatoxins are potent **carcinogens produced by Aspergillus fungi**, often found in contaminated food storage in tropical regions.
*Schistosomiasis*
- This parasitic infection is a risk factor for **squamous cell carcinoma of the bladder** and, to a lesser extent, **cholangiocarcinoma**, but not typically hepatocellular carcinoma with this specific TP53 mutation signature.
- It primarily affects the **urinary bladder** and intestines, leading to chronic inflammation and fibrosis.
*Alcoholism*
- Chronic alcoholism is a major risk factor for **cirrhosis** and **hepatocellular carcinoma** due to continuous liver damage and regeneration.
- However, it does not typically cause the **specific TP53 codon 249 mutation** seen in this patient.
*Hemochromatosis*
- This genetic disorder causes **iron overload**, leading to liver damage, **cirrhosis**, and an increased risk of **hepatocellular carcinoma**.
- While it predisposes to liver cancer, it is not associated with the **specific G:C to T:A TP53 mutation** described.
*Hepatitis C infection*
- Chronic hepatitis C is a leading cause of **cirrhosis** and **hepatocellular carcinoma** worldwide due to chronic inflammation and hepatocyte turnover.
- Similar to alcoholism, it is a significant risk factor for liver cancer but does not specifically cause the **TP53 codon 249 mutation** linked to aflatoxin.
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