Esophageal cancer

Question 1

What are the boundaries of the esophagus that divide it into Cx, upper T, midthoracic, lower T, and abdominal regions?

Answer 1

The esophagus spans from the cricopharyngeus at the cricoid to the esophageal-gastric junction (EGJ). The Cx esophagus spans from
hypopharynx to sternal notch (15 to <20 cm from incisors), the upper T from the sternal notch to the azygos vein (20 to <25 cm), the middle T from azygos vein to inf pulmonary vein (25 to <30 cm), the lower T from the inf pulmonary vein to the EGJ (30 to <40 cm), and the abdominal from EGJ to 2 cm below EGJ (40 to 45 cm).

Question 2

Why is esophageal cancer more prone to locoregional spread than other GI
cancers?

Answer 2

The esophagus has an adventitial layer but does not have a serosal layer, thus reducing the resistance against local spread of cancer.

Question 3

What is the incidence and mortality of esophageal cancer in the United
States?

Answer 3

There are ∼17,000 cases diagnosed and ∼16,000 deaths per yr in the United
States. Males are more commonly affected than females (3:1).

Question 4

Is there an association b/t esophageal cancer and HPV infection?

Answer 4

The single largest case-control studies by Cao B et al. showed a risk of HPV
2.7-fold greater in cases of esophageal SCC than in controls. (Carcinogenesis
2005)

Question 5

What are the risk factors for developing esophageal cancer?

Answer 5

Esophageal SCC risk factors: smoking/alcohol, tylosis, Plummer–Vinson syndrome, Fanconi anemia, Bloom syndrome, caustic injury to the esophagus, Hx of H&N cancer, and achalasia. HPV infection has been associated in ∼20% cases in high-incidence areas (China, Africa, and Japan) but none in low-incidence areas (Europe, United States).

Esophageal adenocarcinoma (adeno) risk factors: obesity/GERD, Barrett esophagus, lack of fruits/vegetables, low socioeconomic status

Question 6

What are some protective factors for developing esophageal cancers?

Answer 6

Protective factors for developing esophageal cancer include

fruits/vegetables and Helicobacter pylori infection (possible atrophic gastritis).

Question 7

How do pts with esophageal cancer typically present?

Answer 7

Dysphagia and weight loss (>90%), odynophagia, pain, cough, dyspnea, and
hoarseness

Question 8

What is the pattern of spread of tumors of the esophagus?

Answer 8

Tumors of the esophagus spread locoregionally through the extensive submucosal lymphatic plexus or distantly through hematogenous routes.

Question 9

What histologies predominate based on the tumor location within the
esophagus?

Answer 9

The proximal three-fourths of the esophagus (Cx to midthoracic) are mostly
SCCs (∼30%–40%), whereas adeno generally is found in the distal esophagus (∼60%–70%).

Question 10

What more uncommon histologies are seen for tumors of the esophagus?

Answer 10

Adenocystic, mucoepidermoid, small cell, and sarcomatous
(leiomyosarcoma) carcinomas (all typically ≤1% of cases). Extremely rare
types are lymphoma, Kaposi sarcoma, and melanoma.

Question 11

What are the common sites of DM seen for esophageal cancers?

Answer 11

Lung, liver, and bone are the most common sites of DM. (Xi M et al., Radiother Oncol 2017)

Question 12

What is the most important factor that determines nodal mets and DM?

Answer 12

DOI is the most important factor dictating nodal and distant spread. (Mariette
C et al., Cancer 2003)

Question 13

What is the extent of submucosal spread of Dz seen for esophageal
cancers, and does it differ by histology?

Answer 13

Gao XS et al. reported the following for SCC: mean microscopic proximal
and distal spread beyond GTV of 10.5 ± 13.5 mm and 10.6 ± 8.5 mm, respectively, with 94% of pts having all tumor contained within a 30-mm margin. For adeno, mean spread of Dz is to 10.3 ± 7.2 mm proximally and 18.3 ± 16.3 mm distally, with a margin of 50 mm required to encompass all tumor in 94% of cases. (IJROBP 2007)

Question 14

What components of the Hx are important in assessing a pt with dysphagia?

Answer 14

Appropriate parts of the Hx in assessing dysphagia Sx include onset, duration, severity (dysphagia to normal solids, soft solids, liquids, or aphagia), weight loss, other Sx of retrosternal pain, bone pain, cough,
hoarseness, Hx of smoking/alcohol, GERD, and Hx of prior H&N cancer.

Question 15

What should be included in the workup of suspected esophageal cancer?

Answer 15

Suspected esophageal cancer workup: H&P, labs (LFTs, alk phos, Cr),
esophagogastroduodenoscopy with Bx. If cancer, then chest/abdominal ± pelvic CT w/ contrast; if not M1, then PET/CT, EUS + FNA for nodal sampling for tumor and node staging, bronchoscopy (if tumor at or above carina to r/o tracheoesophageal fistula), assign Siewert category, nutritional assessment, smoking cessation, and screen for family Hx. Laparoscopic staging is done in some institutions, with reports of upstaging and sparing the
morbidity of more aggressive Tx in 10%–15% of cases. If M1, testing for MSI-H/dMMR including HER2 and PD-L1 if adeno (NCCN 2018).

Question 16

To what anatomic extent is esophageal cancer being defined?

Answer 16

Esophageal cancer is defined as below hypopharynx (15 cm from the incisors) to the EGJ and the proximal 2 cm of the stomach. A tumor epicenter ≥2 cm distal to the EGJ, even if it involves EGJ, is considered stomach cancer.

Question 17

What is different about the AJCC 8th edition (2017) of the TNM staging for esophageal cancer?

Answer 17

The AJCC 8th edition redefines tumor location based on location of epicenter rather than proximal border, adds unique tumor, nodes, & metastases clinical staging (cTNM) and tumor, nodes, & metastases pathologic staging postneoadjuvant therapy (ypTNM) prognostic stage groupings, incorporates pT1a
and pT1b into stage grouping, and separates pT2–T3 into pT2 and pT3 for
stage grouping.

Tis: high-grade dysplasia and CIS
T1a: invades lamina propria or muscularis mucosae
T1b: invades submucosa
T2: invades muscularis propria
T3: invades adventitia (Note: No serosal layer.)
T4a: invades pleura, pericardium, azygos vein, diaphragm, or peritoneum
T4b: invades other adjacent organs (aorta, vertebral body, airway)
Nx: regional nodes cannot be assessed
N0: no regional node mets
N1: 1–2 regional LN mets, including nodes previously labeled as M1a in
AJCC 6th*
N2: 3–6 regional LN mets, including nodes previously labeled as M1a*
N3: ≥7 regional LN mets, including nodes previously labeled as M1a*
*M1a (differ by site): upper T includes Cx LN mets; midthoracic is not
applicable; lower T/GE junction includes celiac LN mets. (Note: M1a
designation is no longer recognized in the 7th or 8th editions.)
M1: DM (retroperitoneal, P-A LN, lung, liver, bone, etc.)

Question 18

What are the AJCC 8th edition (2017) stage groupings for esophageal
cancer, and what new feature has been added?

Answer 18

For SCC;
Stage 0: TisN0M0
Stage I: T1N0–1M0
Stage II: T2N0–1M0; T3N0M0
Stage III: T3N1M0; T1–3N2M0
Stage IVA: T4 or N3
Stage IVB: M1
Tumor, Nodes, & Metastases pathologic staging (pTNM) (Location is
“Any” unless specified)
Stage 0: TisN0M0, N/A
Stage IA: T1aN0M0, G1/GX
Stage IB: T1aN0M0, G2–3; T1bN0M0, any G; T2N0M0, G1
Stage IIA: T2N0M0, G2–3/GX; T3N0M0, any G, Lower; T3N0M0, G1,
Upper/Middle
Stage IIB: T3N0M0, G2–3, Upper/Middle; T3N0M0, GX; T1N1M0, any G
Stage IIIA: T1N2M0, any G; T2N1M0, any G
Stage IIIB: T2N2M0, any G; T3N1–2M0, any G; T4aN0–1M0, any G
Stage IVA: T4aN2M0, any G; T4b or N3, any G
Stage IVB: M1
ypTNM
Stage I: T0–2N0M0
Stage II: T3N0M0
Stage IIIA: T0–2N1M0
Stage IIIB: T3N1M0; T0–3N2M0; T4aN0M0
Stage IVA: T4aN1–2/NXM0; T4b or N3
Stage IVB: M1

For adeno:
Stage 0: TisN0M0
Stage I: T1N0M0
Stage IIA: T1N1M0
Stage IIB: T2N0M0
Stage III: T2N1M0; T3N0–1M0; T4aN0–1M0
Stage IVA: T4b or N2–3
Stage IVB: M1
pTNM
Stage 0: TisN0M0, N/A
Stage IA: T1aN0M0, G1/GX
Stage IB: T1aN0M0, G2; T1bN0M0, G1–2/GX
Stage IC: T1N0M0, G3; T2N0M0, G1–2
Stage IIA: T2N0M0, G3/GX;
Stage IIB: T1N1M0, any G; T3N0M0, any G
Stage IIIA: T1N2M0, any G; T2N1M0, any G
Stage IIIB: T2N2M0, any G; T3N1–2M0, any G; T4aN0–1M0, any G
Stage IVA: T4aN2M0, any G; T4b or N3, any G
Stage IVB: M1
ypTNM
Stage I: T0–2N0M0
Stage II: T3N0M0
Stage IIIA: T0–2N1M0
Stage IIIB: T3N1M0; T0–3N2M0; T4aN0M0
Stage IVA: T4aN1–2/NXM0; T4b or N3
Stage IVB: M1

Question 19

Why does SCC have a separate stage grouping from Adeno?

Answer 19

Tumor location is accounted for in the stage grouping for SCC, with lower regions having better prognosis c/w upper and middle regions.

Question 20

What are the most important features that predict for poor outcomes in pts with T1 esophageal cancers treated with surgical resection alone?

Answer 20

T1b Dz, LVI, and tumor length predict poor outcomes in these pts. (Cen P et al., Cancer 2008; Bolton WD et al., J Thorac Cardiovasc Surg 2009)

Question 21

What are the types of surgical procedures employed for the management of esophageal cancers?

Answer 21

Minimally invasive esophagectomy using laparoscopy, thoracoscopy, or a combination. Traditional surgical approaches include radical esophagectomy, transhiatal, or transthoracic esophagectomies.

Question 22

How do transhiatal and transthoracic esophagectomy procedures compare
in terms of dissection extent and location of the Dz?

Answer 22

In general: A transhiatal approach may be less morbid but will have less
exposure for tumor clearance and thorough LND c/w a transthoracic
approach. Anastomotic leak for the transhiatal approach is easier to manage than the transthoracic approach (Cx vs. intrathoracic leaks).

Transhiatal esophagectomy: Pros: good for distal tumors with possible en bloc resection, laparotomy and a Cx approach (no thoracotomy) with Cx
anastomosis, less morbid with less pain, and avoids fatal intrathoracic anastomotic leak. Cons: poor visualization of upper/midthoracic tumors,
LND limited to blunt dissection, more anastomotic leaks, and more
recurrent laryngeal nerve palsy.

Transthoracic esophagectomy: Pros: Ivor–Lewis (right thoracotomy) is the most common and preferred route and best for exposure for all levels of
the esophagus, whereas left thoracotomy provides access to only the distal
esophagus. Ivor–Lewis (right thoracotomy and laparotomy) provides direct
visualization and exposure with a better radial margin and a more thorough LND. Cons: intrathoracic leak that can lead to fatal mediastinitis. Generally considered to have higher morbidity and mortality than
transhiatal.

Question 23

Does the # of nodes removed from esophagectomy predict for better outcome?

Answer 23

Yes. Data suggest that the # of nodes removed is an independent predictor of
survival. In 1 large study, the optimal # was ≥23. (Peyre CG et al., Ann Surg
2008)

Question 24

Is there evidence to prove that either transhiatal or transthoracic esophagectomy would be sup for Dz control and outcome?

Answer 24

No. There are no data to date showing that 1 approach is sup to the other. 2 large meta-analyses comparing transhiatal with transthoracic esophagectomy have shown equivalence. (Rindani R et al., Aust N Z J Surg 1999; Hulscher
JB et al., Ann Thorac Surg 2001) In general, transthoracic approaches carry greater operative mortality and pulmonary complications, but transhiatal approaches have greater anastomotic leaks and stricture rates as well as recurrent laryngeal nerve injury. 5-yr OS rates are similar b/t the 2
approaches (20%–25%).

Question 25

What is the 5-yr OS for pts managed with Sg alone for localized esophageal cancers?

Answer 25

5-yr OS is 20%–25% for pts managed with Sg alone for localized Dz. This is higher for earlier-stage Dz (T1N0 ∼77%) but lower for stage III Dz (∼10%– 15%).

Question 26

Is there evidence to support the use of preop chemo (no RT) for Tx of resectable esophageal cancers?

Answer 26

This is controversial. Several phase II studies have demonstrated benefit,
and randomized studies have reported conflicting results on the benefit of
preop chemo. U.S. Intergroup trial (Kelsen DP et al., NEJM 1998; Long-term updated, Kelsen DP et al., JCO 2007): 467 pts (53% adeno, 47% SCC) randomized to 3 × 5-FU/cisplatin preop and 2 × 5-FU/cisplatin postop or immediate surgical resection alone. There were no differences in resectability or survival (4-yr OS 26% vs. 23%, respectively; MS 16 mos vs. 15 mos, respectively). pCR was 2.5%. Pts with complete resection had a 5-yr DFS
of 32% vs. 5% with R1–R2 resection.

Question 27

Is there evidence to support adding radiation to neoadj chemo?

Answer 27

MRC randomized trial of preop chemo (MRC, Lancet 2002): 802 pts (66%
adeno, 31% SCC, 3% undifferentiated) randomized to (a) 2 × cisplatin/5- FU preop or (b) immediate Sg. There was a significant benefit of neoadj chemo. MS was 13.3 mos vs. 16.8 mos, respectively, and 2-yr OS was 34% vs. 43%, respectively. The complete resection rate was also improved by chemo (54% vs. 60%, respectively).

German Esophageal Cancer Study Group (POET) trial (Stahl M et al., JCO 2009; Long-term update, Stahl M et al., Eur J Cancer 2017):
randomized phase III in pts with T3–4N any M0 adeno of the GE junction or gastric cardia. The study closed early d/t poor accrual (126 of 354 intended). Randomization: (a) induction chemo → Sg or (b) induction
chemo → preop CRT → Sg. Chemo was cisplatin/5 FU/leucovorin. RT was 30 Gy in 15 fx. pCR was better in the preop CRT group (15.6% vs.
2%) and in tumor-free LNs (64% vs. 38%). 5-yr OS trended better in the CRT group (39.5% vs. 24.4%, p = 0.055). Postop mortality higher in the CRT group (10% vs. 3.8%, p = 0.26).

Neoadjuvant Chemotherapy Versus Radiochemotherapy for Cancer of the Esophagus or Cardia (NeoRes) (Klevebro F et al., Ann Oncol 2016):
181 pts with esophageal/EGJ adeno or SCC randomized to (a) preop chemo alone cisplatin/5-FU × 3 or (b) same chemo + concurrent RT (CRT)
(40 Gy/20 fx). Primary endpoint met showing CRT improved pCR (28% vs. 9%) and also improved R0 rate (87% vs. 74%), but 3-yr OS (47% vs. 49%) and 3-yr PFS (44% both arms) not improved. CRT increased noncancer causes of death in 1st year post randomization (46% vs. 15%, p = 0.036).

Question 28

What is the phase III evidence to support preop CRT over Sg alone?

Answer 28

This had been controversial until the recent publication of the CROSS trial. Urba SG et al. (JCO 2007): 100 pts (75% adeno, 25% SCC) randomized to cisplatin/vinblastine/5-FU + RT to 45 Gy bid vs. Sg alone. 3-yr OS was 30% vs. 16%, respectively (p = 0.18). DM same in both arms (60%).
Burmeister B et al. (Lancet 2007, TTROG): 256 pts (67% adeno, 33% SCC) randomized to cisplatin + 5-FU with RT to 35 Gy/15 fx. Less intensive
chemo (5-FU 800 mg/m2 vs. 1,000 mg/m2 in other studies) was used. There was no difference in OS overall, but there was a trend to improved
OS in SCC.

Question 29

In the CROSS trial, what % of pts had R0 resection in the CRT arm vs. Sg alone arm and what % had a pCR to CRT?

Answer 29

In the CROSS trial, 92% had an R0 resection in the CRT arm vs. 69% in the Sg alone arm. 29% (23% of adeno and 49% of SCC) had a pCR to CRT (typical CR avg of randomized trials 25%–30%). (van Hagen P et al., NEJM 2012)

Question 30

Is there a role for preop RT alone for esophageal cancers?

Answer 30

No. Studies demonstrate no benefit of preop RT alone.

Question 31

Is there a role for postop RT alone for esophageal cancers?

Answer 31

Postop RT alone has failed to demonstrate a benefit in several randomized trials. Incomplete resection should rcv definitive CRT or palliative chemo or RT alone. Completely resected stages II–III adeno of the EGJ should rcv postop CRT based on the Intergroup gastric trial (20% EGJ tumors). (MacDonald JS et al., NEJM 2001)

Question 32

What are the data demonstrating efficacy of definitive CRT vs. RT alone?

Answer 32

RTOG 85-01 (Herskovic A et al., NEJM 1992; Cooper JS et al., JAMA 1999): 130 pts (82% SCC, 18% adeno) randomized to 64 Gy RT alone vs. 50 Gy RT + cisplatin/5-FU × 2 during RT and 2 cycles after RT. There was SCC in 88% pts. 5-yr OS was 27% vs. 0% for RT alone. 10-yr OS was 20% for CRT. No outcome difference b/t adeno and SCC. RT technique used in this trial: initial RT field was the whole esophagus to 50 Gy (RT alone) or 30 Gy
(CRT) → CD to 14 Gy (RT) or 20 Gy (CRT) to tumor + 5-cm sup/inf margin.

Question 33

Is there a benefit of escalating the RT dose during CRT for esophageal
cancer?

Answer 33

This is controversial, b/c INT 0123 (Minsky BD et al., JCO 2002) is a phase III study that randomized pts to 50.4 Gy vs. 64.8 Gy with cisplatin + 5-FU × 2 → adj cisplatin/5-FU × 2. There was no difference in LC (44% vs.
48%). Excessive deaths in 64.8-Gy arm (11 vs. 2) were seen even before the 50.4-Gy dose (7 of 11 deaths). However, separate analysis excluding the early deaths still did not find a benefit to a higher dose. RTOG 9207 (Gaspar et al., Cancer 2000) incorporated a brachytherapy boost and resulted in unacceptable toxicity: 10% mortality and 12% esophageal fistula.

Question 34

Is there evidence to suggest that Sg can be omitted in operable pts with localized esophageal cancer?

Answer 34

There are no strong data suggesting Sg can be omitted in pts with adeno
of the esophagus. However, there are 2 randomized trials examining CRT +
Sg vs. CRT alone in pts with SCC that demonstrated an LC benefit of adding
Sg but not an OS benefit. This is possibly d/t increased postop mortality in pts with SCC.

Bedenne L et al. (JCO 2007): 444 pts enrolled, treated 1st with CRT (45 Gy
or split course 15 Gy × 2); the 230 responding pts (88% SCC) were randomized to Sg or no Sg. LC was better with Sg (66% vs. 57%). There was no difference in survival (34% vs. 40%). The mortality rate was higher in the Sg group (9.3% vs. 0.8%).

Stahl M et al. (JCO 2005): 172 pts with SCC randomized to induction chemo + 40 Gy/chemo + Sg vs. induction chemo + 65 Gy/chemo alone. PFS was
better with Sg (64% vs. 41%). Survival was the same b/t arms, with a trend to better survival with Sg. Postop mortality rate was also high in the surgical group (12.6% vs. 3.2%).

The benefit of Sg after CRT may be seen if postop mortality could be minimized, such as operation in high-volume facilities, where postop
mortality should be in the range of 2%–4%.

Question 35

Could salvage therapies (Sg or RT) be performed after definitive CRT or Sg for esophageal cancer management?

Answer 35

Yes. Salvage Sg could be performed for select pts who recur after definitive CRT but with increased operative morbidity/mortality (Tachimori Y et al.,
J Thorac Cardiovasc Surg 2009). RTOG 0246 (Swisher S et al., IJROBP
2012) was a phase II trial looking at selective Sg for pt with residual or recurrent Dz after induction chemo + CRT. 51% of pts underwent Sg (19% had recurrent Dz, other had residual). 10% Tx-related mortality. 1-yr OS 71%, which failed to meet hypothesized 1-yr survival of 77.5%.
Salvage RT can be performed for isolated LR after Sg alone, but the dose
should be limited to 45 Gy with concurrent chemo b/c of gastric pull through.

Question 36

Can RT be performed in pts with tracheoesophageal fistula?

Answer 36

Yes. Although historically it was contraindicated b/c of fear that RT may worsen the fistula, available studies demonstrate that RT does not worsen the fistula and may even cause healing and closure (Muto M et al., Cancer 1999).
Also, per NCCN guidelines an esophageal stent may be considered to decrease tracheoesophageal fistula Sx but complications are common. (Ross W et al., Gastrointestinal endoscopy 2007)

Question 37

How are cancers of the Cx esophagus managed in general?

Answer 37

B/C of the difficult and morbid Sg (total laryngopharyngoesophagectomy),
cancers of the Cx esophagus are Tx like an H&N primary with a
nonsurgical approach and definitive CRT. Case series using IMRT + 5- FU/cisplatin (Wang SL et al., WJG 2006; Burmeister B et al., AOHNS 2000; McDowell L et al., IJROBP 2017) show that high doses from 60–70 Gy offers good LC and response (LC 88% and 5-yr OS 55% from the Burmeister
B et al. series) but an NCDB analysis did not find an association between increased dose and improved OS (De B et al., Dis Esoph 2017). However,
late toxicity, such as esophageal stricture, is a problem.

Question 38

Can definitive RT be used for early-stage (Tis, IA) esophageal cancers?

Answer 38

Yes, for SCC. With doses 60–72 Gy or 55–60 Gy + a brachytherapy boost,
the LC and DFS is ∼80% in pts with SCC. Tumors >5 cm should rcv CRT b/c
of poorer LC (∼50%–60%). (Hishikawa Y et al., Radiother Oncol 1991)

Question 39

What are the radiotherapy doses and techniques for the management of esophageal cancer?

Answer 39

Preop CRT: 41.4–50.4 Gy for adeno and SCC
Definitive CRT: 50–50.4 Gy for adeno and SCC. Higher doses (60–66 Gy
per NCCN) may be considered for SCC of the Cx esophagus.

Field size: Respecting anatomic boundaries, CTV = GTV+3–4 cm sup and
inf along esophagus and cardia and 1 cm radial expansion & Nodal CTV =
nodal GTV + 0.5–1.5 cm. Elective mediastinal or celiac nodes included
based GTV location.

Consider IMRT for cardiac, lung and/or kidney sparing as needed, with possible benefit of IMRT vs. 3D in reducing cardiac mortality based on MDACC retrospective and SEER-Medicare data (Lin SH et al., IJROBP 2012; Cancer 2016) and postop complications
(Wang J et al., IJROBP 2013). (See IMRT contouring atlas: Wu J et al.,
IJROBP 2015)

Question 40

Is there a role for induction chemo prior to neoadj CRT?

Answer 40

Possibly. The CALBG 80803 phase II crossover trial (Goodman KA et al.,
ASCO GI 2017) looked at 257 pts randomized to induction chemo, either modified FOLFOX-6 or carboplatin/ paclitaxel f/b a repeat PET. Pt who responded (>35% decrease in standardized uptake value [SUV]) went onto
CRT (50.4 Gy/28 fx) then Sg. Nonresponders crossed over to alternative chemo with RT, then Sg. The hypothesis was that cross over chemo will
improve pCR from the null of <5% to 5–20%. In the FOLFOX group, the responders had a pCR 38% and the nonresponders had pCR 16.2%. In the carboplatin/ paclitaxel group, the responders had a pCR 10.7% and the nonresponders had a pCR of 15%. Conclusion was nonresponders had improved pCR from induction and cross-over chemo.

Question 41

Is there any benefit to adding targeted EGFR inhibition to definitive CRT?

Answer 41

No, 2 randomized trials showed no benefit with the addition of cetuximab.
SCOPE1 phase II/III randomized trial (Crosby T et al., Lancet Oncol 2013)
had randomized 258 pts to definitive CRT vs. definitive CRT with cetuximab, before closing trial early before going to phase III d/t futility of
experimental arm. The cetuximab arm performed worse than CRT alone for MS (22.1 mos vs. 25.4 mos, HR 1.53, p = 0.035) and with greater grade 3–4 nonhematologic toxicities (79% vs. 63%, p = 0.004). RTOG 0436 Phase III trial (Suntharalingam M et al., JAMA Oncol 2017) randomized 344 pts to definitive CRT with cisplatin/paclitaxel ± cetuximab regardless of EGFR expression. Cetuximab did not improve cCR (56% vs. 58% control), LF (3-yr 49% both arms), or OS (3-yr 45%
vs. 44%).

Question 42

What Tx options exist for malignant dysphagia in a metastatic pt?

Answer 42

Consider starting with chemo alone with diet changes as indicated. RT
(mainly 20 Gy/5 fx) decreased dysphagia in 75%, lasting for about 5 mos
(Murray LJ et al., PRO 2012). Stents work faster but with less durable responses, and complications include pain, migration, and reflux.

Question 43

What is the rate of esophageal stricture following RT alone & CRT?

Answer 43

For esophageal cancer, series of RT alone reveal benign strictures in 12%–
30% of pts, and 1 series showed a 12% rate >1 yr after CRT (Adebahr S et
al., Best Pract Res Clin Gastroenterol 2016). Balloon dilation is successful for ∼80%–90%.

Question 44

What types of toxicities are experienced during radiotherapy, and what
measures should be taken to help minimize these toxicities?

Answer 44

Relief is obtained with topical anesthesia, narcotics, H2 blockers, feeding tube (J-tube if preop CRT, PEG if definitive CRT), and limiting the dose
to critical structures.

Acute: esophagitis, skin irritation, fatigue, weight loss

Late: dysphagia, stricture, pneumonitis, laryngeal edema, cardiac injury, renal
insufficiency, liver injury

Question 45

Describe an appropriate f/u schedule for pts after completion of Tx for
esophageal cancer?

Answer 45

Majority of relapses within 2 yrs. F/u for esophageal cancer after Tx: H&P
q3–6 mos for 2 yrs, q6–12 mos for next 3 yrs, then annually; at each visit,
basic labs such as CBC/ chemistry panel; consider CT chest/abd every 6 mos × 2 yrs, and if bimodality therapy EGD every 3–6 mos × 2 yrs, q6mos for 3rd yr, then as clinically indicated (NCCN 2018); and dilatation for stenosis and nutritional counseling as needed.