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Ann Thorac Surg 2007;84:393-400
© 2007 The Society of Thoracic Surgeons

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Original Articles: General Thoracic

Positron Emission Tomographic Scanning Predicts Survival After Induction Chemotherapy for Esophageal Carcinoma

Division of Thoracic Surgery, Department of Cardiothoracic Surgery, New York Presbyterian Hospital, Weill Medical College of Cornell University, New York, New York

Accepted for publication March 26, 2007.

^_* Address correspondence to Dr Altorki, Division of Thoracic Surgery, Department of Cardiothoracic Surgery, Suite M404, Weill Medical College of Cornell University, East 68th Street, New York, NY 10021 (Email: nkaltork{at}med.cornell.edu).

Presented at the Forty-third Annual Meeting of The Society of Thoracic Surgeons, San Diego, CA, Jan 29–31, 2007.

	Abstract

Top Abstract Introduction Patients and Methods Results Comment Discussion References

 
Background: The ability to accurately predict clinical and pathological response and survival in patients undergoing preoperative chemotherapy may have a significant impact on treatment strategy for esophageal carcinoma. This study assessed the predictive accuracy of clinical response (CR) and positron emission tomography (PET) scanning in determining pathological downstaging and disease free survival (DFS) after chemotherapy.

Methods: This is a retrospective review of patients who underwent chemotherapy prior to complete surgical resection for esophageal carcinoma between 1999 and 2005. Clinical response was correlated with pathological downstaging and survival. For PET scanning, the percent reduction in maxSUV after induction therapy was determined and we identified the optimal threshold of percent reduction in maxSUV for predicting clinical response and pathological downstaging.

Results: Sixty-two patients (52 men, median age 62.3) were evaluated. Thirty-nine patients (62.9%) had either a partial (n = 32) or complete clinical response (n = 7) to induction therapy. The sensitivity, specificity, positive, and negative predictive value of an objective clinical response in predicting downstaging in T and (or) N were 85.7%, 55.9%, 61.5%, and 82.6%, respectively. There was no difference in DFS between responders and nonresponders. The PET sensitivity, specificity, positive, and negative predictive values for predicting pathologic downstaging were 77.8%, 52.9%, 56.8%, and 75%, respectively. Thirty-seven patients (59.7%) had a 50% or greater reduction in the maxSUV of their primary tumor and had a significant improvement in DFS compared with patients with a less than 50% reduction in maxSUV (median DFS time: 35.5 months vs 17.9 months, respectively, p = 0.03). Significantly, 11 patients had a 100% reduction in maxSUV despite the presence of residual tumor.

Conclusions: Complete response and PET appear equivalent in predicting pathological downstaging. However, a 50% reduction in the maxSUV after induction therapy is more significantly associated with improved DFS than CR or pathological downstaging. Additionally, a complete absence of PET signal cannot be equated with a complete pathological response.

	Introduction

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Survival of patients with esophageal cancer is poor [1]. While surgical resection remains the mainstay of treatment for locally advanced disease, five-year survival after surgery alone is in the range of 15 to 30% [2, 3]. These results have prompted many clinicians to adopt a multimodality approach for the treatment of this disease, combining chemotherapy, radiotherapy, and surgery [3–5]. While the effect of this strategy on overall survival remains controversial, it appears that patients in whom a major pathological response is achieved derive a survival benefit [4, 5]. Therefore, accurate assessment of pathological response to therapy prior to esophagectomy may allow better prognostic stratification and (or) tailoring of subsequent therapy for individual patients. Unfortunately, standard restaging modalities, such as computed tomography (CT), endoscopy, and endoscopic ultrasonography (EUS), do not reliably predict significant response to preoperative therapy, much less subsequent patient survival [6–8].

F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) has emerged as an important functional imaging tool for the staging and restaging of a number of solid tumors including breast cancer, lung cancer, gastric cancer, and rectal cancer [9–13]. Its potential value as a predictor of pathological response to therapy in esophageal cancer was explored by several investigators principally, if not exclusively, in the setting of preoperative chemoradiotherapy (CRT) [14–19]. Most of these studies have shown that PET scanning after preoperative CRT can reliably identify patients with a complete pathological response (cPR) and those with microscopic residual disease (MRD) who usually derive the greatest survival benefit after resection. In contrast to preoperative CRT, major pathological responses after induction chemotherapy alone are less common, leading some to question the survival benefit of this treatment strategy. However, we have previously reported that patients whose tumors are pathologically downstaged for T and (or) N had a five-year survival exceeding 60% despite the persistence of residual gross disease [20]. In contrast, patients whose tumors were not similarly downstaged had a five-year survival of only 25%. Thus, the preoperative identification of pathological downstaging may be helpful in guiding further treatment strategy. The primary objective of the current study was to examine the hypothesis that PET scanning, rather than conventional clinical response assessment, may better predict pathological downstaging, pathological response, and survival after resection.

	Patients and Methods

Top Abstract Introduction Patients and Methods Results Comment Discussion References

 
Patients
This study was a retrospective review of a prospectively assembled, Institutional Review Board approved, thoracic database. It was approved by the Institutional Review Board of the Weill Medical College of Cornell University and patient consent was waived. Patients were only eligible for this review if a PET scan with a reported maximal SUV (maxSUV) was performed prior to, and two to three weeks after, preoperative chemotherapy. Sixty-two patients who underwent esophagectomy for cancer between January 1999 and December 2005 met these eligibility criteria. All patients were initially staged by a thorough history and physical examination, computed tomographic (CT) scan of the thorax and upper abdomen, whole body PET scan, EUS, and endoscopy. After chemotherapy, restaging was performed by CT scanning, PET scanning, and a repeat endoscopic evaluation. All endoscopic evaluations were performed by the attending surgeon with particular attention to the length of the tumor and pathological documentation of endoluminal disease. Endoscopic ultrasonography was not done for restaging purposes.

Chemotherapy
Patients were considered for preoperative chemotherapy if they had T2-T3N0M0, T1- T3N1M0 or T1-T3M1a, or M1b (lymph node) stages. All patients received two to three cycles of platinum-based chemotherapy. Paclitaxel/carboplatin was the most common doublet utilized (74%). All but one patient completed at least two cycles of therapy. There were no chemotherapy-related deaths.

PET Scanning
All PET scans were performed on a dedicated whole body PET scanner (General Electric Medical Systems, Milwaukee WI). After six hours of fasting, 10 to 15 millicuries of 18F-FDG were injected and followed by image acquisition 45 to 60 minutes after injection. Positron emission tomographic scans were read by a nuclear radiologist unaware of the clinical data. Scans were interpreted for the presence or absence of visceral metastases and the maxSUV in the primary tumor. The maxSUV was calculated using commercially available software.

Assessment of Response
In the absence of distant metastases by CT and PET scanning, an objective clinical response was determined solely on the basis of changes in tumor length as determined by endoscopic examination. While both CT and PET were used to assess distant disease, neither was employed in assessing response of the primary tumor to chemotherapy. A complete clinical response (CR) was considered present if there was no visible and histologic evidence of endoluminal disease. A partial response (PR) was determined if there was at least a 50% reduction in the length of the primary tumor as determined by endoscopy. Patients with a change in the length of tumor between 25% and 50% were considered to have a minimal response (MR) while those with a lesser decrement or no change in length were considered to have stable disease (SD). The PET activity in the primary tumor was not a criterion for response assessment. However, patients with a complete response at the primary site, but with a persistent PET signal at a distant nodal site (celiac, recurrent laryngeal, and supraclavicular), were assigned to the partial response category.

Surgical Resection
One patient was unresectable at exploration due to tracheal invasion by the primary tumor. The remaining 61 patients had an R0 resection; 58 by en bloc resection (11 two- field, 47 three-field) and three by transhiatal approach. All but one of the resected patients survived the perioperative period. Follow-up was available in 100% of patients.

Pathologic Downstaging and Response
To assess downstaging from chemotherapy, the pretreatment clinical stage (cTNM) was compared with the postsurgical, pathologic stage (pTNM). Downstaging was defined as either a reduction in the T descriptor, the N descriptor, or both.

Pathological Response
A major pathologic response was defined as either complete disappearance of all tumors (pCR) or the presence of less than 10% viable tumor in the resected specimen (MRD).

Statistical Analysis
The percent reduction in maxSUV after induction therapy was determined and receiver operating characteristic (ROC) analysis was performed to identify a threshold value of percent reduction in maxSUV for predicting (1) clinical response (defined as complete/partial response [CR/PR] versus minimal response/stable disease [MR/SD]) and (2) pathological downstaging (defined as a reduction in pT and [or] pN). Sensitivity, specificity, positive and negative predictive values, and area under the ROC curve (AUC) are reported. The ² test was used for categoric outcomes and the nonparametric Wilcoxon rank sum test was used for continuous outcomes, as appropriate. Kaplan-Meier survival analysis was performed to compare disease-free survival (DFS) between patients with a 50% and greater reduction and less than 50% reduction in maxSUV after induction therapy (threshold value as determined from the ROC analysis), DFS between clinical responders (CR/PR) and nonresponders (MR/SD), DFS between pathological responders (pCR/MRD) and nonresponders, and DFS between pathologically downstaged and nondownstaged patients. Patient "events" counted for disease-free survival included alive with disease, died from disease, and died other cause. A multivariate Cox proportional hazards regression model of independent prognostic factors for DFS was performed, including clinical stage, clinical response, reduction by 50% or greater in maxSUV (compared with < 50%), pathological stage, and pathological downstaging. Pathologic response could not be included in the model because of too few events. All p values are two-sided with statistical significance evaluated at the 0.05 alpha level. All analyses were performed in SAS version 9.1 (SAS Institute, Inc, Cary, NC) and STATA version 8.0 (Stata Corp, College Station, TX).

	Results

Top Abstract Introduction Patients and Methods Results Comment Discussion References

 
Sixty-two patients (52 male) with a median age of 62 (36 to 79) were included in this review, the majority of whom had adenocarcinoma (82%). The clinical and pathological characteristics are shown in Table 1. Seventy-five percent of patients had clinical stage III or IV disease at presentation. Twenty-eight patients (45%) were downstaged in their pT and/or pN descriptor. Ten patients (16%) had either a pathological complete response (pCR) (n = 3) or MRD. The DFS was significantly improved in downstaged (n = 28) versus nondownstaged patients (median DFS time: not reached vs 20.6 months, respectively, p = 0.01 [Fig 1]).. Similarly, DFS was significantly improved in pathologic responders (pCR and MRD) compared with nonresponders (median DFS time: not reached vs 21 months, respectively, p = 0.007) (Fig 2).

View larger version (9K): [in this window] [in a new window]   Fig 1. Disease-free survival (DFS) by downstaged status. Nondownstaged: n = 33 patients, 17 events. Median DFS-time = 20.6 months (95% confidence interval [CI] = 15.6 months, 30.4 months); two-year DFS probability = 40.9% (95% CI = 20.4%, 60.5%). Number of patients at risk over time: at 0 months, n = 33; at 12 months, n = 18; at 24 months, n = 6; at 36 months, n = 0. Downstaged: n = 28 patients, 7 events. Median DFS-time = not reached. Two-year DFS probability = 68.7% (95% confidence interval = 42.4 to 84.9. Number of patients at risk over time: at 0 months, n = 28; at 12 months, n = 15; at 24 months, n = 10; at 36 months, n = 6. (p value by log-rank test = 0.01.)

View larger version (9K): [in this window] [in a new window]   Fig 2. Disease-free survival (DFS) by pathological response. Clinical response/microscopic residual disease (CR/MRD): n = 10 patients, 1 event. Median DFS time = not reached. Two-year DFS probability = 88.9% (95% confidence interval = 43.3 to 98.4). Number of patients at risk over time: at 0 months, n = 10; at 12 months, n = 9; at 24 months, n = 6; at 36 months, n = 3. None: n = 51 patients, 23 events. Median DFS time = 20.6 months (95% CI = 15.7 months to 30.9 months). Two-year DFS probability = 43.9% (95% CI = 26.2 to 60.2). Number of patients at risk over time: at 0 months, n = 51; at 12 months, n = 25; at 24 months, n = 10; at 36 months, n = 3. (p value by log-rank test = 0.007.)

View larger version (9K): [in this window] [in a new window]   Fig 3. Disease-free survival (DSF) by clinical response. Complete response/partial response (CR/PR): n = 39 patients, 17 events. Median DFS time = 27.6 months (95% confidence interval [CI] = 18.4 months, upper limit not estimated). Two-year DFS probability = 53.0% (95% CI = 33.3 to 69.2). Number of patients at risk over time: At 0 months, n = 39; at 12 months, n = 24; at 24 months, n = 12; at 36 months, n = 5. Minor response/stable disease (MR/SD): n = 22 patients, 7 events. Median DFS time = 30.4 months (95% CI = 15.6 months, upper limit not estimated). Two year DFS probability = 54.1% (95% CI = 24.3 to 76.6). Number of patients at risk over time: at 0 months, n = 22; at 12 months, n = 10; at 24 months, n = 4; at 36 months, n = 1. (p value by log-rank test = 0.77.)

View larger version (11K): [in this window] [in a new window]   Fig 4. Receiver operating curve (ROC) curve for percent reduction in standardized uptake value (SUV) after chemotherapy as a predictor of clinical response (response defined as complete response/partial response [CR/PR] versus minor response/stable disease [MR/SD]) (referent). Optimal "percent reduction in SUV after chemotherapy" cutpoint for predicting CR/PR versus MR/SD is 50% or greater reduction in SUV after chemotherapy (sensitivity = 73.7%, specificity = 60.9%).

View larger version (16K): [in this window] [in a new window]   Fig 5. Median positron emission tomographic values before chemotherapy and by clinical response.

View larger version (11K): [in this window] [in a new window]   Fig 6. Receiver operating characteristic (ROC) curve for percent reduction in standardized uptake value (SUV) after chemotherapy as a predictor of downstaging status. Optimal "percent reduction in SUV after chemotherapy" cutpoint for predicting downstaging versus non-downstaging is 50% or greater reduction in SUV after chemotherapy [sensitivity = 77.8%, specificity = 52.9%].

Predicting Survival
The median follow-up time for the cohort was 24 months (range, 7.8 to 146.1). Five-year DFS for the entire cohort was 35% (Fig 7). Thirty-seven patients (59.7%) had a reduction in maxSUV of their primary tumor equal to or exceeding 50%. Disease-free survival was significantly improved in patients with a 50% or greater reduction in maxSUV compared with those patients with a less than 50% reduction in maxSUV (median DFS time: 35.5 months vs 17.9 months, respectively, p = 0.03; Fig 8).

View larger version (7K): [in this window] [in a new window]   Fig 7. Disease-free survival (DSF) for the entire study group (n = 61 patients with 24 events [n = 2 alive with disease, n = 20 died from disease, n = 2 died other cause]). Median DFS time = 27.6 months (95% confidence interval [CI] = 18.2 months, upper limit not estimated). Two-year DFS probability = 53.1% (95% CI = 36.6 to 67.0). Number of patients at risk over time: at 0 months, n = 61; at 12 months, n = 34; at 24 months, n = 16; at 36 months, n = 6.

View larger version (11K): [in this window] [in a new window]   Fig 8. Disease-free survival (DSF) for percent reduction in maxSUV after induction chemotherapy. A 50% or greater reduction in maxSUV: n = 36 patients with 11 events (n = 2 alive with disease, n = 9 died from disease). Median DFS time = 35.5 months (95% confidence interval [CI] = 24.0 months, upper limit not estimated). Two-year DFS probability = 65.9% (95% CI = 42.6 to 81.5). Number of patients at risk over time: at 0 months, n = 36; at 12 months, n = 23; at 24 months, n = 12; at 36 months, n = 4. Less than 50% reduction in maxSUV: n = 24 patients with 12 events (n = 11 died from disease, n = 1 died other cause). Median DFS time = 17.9 months (95% CI = 11.0 months to 30.4 months). Two-year DFS probability = 36.4% (95% CI = 15.1 to 58.2). Number of patients at risk over time: at 0 months, n = 24; at 12 months, n = 10; at 24 months, n = 4; at 36 months, n = 1. (n =2 patients with missing information.)

	Comment

Top Abstract Introduction Patients and Methods Results Comment Discussion References

We initiated the present study to evaluate the comparative efficacy of PET scanning and clinical response in predicting tumor downstaging, pathological response, and survival after preoperative chemotherapy alone, thus avoiding the possible confounding effects of radiation. Our results show that current estimates of clinical response inadequately predict tumor downstaging. Although an objective clinical response identified 24 of 28 downstaged patients, nearly 40% of clinical responders were not downstaged. The high sensitivity for clinical response in detecting tumor downstaging was offset by its poor specificity. Contrary to what is commonly assumed, the DFS of clinical responders was not significantly different from that of nonresponders. Unfortunately, the ability of PET to detect downstaging was similarly inadequate. Although the sensitivity of PET for predicting downstaging was an acceptable 75%, specificity was poor at 53%. In fact, 43% of tumors with a reduction in maxSUV 50% or greater were not downstaged after chemotherapy. Nonetheless, a 50% or greater reduction in maxSUV was a significant predictor of an improvement in DFS, regardless of pathological downstaging (two-year survival: 66% vs 36%). In the multivariate analysis, a 50% or greater reduction in maxSUV of the primary tumor was confirmed to be a more significant determinant of survival than cTNM stage, pTNM stage, and tumor downstaging. It is intriguing to speculate that PET detects a biological "signal" beyond that of simple tumor downstaging alone. The inherent ability of PET to assess tumor cellular metabolism may allow for the identification of tumors with a more biologically favorable behavior or those with a higher sensitivity to chemotherapy. Future neoadjuvant studies should further explore the possibility of utilizing a 50% or greater reduction in maxSUV as a criterion for resection rather than the standard guideline of a clinical response to therapy. Finally, we have extended the observation made by several investigators that the absence of a PET signal in the primary tumor cannot be construed as evidence of tumor sterilization. In fact, 11 of 13 patients with 100% reduction in PET signal had residual disease.

This study is limited by its retrospective nature and the post hoc determination of a cutoff maxSUV value. Future studies should attempt to validate our results and those of other investigators, in a prospective manner, using a predefined maxSUV cutoff value in a large cohort of patients, receiving uniform preoperative therapy. However, the results of this and previously reported studies suggest that PET scanning after induction therapy may be a useful and important adjunct in patient management.

	Discussion

Top Abstract Introduction Patients and Methods Results Comment Discussion References

 
DR ERIC VALLIÈRES (Seattle, WA): Nice presentation and nice piece of work Jeffrey. In this series, what was the timing of the PET scan after chemotherapy and before surgery, and what do you recommend as the best time to obtain the test after induction therapy?

DR PORT: We have been performing the PET scans about two to three weeks after the patient’s completion of preoperative chemotherapy. There have been reports in which the repeat PET scan was performed at even earlier intervals and have shown the scans to be predictive. However, for this study the timing was two to three weeks following therapy.

DR FREDERIC W. GRANNIS (Duarte, CA): In the case of non-small cell lung cancer, some investigators argue that if you do not have a reduction in the PET that you shouldn’t operate on the patient. What conclusions do you draw? Are you operating on the patients who don’t have a 50% reduction or do you recommend that they be treated by other means?

DR PORT: We have not yet altered treatment for these patients. Currently, I have a discussion with the patients and I indicate that the repeat PET results are a new risk factor that we need to discuss. But I think that the results are intriguing, and there is now enough cumulative PET data available to stimulate a discussion about altering the treatment algorithm for poor responders.

DR JOSHUA R. SONETT (New York, NY): Excellent study and presentation. I enjoyed it. I’m just wondering about your choice of just induction chemo versus chemo and radiation therapy, as chemo and radiation has been shown as the treatment of choice nonoperatively and clearly shows better response rates. Why would you go with chemo alone?

DR PORT: Well, we beg to differ. I think that there are now at least seven randomized trials showing no benefit to induction chemoradiotherapy. In fact, there are two recent European trials with over 800 patients demonstrating a benefit for induction chemotherapy alone, Medical Research Council (MRC), and Medical Research Council Adjuvant Gastric Infusional Chemotherapy (MAGIC) Trial. Yet, here in the US we have embraced induction chemoradiotherapy for reasons which are just not well supported by the data. We must remember that, while chemoradiotherapy does give result in higher pathological response rates, it has yet to translate into improved survival.

DR STEPHEN C. YANG (New York, NY): Very nice presentation. Does your PET downstaging correlate with the stage downstaging; ie, is there a greater SUV decrease in those patients with a higher stage versus those who have, say, N0 disease but have T2/T3N0 disease? Second, if you still have persistent M1a or M1b disease, do you still operate on those patients, and why?

DR PORT: Nine out of the ten patients with a pathologic complete response or microscopic residual disease had a greater than 50% reduction in their primary tumor maxSUV. PET sensitivity and specificity for predicting either pCR or MRD was 90.0% and 45.1%, respectively. In regards to patients with persistent M1a or M1b disease, we will resect these patients and make every effort to completely dissect the affected nodal basins.

DR WAYNE HOFSTETTER (Houston, TX): Dr. Port that was a nice presentation, which I enjoyed. Generally, I agree with your conclusions. I just have one question and a comment as well. We have reviewed our data regarding those patients who underwent induction chemotherapy followed by chemoradiotherapy and looked at pathologic response in terms of downstaging. We found that in patients who have had a significant pathologic response there is an associated improvement in survival. Now, this is retrospective. We also looked at the patients who had only received chemoradiotherapy and looked at pathologic response. If they had a complete response it was associated with improved survival and I think the other studies have corroborated this finding. Our data indicated that patients who had partial responses had improvement in survival as well. When you reviewed your data, did you look at pathologic response or clinical response.

DR PORT: We agree that patients who have a major pathological response derive a survival benefit. However, these make up a small minority of all patients and you need to have the resected specimen to determine pathological response. We therefore looked at other predictors like repeat PET scanning as a means to identify greater numbers of patients who might derive a survival benefit and try to identify them pre-resection.

DR LUIS D. BERRIZBEITIA (Princeton, NJ): Could you elaborate on how you used the ROC curves to determine that a 50% reduction was favorable?

DR PORT: The percent reduction in maxSUV after induction therapy was determined and ROC analysis was performed to identify a threshold value of percent reduction in maxSUV for predicting (1) clinical response (defined as complete/partial response [CR/PR] versus minimal response/stable disease [MR/SD]) and (2) pathological downstaging (defined as a reduction in pT and/or pN).

DR SCOTT J. SWANSON (New York, NY): If about 60 or so patients went through this trial and you’re using T2a and above, that seems like a small percentage of the patients you’re seeing with those stages. Did everyone who was stage IIA and above get chemotherapy and, if not, how do you decide who gets induction or not?

DR PORT: The study spans six years. It is our current practice to offer induction chemotherapy to patients with cIIa and above with good performance status. The reason for smaller numbers is that patients had to have pre and post PET scans performed and this was not our standard practice early in the study period.

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Top Abstract Introduction Patients and Methods Results Comment Discussion References

 

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				X.-B. D'Journo, P. Michelet, L. Dahan, C. Doddoli, J.-F. Seitz, R. Giudicelli, P. A. Fuentes, and P. A. Thomas Indications and outcome of salvage surgery for oesophageal cancer Eur. J. Cardiothorac. Surg., June 1, 2008; 33(6): 1117 - 1123. [Abstract] [Full Text] [PDF]

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Jeffrey L. Port Paul C. Lee Robert J. Korst Nasser K. Altorki Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Port, J. L. Articles by Altorki, N. K. Search for Related Content PubMed PubMed Citation Articles by Port, J. L. Articles by Altorki, N. K. Related Collections Esophagus - cancer