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Radiation Oncology Factoids > Oropharyngeal cancer > Flashcards

Oropharyngeal cancer Flashcards

1
Q

What is the incidence of oropharyngeal cancer (OPC) in the United States?

A

∼36,000 cases/yr of OPC in the United States with 6,850 deaths (2013 data)

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2
Q

How does the incidence of OPC compare to that of other H&N sites?

A

The incidence of OPC is increasing, whereas cancer of other H&N sites is decreasing.

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3
Q

Is there a sex predilection for OPC?

A

Yes. Males are more commonly affected than females (3:1).

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4
Q

What are the 4 subsites of the OPX?

A

Soft palate, tonsils, base of tongue (BOT), and pharyngeal wall

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5
Q

From which subsite do most OPCs arise?

A

The tonsil (ant tonsil pillar and fossa) is the most common primary site.

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6
Q

What are the borders of the OPX?

A

Anterior: oral tongue/circumvallate papillae
Superior: hard palate/soft palate junction
Inferior: valleculae
Posterior: pharyngeal wall
Lateral: tonsil

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7
Q

What 3 structures make up the walls of the tonsillar fossa?

A

Walls of the tonsillar fossa:

  1. Ant tonsillar pillar (palatoglossus muscle)
  2. Post tonsillar pillar (palatopharyngeus muscle)
  3. Inf glossotonsillar sulcus
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8
Q

What are the 4 most important risk factors for the development of OPC?

A

Risk factors for developing OPC:

  1. Smoking
  2. Alcohol
  3. HPV infection (up to 80% of cases now)
  4. Betel nut consumption
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9
Q

What is the 1st-echelon drainage region for most OPCs?

A

The 1st-echelon drainage site for most OPCs is the level II (upper jugulodigastric) nodes.

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10
Q

Are skip mets common for OPC?

A

No. Skip mets are extremely rare in OPC (<1%).

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11
Q

What are the 2 most common histologies encountered in the OPX? Rare histologies?

A

Most common histologies: squamous cell carcinoma (SCC) (90%), non- Hodgkin lymphoma (10% tonsil, 2% BOT)
Rare histologies: lymphoepithelioma, adenoid cystic carcinoma, plasmacytoma, melanoma, small cell carcinoma, mets

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12
Q

What proportion of pts with OPC fail locoregionally vs. distantly?

A

1:1 proportion of locoregional:distant failures

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13
Q

How prevalent is HPV infection in OPC?

A

Depending on the series, 40%–80% of OPCs are associated with HPV infection.

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14
Q

Which HPV serotype is most commonly associated with OPC?

A

HPV 16 is the most common serotype in OPC (80%–90%).

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15
Q

What is a surrogate marker of HPV infection in OPC that can be used as an indirect indication of HPV seropositivity?

A

The surrogate marker for HPV infection is p16 staining; E7 protein inactivates Rb, which upregulates p16.

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16
Q

Which pt population is most likely to present with HPV-related OPC?

A

Nonsmokers and nondrinkers are most likely to have HPV+ SCC of the OPX.

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17
Q

Do HPV+ or HPV– OPC pts have a better prognosis?

A

HPV+ OPC pts have a better prognosis. Data from RTOG 0129 (Ang KK et al., NEJM 2010) showed better 3-yr OS (82.4% vs. 57.1%) and risk of death (HR 0.42) for HPV+ pts. Smoking was an independent poor prognostic
factor.

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18
Q

What is the hypothesis behind why HPV+ OPC pts have a better prognosis?

A

HPV+ H&N cancers are usually in nonsmokers and nondrinkers, so p53 status is usually nonmutated; p53 mutation (which is common in non–HPV-related H&N cancers) predicts for a poor response to Tx

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19
Q

What nerves are responsible for otalgia in cancers of the oral tongue, BOT, and larynx/hypopharynx (HPX)?

A

Oral tongue: CN V (auriculotemporal) → preauricular area
BOT: CN IX (Jacobson nerve) → tympanic cavity
Larynx/HPX: CN X (Arnold nerve) → postauricular area

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20
Q

What are the 4 extrinsic tongue muscles, and what are their anatomic spans?

A

Extrinsic tongue muscles (-glossus) and anatomic spans:

  1. Genioglossus (ant mandible to tongue)
  2. Styloglossus (styloid process to tongue)
  3. Palatoglossus (palate to tongue; also forms ant tonsillar pillar)
  4. Hyoglossus (hyoid bone to tongue)
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21
Q

What is the most common presentation of OPC?

A

The most common presentation is a neck mass, especially with HPV+ OPC.

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22
Q

What are additional common presenting Sx by OPX subsite?

A

Base of tongue: sore throat, dysphagia, otalgia, neck mass
Tonsils: sore throat, trismus (T4b), otalgia, neck mass
Soft palate: leukoplakia, sore throat with swallowing, trismus/perforation, phonation defect with advanced lesions
Pharyngeal wall: pain/odynophagia, bleeding

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23
Q

Describe the workup for a pt with an OPX mass (per NCCN 2018).

A

OPX mass workup: H&P (bimanual exam of the floor of mouth), labs, laryngoscopy, CT/MRI with contrast H&N, tissue Bx with HPV testing (EUA if necessary), CT chest, consider PET/CT for stages III–IV Dz, nutrition, speech/swallow, audiogram

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24
Q

If the neck mass Bx is positive, is an additional Bx of the primary lesion necessary?

A

Yes. A Bx of the primary (or suspected primary) should also be done.

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25
Q

What % of OPC pts have clinically +nodes? Clinically occult nodes? Bilat nodes?

A

∼75% of OPC pts have clinically+ nodes at presentation, 30%–50% have clinically occult nodes, and ∼30% have bilat nodes (especially BOT/midline).

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26
Q

What is the T staging of p16(-) OPC? How is it different for p16(+) OPC?

A

T1: ≤2 cm
T2: >2 cm, ≤4 cm
T3: >4 cm or extension to lingual surface of epiglottis
T4a (moderately advanced): invades larynx, deep/extrinsic tongue muscles,
medial pterygoid, hard palate, mandible
T4b (very advanced): invades lat pterygoid muscle, pterygoid plate, lat NPX, skull base, carotid encasement

For p16+ OPC, T4a and T4b are combined into a single T4 designation.

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27
Q

What is the N staging of p16(-) OPC?

A 
N1: single ipsi, ≤3 cm, ENE(–)
N2a: single ipsi, >3 cm, ≤6 cm, ENE(–)
N2b: multiple ipsi, ≤6 cm, ENE(–)
N2c: any bilat or contralat, ≤6 cm, ENE(–)
N3a: any >6 cm, ENE(–)
N3b: any clinically overt ENE(+)
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28
Q

What is the summary staging for p16(-) OPC?

A 
Stage I: T1N0
Stage II: T2N0
Stage III: T3N0 or T1–3N1
Stage IVA: T4aN0–1 or T1–4aN2
Stage IVB: T4b any N or any T N3
Stage IVC: any T any N M1
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29
Q

What is the N staging of p16(+) OPC?

A

Clinical
N1: any ipsi, ≤6 cm
N2: any contra or bilat LNs, ≤6 cm
N3: any >6 cm

Pathologic
N1: ≤4 LN positive
N2: >4 LN positive

30
Q

What is the overall stage grouping for p16(+) OPC?

A 
Clinical
Stage I: T1–2 N0–1
Stage II: T1–2 N2 or T3 N0–2
Stage III: any T N3 or T4 any N
Stage IV: M1
Pathologic
Stage I: T1–2 N0–1
Stage II: T1–2 N2 or T3–T4 N0–1
Stage III: T3–4 N2
Stage IV: M1
31
Q

Broadly speaking, what OPC pts/stage groups are deemed early, intermediate, and advanced?

A

Based on RTOG 0129 and AJCC 8th edition staging:
Early: stages I–II (cT1–2N0) and select III (T2N1)
Intermediate/favorable: HPV(+) stages III–IV (without T2N1) in nonsmokers/drinkers, T3N0 (exophytic) regardless of HPV/smoking status
Advanced/unfavorable: HPV(–) smokers with stages III–IV Dz, T4 Dz regardless of HPV/smoking status

32
Q

What are the Tx paradigms for early oropharyngeal tumors?

A

Early oropharyngeal tumor Tx paradigm: surgical resection with selective neck dissection +/- PORT or definitive RT alone

33
Q

What are the Tx paradigms for intermediate oropharyngeal tumors?

A

Intermediate-group oropharyngeal tumor Tx paradigms: Sg +/- postop CRT, altered fractionation RT, and CRT (conventional fractionation)

34
Q

What are the Tx paradigms for advanced/unfavorable oropharyngeal tumors?

A

Advanced/unfavorable oropharyngeal tumor Tx paradigm: CRT (conventional)

35
Q

When is WLE alone appropriate for OPC?

A

Rarely. WLE may suffice in the rare instance of a small (<1 cm), ant tonsillar pillar lesion.

36
Q

Is tonsillectomy ever adequate as a definitive Tx for tonsillar cancers?

A

Generally, no. Simple tonsillectomy is considered an excisional Bx and thus needs further definitive Tx. Radical tonsillectomy may be adequate in select
cases but results in worse functional outcomes than RT.

37
Q

What type of Sg is required for the surgical management of OPC?

A

Historically, labiotomy and mandibulotomy were required to gain access to the OPX, but there is growing experience with transoral approaches with transoral laser microsurgery (TLM) and transoral robotic surgery (TORS).

38
Q

When is PORT indicated for OPC? When is postop CRT indicated for OPC?

A

Similar to other H&N sites, PORT is generally for intermediate-risk factors such as T3–T4, LN+, LVSI, and PNI, while postop CRT is indicated for +margin or +ENE.

39
Q

When can unilat neck Tx be considered for OPC pts?

A

Unilat neck Tx can be considered if the lesion is well lateralized (T1–T2, <1 cm soft palate extension, no BOT involvement) and 1 or few regional ipsi nodes <6 cm based on multiple retrospective reviews showing a very low contralat failure rate (<3%).

40
Q

Which LN regions/levels should be irradiated in pts with an early T stage but N+ OPC?

A

Levels II–IV should always be included/irradiated; however, some data (Sanguineti G et al., IJROBP 2009) suggest that levels I and V may be omitted d/t a significantly lower incidence of nodal spread.

41
Q

What is the main indication for a neck dissection after definitive CRT for OPC?

A

The main indication for a neck dissection after CRT is persistent nodal Dz that can be documented by fine-needle sampling, CT (at 4–6 wks), or PET/CT (at 10–12 wks).

42
Q

What is the recommended timing for a neck dissection after CRT?

A

Neck dissection should typically occur at 6–8 wks (12–15 wks if evaluated by PET/CT).

43
Q

How should OPC pts be set up for simulation?

A

OPC pts should be simulated supine, with arms pulled inferiorly and the head extended with a bite block or stent. Contrast is recommended with CT.

44
Q

What type of custom stent can be used for OPC simulation?

A

Mouth opening, tongue depressing stent

45
Q

What should the pre-RT evaluation/preparation include for OPC?

A

Dental evaluation/fluoride prophylaxis, speech and swallow evaluation/exercises, and nutrition evaluation with a PEG tube if the pre-Tx weight loss is >10% over 3 mos

46
Q

What are the typical CTVs for IMRT planning for OPC?

A

CTV high dose (CTVHD): primary tumor and nodal GTV with 0.5–1-cm margin
CTV intermediate dose (CTVID): soft palate, adjacent parapharyngeal space, sup tonsillar pillars for lat tumors, and nodal levels adjoining involved nodes
CTV elective dose (CTVED): levels II–IV, RP nodes. If node+, most include ipsi IB and V.

47
Q

What are the typical RT doses and volumes used for OPC?

A

T1 and superficial T2N0: 66–70 Gy to CTVHD, 60 Gy to CTVID, and 54 Gy to CTVED, given in 30–35 fx over 6–7 wks

> T2+ without chemo:

(1) 70 Gy to CTVHD, 63 Gy to CTVID, and 56 Gy to CTVED given in 35 fx over 6 wks (per Danish Head and Neck Cancer Group [DAHANCA]);
(2) 70 Gy to CTVHD, 60 Gy to CTVID, and 57 Gy to CTVED given in 33 fx

> T3 or >N2 with chemo: 70 Gy to CTVHD, 63 Gy to CTVID, and 59.5 Gy to CTVED in 35 fx

48
Q

What is the 2-yr LF rate after IMRT alone for early (T1–2N0–1) OPC?

A

RTOG 00–22 (Eisbruch A et al., IJROBP 2010) demonstrated excellent results with accelerated hypofractionated IMRT for early OPC: 2-yr LF rate
was 9% (if major deviations, 50%; otherwise, 6%, SS).

49
Q

What were the RT techniques and doses employed in RTOG 00–22? How was the N stage established?

A

In RTOG 00–22 (Eisbruch A et al., IJROBP 2010), RT was delivered with accelerated hypofractionated IMRT as follows: 66 Gy in 30 fx (2.2 Gy/fx) to the primary PTV and 54–60 Gy in 30 fx (1.8–2 Gy/fx) to the secondary
PTV. Neck staging was clinical (not from CT); however, pts “upstaged” by CT (e.g., cN1 but N2 after CT) were also eligible.

50
Q

What did the RTOG 90–03 study demonstrate about the use of altered fractionation in H&N cancers?

A

RTOG 90–03 (Fu KK et al., IJROBP 2000): 1,073 pts with H&N cancers (10% OC, 60% OPX, 13% HPX) with stage III (28%) or stage IV (68%) Dz randomized to (a) conventional 70 Gy qd, (b) 81.6 Gy in 1.2 Gy/fx bid, (c)
accelerated with split, and (d) concomitant boost (1.8 Gy/fx qd × 17, with last 12 fx bid with 1.8 Gy AM, 1.5 Gy PM to 72 Gy). There was better LC with altered fx (54% vs. 46%) but no OS/DFS benefit. There was worse acute
toxicity but no difference in late toxicity.

51
Q

What randomized studies demonstrated better outcomes with hyperfractionated RT over conventional RT for OPC?

A 
RTOG 90–03 (Fu KK et al., IJROBP 2000): see above.
EORTC 22791 (Horiot JC et al., Radiother Oncol 1992): 325 pts (all OPX, but no BOT): 70 Gy vs. 80.5 Gy at 1.15 Gy bid. There was better LC (60% vs. 40%) but no OS benefit. LC was best for T3 Dz.
52
Q

What data showed good LC rates with RT alone for select advanced (stages III–IV) OPCs?

A

MDACC data (Garden AS et al., Cancer 2004): pts with small primaries but stages III–IV Dz by virtue of +LNs; treated with RT alone. There were acceptable 5-yr LF (15%), DM (19%), and OS (64%) rates.

53
Q

What are 2 important randomized trials that demonstrated the importance of adding chemo to conventionally fractionated RT in OPC?

A

GORTEC 94–01 (Calais G et al., JNCI 1999): 222 pts with stages III–IV OPC randomized to conventional RT alone vs. conventional RT + carboplatin/5-FU, no planned neck dissection for N2–3 Dz. The CRT arm had better 3-yr OS (51% vs. 31%), DFS (30% vs. 15%), and LC (66% vs.
42%); however, there was significantly worse grades 3–4 mucositis and weight loss/feeding tube use in the CRT arm.
Head and Neck Intergroup Study (Adelstein DJ et al., JCO 2003): 295 pts with unresectable stages III–IV H&N cancers (15% OC, 55% OPX, 20% HPX), RT alone vs. CRT with cisplatin 100 mg q3 wks × 3. 3-yr OS was
better in the CRT arm (37% vs. 23%). There also was improved DFS (51% vs. 33%) in the CRT arm.

54
Q

Pooled analysis from which 2 important RCTs support adding chemo to PORT in H&N cancers for +margin and ECE?

A

EORTC 22931 (Bernier J et al., NEJM 2004): 334 pts randomized to PORT 66 Gy vs. PORT + cisplatin 100 mg/m2 on days 1, 22, and 43. Eligibility: ECE, +margin, PNI, LVI, and levels 4–5 +N from OCC/OPC. There was
better OS, DFS, and 5-yr LC with CRT but ↑ grades 3–4 toxicity.
RTOG 95–01 (Cooper JS et al., NEJM 2004): 459 pts randomized to 60–66 Gy PORT vs. PORT + cisplatin 100 mg/m2 on days 1, 22, and 43. Eligibility: >2 LN, ECE, +margin. There was better DFS (43% vs. 54%)
and 2-yr LRC (72% vs. 82%) but only a trend to improvement in OS (57% vs. 63%).

55
Q

What study demonstrated improvement in OS with the addition of cetuximab (C225) to RT in H&N cancers?

A

Bonner JA et al. (NEJM 2006): 424 pts with stages III–IV SCC of the OPX, laryngeal cancer, or HPX randomized to RT vs. RT + C225. RT options were conventional to 70 Gy, 1.2 bid to 72–76.8 Gy, or concomitant boost to 72 Gy. There was better 3-yr LRC (47% vs. 34%) and OS (55% vs. 45%) with C225 + RT. Subset analysis showed improvement mostly in OPC and in the altered fractionation RT arms (∼50% treated with altered fractionation).

56
Q

What studies are looking at Tx deintensification for HPV+ OPX?

A
  1. E1308: Phase II, stages III/IV, induction chemo (paclitaxel, cisplatin,cetuximab) f/b 54 Gy in 27 fx if CR or 69.3 Gy in 33 fx if PR, both with concurrent cetuximab. Although the study (Marur S et al., J Clin Oncol 2017) met its 2-yr PFS target based on historical control, other phase III trials indicate induction chemo adds toxicity without survival benefit (PARADIGM, DeCIDE).
  2. RTOG 1016: Phase III, stages III/IV, treated with accelerated IMRT to 70 Gy/6 wks randomized to concurrent cisplatin vs. cetuximab.
  3. NRG HN002: Phase II, stages III/IV, randomized to dose-reduced cisplatin CRT (60 Gy in 6 wks) vs. accelerated RT alone (60 Gy in 5 wks).
57
Q

What 2 randomized studies demonstrated a benefit with induction taxane/platinum/5-FU (TPF) chemo over PF in pts with unresectable H&N cancers?

A

TAX 324 study (induction chemo → CRT) (Posner MR et al., NEJM 2007): 501 pts, unresectable stages III–IV H&N cancers (52% OPX, 13%–18% OC, larynx, HPX) randomized to induction platinum + 5-FU or TPF
→ CRT with carboplatin. There was better 3-yr OS (62% vs. 48%), MS (71 mos vs. 30 mos), and LRC (70% vs. 62%) in the TPF arm. Pts in the TPF arm had fewer Tx delays than in the platinum/5-FU arm despite
higher myelotoxicity in the TPF arm (98% rcvd planned Tx in the TPF arm vs. 90% in the PF arm).

TAX 323 study (induction chemo → RT) (Vermorken JB et al., NEJM 2007): 358 pts, unresectable stages III–IV H&N cancers (46% OPX, 18% OC, 29% HPX, 7% larynx) randomized to induction platinum + 5-FU or
TPF → RT alone. TPF resulted in better median PFS (11 mos vs. 8.2 mos), MS (18.8 mos vs. 14.5 mos), and HR 0.73. The rate of toxic deaths was greater in the platinum/5-FU group (5.5% vs. 2.3%). Also, there was more grades 3–4 thrombocytopenia, anemia, stomatitis, n/v, diarrhea, and hearing loss in the platinum/5-FU arm. Neutropenia, leukopenia, and alopecia were more common in the TPF arm.

58
Q

What study compared induction chemo vs. upfront CRT?

A 
PARADIGM study (induction TPF → CRT vs. CRT) (Haddad H et al., Lancet Oncol 2013): 145 pts, stages III–IV (55% OPX), randomized to induction TPF → CRT vs. CRT. At a median follow-up of 49 mos, there was
no difference in 3-yr OS (73% for induction vs. 78% for CRT), with a higher rate of febrile neutropenia observed in the induction arm.
59
Q

What are some advantages and disadvantages of split-field IMRT (vs. whole-field IMRT) in the Tx of H&N cancers?

A

There is potentially better laryngeal sparing with split-field IMRT techniques; however, the drawback is that the practitioner may have to junction the RT dose through involved nodes.

60
Q

What are the advantages and disadvantages of IMRT “dose painting” (vs. sequential plans) in the Tx of H&N cancers?

A

The main advantage of IMRT dose painting is that better conformality can be achieved in a single plan. The drawback, however, is that nonstandard doses/fx are required.

61
Q

How do unplanned RT interruptions in H&N cancer affect LC rates and why?

A

Each wk of Tx-time prolongation reduces the LC rate by ∼10%–12% in H&N cancer pts b/c of accelerated repopulation

62
Q

What is the best way to compensate for several/few missed RT sessions and avoid Tx-time prolongation in H&N cancer pts?

A

According to Bese NS et al. the best way to compensate is by preserving total time, dose, and dose/fx (i.e., can treat bid on Fridays or extra fx on Saturdays). Alternatively, dose/fx can be increased (e.g., by 0.5–0.7 Gy/day). (IJROBP 2007)

63
Q

What is the approximate long-term PEG tube dependency rate after CRT for OPC?

A

The long-term PEG tube dependency rate after CRT can be as high as 15%–20%, which is reduced with efforts on sparing swallowing structures (pharyngeal constrictors, larynx) with swallowing exercises and the use of PEG on demand.

64
Q

What are some typical RT dose constraints for the parotid glands?

A

Typical RT dose constraints for the parotid glands are (a) mean dose to either parotid <26 Gy or (b) at least 50% of either parotid gland <30 Gy.

65
Q

What is the typical RT dose constraint for the inner ears?

A

The mean dose to the inner ears should be ≤35 Gy.

66
Q

Appx what % of pts receiving cisplatin-based chemo will experience hearing loss as a result of ototoxicity?

A

∼30% of pts will experience hearing loss.

67
Q

What were the xerostomia rates for OPC pts treated with IMRT in RTOG 00–22?

A

Xerostomia rates in RTOG 00–22 (Eisbruch A et al., IJROBP 2010) were 55% at 6 mos, 25% at 1 yr, and 16% at 2 yrs. Salivary output did not recover over time.

68
Q

What was the observed rate of osteoradionecrosis with accelerated hypofractionated IMRT in RTOG 00–22?

A

The observed rate of osteoradionecrosis was 6% in RTOG 00–22 (Eisbruch A et al., IJROBP 2010), which is higher than expected for IMRT (potentially
b/c of the accelerated hypofractionated approach). Other toxicities were acceptable (grade 2+ for mucosa [24%], salivary [67%], esophagus [19%]).

69
Q

What oral care do all pts need to be instructed on?

A

Fluoride trays. Consult a dental oncologist before any dental procedures.

70
Q

What is the follow-up paradigm for OPC pts?

A

OPC follow-up paradigm: H&P + pharyngolaryngoscopy (q1–3 mos for yr 1, q2–6 mos for yr 2, q4–8 mos for yrs 3–5, q12 mos if >5 yrs), imaging (for signs/Sx), annual TSH, speech/hearing/dental evaluation, and smoking
cessation.

Radiation Oncology Factoids (44 decks)

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