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IP Oncology Exam 2 > Lec 6: Colon Cancer > Flashcards

Lec 6: Colon Cancer Flashcards

1
Q

General Trends and Incidence of Colon Cancer

A
  • It’s the 4th most common cancer
  • It’s the 2nd cause of cancer death in both men and women!
  • Stage at Diagnosis: mostly it is localized (have not spread outside of the colon)
  • 5 year survival rate is higher if caught at localized stage! Caught early = higher survival rate. survival drastically drop when metastasized
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2
Q

Risk factors: NON-MODIFIABLE (things you cannot change)

A
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3
Q

Risk Factors: MODIFIABLE (things you can change)

A
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4
Q

Risk Factors (familial syndromes): LYNCH SYNDROME

A
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5
Q

Risk Factors (familial syndromes): FAP

A
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6
Q

Screening: Average Risk

A

NOTE: Sign and symptoms of CRC such as iron deficiency anemia, rectal bleeding, or changes in bowel habits warrant prompt evaluation with colonoscopy

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7
Q

Screening: Increased Risk/ High Risk? (know general)

A

NOTE: Just know that screening is more frequent in people with high risk!

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8
Q

What is the most appropriate colon cancer screening plan for a 56 year old average risk man who is seen for the first time in his primary care doctors office for an annual wellness exam who absolutely refuses a colonoscopy?
A) No screening needing at this time
B) Flexible sigmoidoscopy every 6 months for 5 years
C) Colonoscopy every 10 years
D) Stool-based, high-sensitivity guaiac-based or immunochemical based test every year

A

D… for pt, who’s adamant about no colonoscopy!

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9
Q

Signs and Symptoms of colon cancer

A
  • A change in bowel habits
  • A feeling the need to have a bowel movement that is not relieved by doing so
  • Rectal bleeding with bright red blood
  • Dark stools, or blood in the stool
  • Cramping or abdominal pain
  • Weakness and fatigue
  • Unintended weight loss
  • Tumor marker elevation
  • Carcinoembryonic Antigen (CEA)
    .
    NOTE: these symp are v general so sometimes patients do not seek help!
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10
Q

Early Stage Colon Cancer (I, II, III) Goal and treatment? (general)

A

Goal: Cure
.
Treatment Modalities:
1.) Surgery –> Resection of primary tumor and sampling of lymph nodes…. Minimum of 12 lymph nodes needed for complete sampling
2.) Chemotherapy
- Adjutant (after surgery)
- Eradicate micro-metastatic disease
- Improve disease free survival
3.) Radiation - Minimal role in colon cancer.. will not focus on this

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11
Q

Early Stage Colon Cancer (I, II, III): Chemotherapy Regimens (Adjuvant Chemotherapy) - chart of different medications/ dosing/ SIG

A
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12
Q

Early Stage Colon Cancer (I, II, III) Adjuvant Chemotherapy: duration? standard of care? benefits?

A
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13
Q

Early Stage Colon Cancer Treatment Recommendation
-Stage I

A
  • Surgery: Removal of primary tumor and regional lymph nodes
  • Observation/Surveillance: No adjuvant therapy !!!
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14
Q

Early Stage Colon Cancer
Treatment Considerations: Stage II
HIGH RISK OF RECURRENCE

A
  • <12 lymph nodes collected (less than 12)
  • Poorly differentiated histology
  • Lymphatic/vascular/perineural invasion
  • Bowel obstruction
  • Localized perforation
  • Close, indeterminate, or positive surgical margins
  • T4 disease
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15
Q

Early Stage Colon Cancer
Treatment Considerations: Stage II
DEFECTIVE DNA MISMATCH REPAIR (dMMR)

A
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16
Q

Early Stage Colon Cancer
Treatment Recommendation
Stage IIA and no high risk factors:

A

Treatment for Stage IIA and no high risk factors:
- Surgery: Removal of primary tumor and regional lymph nodes
- Observation/Surveillance and No adjuvant therapy
.
May consider adjuvant treatment (if drs look at cancer cells and were like ‘wow these are screwed up cells. very differentiated’ then may put patient on meds)
- 5-FU/leucovorin (6 months of treatment)
- Capecitabine (6 months of treatment)

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17
Q

Early Stage Colon Cancer
Treatment Recommendation
Stage IIA with high risk factors, IIB and IIC:

A
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18
Q

MOSAIC Trial: talk about it .. what did they concluded/ findings?

A

Looked at patients with Stage II and III colon cancer getting adjuvant treatment (Compared 5-FU alone vs 5-FU + oxaliplatin (FOLFOX-4))
.
Stage II patients: No difference in disease free survival or overall survival
.
Stage III patient: where the benefit of adding oxaliplatin was seen!

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19
Q

Early Stage Colon Cancer
Treatment Recommendation
Stage III low risk (T 1-3, N1):

A
20
Q

Early Stage Colon Cancer
Treatment Recommendation
Stage III high risk (T4, N1-2; T any, N2):

A

NOTE: Stage III Low Risk? CAPEOX 3 months preferred! for Stage III High Risk? Need 6 months (UNLESS: starting to have side effects)

21
Q

IDEA Trial: talk about it .. what did they concluded/ findings?

A

Looked at patients with Stage III colon cancer getting adjuvant treatment (FOLFOX or CAPEOX administered for 3 months vs 6 months)
.
Conclusion:
Patients with lower risk stage III (T1, T2, or T3 and N1) adjuvant treatment with CAPEOX for 3 months is as effective as 6 months

22
Q

Early Stage Colon Cancer (I, II, III) Long Term Follow-Up
- Stage I

A
  • Colonoscopy at 1 year
    …. If advanced adenoma repeat in 1 year
    …If no advanced adenoma, repeat in 3 years, then every 5 years
23
Q

Early Stage Colon Cancer (I, II, III) Long Term Follow-Up
-Stage II and III

A
  • History and physical, and CEA every 3 – 6 months for 2 years, then every 6 months for a total of 5 years
  • CT of chest, abdomen, pelvis every 6 – 12 month x 5 yrs
  • Colonoscopy in 1 year except if no preoperative colonoscopy then in 3 – 6 months
    —— If advanced adenoma repeat in 1 year
    —— If no advanced adenoma, repeat in 3 years, then every 5 years
24
Q

TE is a 63 year old woman with newly diagnosed stage III low risk colon cancer. She has a good performance status and no other comorbidities. What is the most appropriate treatment plan for this patient?
A) Surgery followed by capecitabine for 6 months
B) Surgery followed by CAPEOX for 3 months
C) Surgery followed by observation
D) Surgery followed by mFOLFOX6 for 3 months

A

B. This is because the patient is stage 3 with LOW RISK and NO comorbidities!

25
Q

Metastatic Colon Cancer: Goal and treatment

A
26
Q

Metastatic Colon Cancer
Treatment Selection: What we know (general)

A

NOTE:
- mFOLFOX6 : 5FU, Leucovorin, oxaliplatin
- FOLFIRI: 5FU, Leucovorin, Irinotecan
- FOLFOXIRI: 5FU, Leucovorin, oxaliplatin, Irinotecan

27
Q

Metastatic Colon Cancer
Treatment Selection… the importance of gene mutations?

A
28
Q

Metastatic Colon Cancer
Initial Chemotherapy (know the general)

A

The most commonly used drugs: 5-FU (+leucovorin), oxaliplatin, and irinotecan.
.
bevacizumab (VEGF inhibitor) can be added
.
cetuximab or panitumumab are Anti EGFR (only used if patients have WT! NO MUTATION of KRAS, BRAS, NRAS and left-sided tumors only!!!!

.
Pembrolizumab (dMMR/MSI-H only!) use if MSI is HIGH!

29
Q

Differences between Right and Left Colon Cancer

A
30
Q

Fluoropyrimidines
FLUOROURACIL (5 – FU): MOA, SE, and gene expression of what is significant?

A
31
Q

Fluoropyrimidines
CAPECITABINE: MOA and SE

A
  • MOA: prodrug of 5-FU. It undergoes hydrolysis in the liver and tissues to form fluorouracil (fluorinated pyrimidine form fluorouracil antimetabolite). Inhibits thymidylate synthetase, blocking the methylation of deoxyuridylic acid to thymidylic acid, interfering with DNA, and to a lesser degree, RNA synthesis
  • SE: Diarrhea, myelosuppression, n/v, handfoot syndrome, mouth sores
32
Q

Platinum Agent: Oxaliplatin
MOA, SE, DLT

A
33
Q

Oxaliplatin-Induced Neurotoxicity
Acute vs Chronic ? prevention?

A

1.) Acute: transient, rapid onset hours to days after infusion
- Oxalate metabolite of oxaliplatin chelates calcium and magnesium and interferes with voltage-gated sodium channels and electrical current
- Prolonged opening of the sodium channels in sensory nerves that results in a hyperexcitable state
- Prevention by prolonging infusion 2 – 6 hrs or dose reductions
.
2.) Chronic: Onset >14 days after infusion, persistent between treatment
- Thought to be related to interference with microtubule-based axonal transport, oxidative stress or drug accumulation in dorsal root ganglinon and sensory nerves
- Prevention: Stop-and-Go approach, discontinuing oxaliplatin after 6 cycles followed by 5-FU maintenance may be considered

34
Q

Irinotecan: MOA, SE, and gene expression of what is significant?

A
35
Q

Irinotecan-Induced Diarrhea.. ACUTE: Prevention/ meds to treat?

A
  • Occurs during or immediately after infusion
  • Cholinergic symptoms! :Cramping, diohoresis (sweating), flushing, salivation, visual disturbances, and lacrimation, Direct inhibition of acetylcholinesterase
    .
  • Treatment: Atropine –> Suppresses cholinergic effect, Start at 0.25 mg IV (max dose 1.2 mg)
    .
    -Monitor blood pressure and heart rate
    -Can consider to give as secondary prophylaxis
36
Q

Irinotecan-Induced Diarrhea.. DELAYED: Prevention/ meds to treat?

A
  • Occurs >24 hr after infusion. Reported 2 – 12 days after… Thought to be do to SN-38 reactivation
    .
    -Treatment:
    Loperamide 4 mg at first sign of diarrhea, then 2 mg
    every 2 hrs until 12 hrs following last bowel movement, then PRN up to 24 mg/day (higher that the 16 mg/day max)..go over max to 24mgQD is recommended!!!!
    .
    -Supportive care: Fluids and electrolyte replacement, Nutrition
37
Q

VEGF Inhibitors
Bevacizumab: VEGF monoclonal antibody - MOA and SE

A

MOA: Bind to VEGF preventing its association with endothelial receptors… VEGF binding initiates angiogenesis so inhibiting it = The inhibition of microvascular growth is believed to retard the growth of all tissues
- Not indicated as single agents!!!!!!
.
SE: hypertension, proteinuria, wound dehiscence, bleeding, thrombotic events

38
Q

Anti-EGFR Monoclonal Antibodies
Cetuximab and Panitumumab - MOA and SE and important thing to note!

A
  • MOA: binds specifically to EGFR and competitively inhibits the binding of epidermal growth factor (EGF) and other ligands
  • SE: Skin rash, hypersensitivity reactions, hypomagnesemia
    .
    NOTE:
  • Only for KRAS/NRAS wild-type tumors! NO MUTATION
  • Mutation in RAS predicts lack of response to EGFR inhibitors!!!
  • Recommended for left-sided primary tumors for front-line
  • If used in initial treatment, no evidence to use them in subsequent treatments (no need to continue using them if they are not working)
39
Q

EGFR Inhibitor SIDE EFFECT: Papulopustular Rash (Acne lookin’ shit) and treatments?

A
  • Acneiform Rash characterized by papules and pustules coupled with itching and pain: Develops on face and scalp…THIS IS NOT acne (but looks like it) using acne products make it worst!
  • Positive correlation between rash severity and tumor response
  • Pre-emptive management: Hydrocortisone 1% + moisturized, sunscreen, and doxycycline 100 mg BID (For at least the 1st 6 weeks)
    .

Treatment (based on CTCAE grade)
 Grade 1: continue same dose, topical hydrocortisone, and clindamycin
 Grade 2: continue same dose, topical hydrocortisone, and oral doxycycline or minocycline
 Grade 3/4: dose reduce, topical hydrocortisone, and oral doxycycline or minocycline, oral prednisone

40
Q

PD-1 Monoclonal Antibodies
Pembrolizumab, Nivolumab, Dostarlimab-gxly: MOA and SE and important thing to note

A
  • MOA: inhibits programmed cell death-1 (PD-1) activity by binding to the PD-1 receptor on Tcells to block PD-1 ligands from binding….The negative PD-1 receptor signaling that regulates T-cell activation and proliferation is therefore disrupted….This releases PD-1 pathway-mediated inhibition of the immune response, including the antitumor immune response
    .
  • Only used in patients with dMMR/MSI-H
    .
  • If progression on one agent no use to switching to the other agents
    .
  • SE: Immune-mediated toxicities (pneumonitis, colitis, hepatitis, nephritis, and thyroid dysfunction)
41
Q

Metastatic Colon Cancer
Second Line Treatment: … PREVIOUS OXALIPLATIN BASED TREATMENT (WITHOUT IRINOTECAN) - aka if patient was previously on a oxaliplatin regimen…switch to irinotecan continuing 5-FU!

A
42
Q

Metastatic Colon Cancer
Second Line Treatment… PREVIOUS IRINOTECAN BASED TREATMENT (WITHOUT OXALIPLATIN)- aka if patient was previously on an irinotecan regimen …then switch it to oxaliplatin containing 5-FU !

A
43
Q

Metastatic Colon Cancer
Other Agents . . . these are last lines if the previous ones do not work…
1.) REGORAFENIB - MOA and SE

A
  • MOA: multikinase inhibitor; it targets kinases involved with tumor angiogenesis, oncogenesis, and maintenance of the tumor microenvironment which results in inhibition of tumor growth
  • SE: hypertension, fatigue, diarrhea, mucositis, n/v,
    hand-foot syndrome, myelosuppression, proteinuria, liver toxicity
44
Q

Metastatic Colon Cancer
Other Agents . . . these are last lines if the previous ones do not work…
2.) TRIFLURIDINE + TIPRACIL - MOA and SE

A
  • MOA: Trifluridine, is a thymidine-based nucleic acid
    analogue which is incorporated into DNA and
    interferes with DNA synthesis and inhibits cell
    proliferation…. Tipiracil is a potent thymidine phosphorylase inhibitor which prevents the rapid degradation of trifluridine, allowing for increased trifluridine exposure
    .
  • SE: diarrhea, n/v, decrease appetite, fatigue,
    myelosuppression
45
Q

Metastatic Colon Cancer
Other Agents . . . these are last lines if the previous ones do not work…
3.) LAROTRECTINIB - MOA and SE

A
  • MOA: Inhibits tropomyosin receptor kinase (TRK)
    TRKA, TRKB, and TRKC proteins encoded by neurotrophic receptor tyrosine kinase (NTRK) genes, NTRK1, NTRK2, and NTRK3.
    -Anti-tumor activity in cells with constitutive activation
    of TRK proteins resulting from gene fusions, deletion of
    a protein regulatory domain, or in cells with TRK
    protein overexpression
  • SE: fatigue, n/v, anemia, neutropenia, liver toxicity,
    neurotoxicity (dizziness), cough, constipation,
    diarrhea
46
Q

Metastatic Colon Cancer
Other Agents . . . these are last lines if the previous ones do not work…
4.) ENTRECTINIB- MOA and SE

A
  • MOA: Inhibits tropomyosin receptor kinase (TRK)
    TRKA, TRKB, and TRKC proteins encoded by neurotrophic receptor tyrosine kinase (NTRK) genes, NTRK1, NTRK2, and NTRK3.
    -Inhibits cancer cell lines derived from multiple tumor
    types harboring NTRK, ROS1, and ALK fusion genes
    thus inhibiting tumorigenic potential through
    hyperactivation of downstream signaling pathways and
    uncontrolled cell proliferation caused by fusion
    proteins
  • SE: edema, weight increase, constipation, diarrhea,
    n/v, taste changes, arthralgia, myalgia, fatigue,
    cough, shortness of breath, fever, neurotoxicity
47
Q

Resectable Liver or Lung Metastases

A
  • Can go for cure in 20-25% of patient
  • Resection of primary tumor and liver or lung metastases
  • Followed by FOLFOX or CapeOx (preferred)
    .
    Neoadjuvant chemotherapy
  • 2 – 3 months to increase curative resection and convert from unresectable to resectable
    —- mFOLFOX6, CapeOx (preferred)

IP Oncology Exam 2 (9 decks)

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