Lymphovascular invasion as a tool to further subclassify T1b esophageal adenocarcinoma

Putao Cen, Wayne L. Hofstetter, Arlene M. Correa, Tsung Teh Wu, Jeffery H. Lee, William A. Ross, Marta Davilla, Stephen G. Swisher, Norio Fukami, Asif Rashid, Dipen Maru, Jaffer A. Ajani

Research output: Contribution to journalArticle

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Abstract

BACKGROUND. Lymphovascular invasion (LVI) and/or lymph node metastases (LNM) adversely influence the overall survival (OS) of patients with T1 esophageal adenocarcinoma. Although endoscopic therapy may be adequate for patients with T1a cancer, patients with T1b cancer require esophagectomy/ lymphadenectomy. The authors hypothesized that LVI status would subclassify T1b cancers and facilitate new therapeutic strategies. METHODS. Ninety-nine consecutive patients with T1 adenocarcinoma were analyzed after they underwent esophagectomy/lymphadenectomy. LNM was assessed in all patients, and LVI was assessed in 89 patients. OS was correlated with pathologic cancer stage in association with LVI and LNM. RESULTS. The 5-year OS rate for patients with T1a tumors (88%) was superior to that for patients with T1b tumors (62%; P = .001). The 5-year OS rate for patients who had cancers without LVI (85%) was superior to the rate for patients who had cancers with LVI (36%; P = .0001). It is noteworthy that, for cancers without LVI, the 5-year OS rate for patients with T1b tumors (77%) was similar to the rate for patients with T1a tumors (90%; P = .08), but it was superior to the rate for patients with T1b tumors that had LVI (27%; P = .006). The presence of LVI and/or LNM resulted in worse 5-year OS (≤37%) compared with the lack of LVI and/or LNM (88%; P < .001). The rate of LNM for patients who had T1b tumors without LVI still was 19%, and the relapse rate was 16%. CONCLUSIONS. The current results demonstrated that LVI distinguishes the biologic behavior of early esophageal cancer, and patients who have T1b cancer without LVI have a clinical biology similar to that of patients with T1a cancer. If LNM before surgery can be diagnosed with high sensitivity by better endoscopic techniques and/or molecular biomarkers, then a new therapeutic paradigm for T1b cancers could emerge. Further research is needed on patients with T1b esophageal adenocarcinoma.

Original languageEnglish (US)
Pages (from-to)1020-1027
Number of pages8
JournalCancer
Volume112
Issue number5
DOIs
StatePublished - Mar 1 2008
Externally publishedYes

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Adenocarcinoma
Neoplasms
Lymph Nodes
Neoplasm Metastasis
Esophagectomy
Survival Rate
Lymph Node Excision
Survival
Esophageal Neoplasms
Therapeutics
Biomarkers

Keywords

  • Adenocarcinoma
  • Esophageal cancer
  • Lymphovascular invasion
  • T1b

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Cen, P., Hofstetter, W. L., Correa, A. M., Wu, T. T., Lee, J. H., Ross, W. A., ... Ajani, J. A. (2008). Lymphovascular invasion as a tool to further subclassify T1b esophageal adenocarcinoma. Cancer, 112(5), 1020-1027. https://doi.org/10.1002/cncr.23265

Lymphovascular invasion as a tool to further subclassify T1b esophageal adenocarcinoma. / Cen, Putao; Hofstetter, Wayne L.; Correa, Arlene M.; Wu, Tsung Teh; Lee, Jeffery H.; Ross, William A.; Davilla, Marta; Swisher, Stephen G.; Fukami, Norio; Rashid, Asif; Maru, Dipen; Ajani, Jaffer A.

In: Cancer, Vol. 112, No. 5, 01.03.2008, p. 1020-1027.

Research output: Contribution to journalArticle

Cen, P, Hofstetter, WL, Correa, AM, Wu, TT, Lee, JH, Ross, WA, Davilla, M, Swisher, SG, Fukami, N, Rashid, A, Maru, D & Ajani, JA 2008, 'Lymphovascular invasion as a tool to further subclassify T1b esophageal adenocarcinoma', Cancer, vol. 112, no. 5, pp. 1020-1027. https://doi.org/10.1002/cncr.23265
Cen P, Hofstetter WL, Correa AM, Wu TT, Lee JH, Ross WA et al. Lymphovascular invasion as a tool to further subclassify T1b esophageal adenocarcinoma. Cancer. 2008 Mar 1;112(5):1020-1027. https://doi.org/10.1002/cncr.23265
Cen, Putao ; Hofstetter, Wayne L. ; Correa, Arlene M. ; Wu, Tsung Teh ; Lee, Jeffery H. ; Ross, William A. ; Davilla, Marta ; Swisher, Stephen G. ; Fukami, Norio ; Rashid, Asif ; Maru, Dipen ; Ajani, Jaffer A. / Lymphovascular invasion as a tool to further subclassify T1b esophageal adenocarcinoma. In: Cancer. 2008 ; Vol. 112, No. 5. pp. 1020-1027.
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abstract = "BACKGROUND. Lymphovascular invasion (LVI) and/or lymph node metastases (LNM) adversely influence the overall survival (OS) of patients with T1 esophageal adenocarcinoma. Although endoscopic therapy may be adequate for patients with T1a cancer, patients with T1b cancer require esophagectomy/ lymphadenectomy. The authors hypothesized that LVI status would subclassify T1b cancers and facilitate new therapeutic strategies. METHODS. Ninety-nine consecutive patients with T1 adenocarcinoma were analyzed after they underwent esophagectomy/lymphadenectomy. LNM was assessed in all patients, and LVI was assessed in 89 patients. OS was correlated with pathologic cancer stage in association with LVI and LNM. RESULTS. The 5-year OS rate for patients with T1a tumors (88{\%}) was superior to that for patients with T1b tumors (62{\%}; P = .001). The 5-year OS rate for patients who had cancers without LVI (85{\%}) was superior to the rate for patients who had cancers with LVI (36{\%}; P = .0001). It is noteworthy that, for cancers without LVI, the 5-year OS rate for patients with T1b tumors (77{\%}) was similar to the rate for patients with T1a tumors (90{\%}; P = .08), but it was superior to the rate for patients with T1b tumors that had LVI (27{\%}; P = .006). The presence of LVI and/or LNM resulted in worse 5-year OS (≤37{\%}) compared with the lack of LVI and/or LNM (88{\%}; P < .001). The rate of LNM for patients who had T1b tumors without LVI still was 19{\%}, and the relapse rate was 16{\%}. CONCLUSIONS. The current results demonstrated that LVI distinguishes the biologic behavior of early esophageal cancer, and patients who have T1b cancer without LVI have a clinical biology similar to that of patients with T1a cancer. If LNM before surgery can be diagnosed with high sensitivity by better endoscopic techniques and/or molecular biomarkers, then a new therapeutic paradigm for T1b cancers could emerge. Further research is needed on patients with T1b esophageal adenocarcinoma.",
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T1 - Lymphovascular invasion as a tool to further subclassify T1b esophageal adenocarcinoma

AU - Cen, Putao

AU - Hofstetter, Wayne L.

AU - Correa, Arlene M.

AU - Wu, Tsung Teh

AU - Lee, Jeffery H.

AU - Ross, William A.

AU - Davilla, Marta

AU - Swisher, Stephen G.

AU - Fukami, Norio

AU - Rashid, Asif

AU - Maru, Dipen

AU - Ajani, Jaffer A.

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N2 - BACKGROUND. Lymphovascular invasion (LVI) and/or lymph node metastases (LNM) adversely influence the overall survival (OS) of patients with T1 esophageal adenocarcinoma. Although endoscopic therapy may be adequate for patients with T1a cancer, patients with T1b cancer require esophagectomy/ lymphadenectomy. The authors hypothesized that LVI status would subclassify T1b cancers and facilitate new therapeutic strategies. METHODS. Ninety-nine consecutive patients with T1 adenocarcinoma were analyzed after they underwent esophagectomy/lymphadenectomy. LNM was assessed in all patients, and LVI was assessed in 89 patients. OS was correlated with pathologic cancer stage in association with LVI and LNM. RESULTS. The 5-year OS rate for patients with T1a tumors (88%) was superior to that for patients with T1b tumors (62%; P = .001). The 5-year OS rate for patients who had cancers without LVI (85%) was superior to the rate for patients who had cancers with LVI (36%; P = .0001). It is noteworthy that, for cancers without LVI, the 5-year OS rate for patients with T1b tumors (77%) was similar to the rate for patients with T1a tumors (90%; P = .08), but it was superior to the rate for patients with T1b tumors that had LVI (27%; P = .006). The presence of LVI and/or LNM resulted in worse 5-year OS (≤37%) compared with the lack of LVI and/or LNM (88%; P < .001). The rate of LNM for patients who had T1b tumors without LVI still was 19%, and the relapse rate was 16%. CONCLUSIONS. The current results demonstrated that LVI distinguishes the biologic behavior of early esophageal cancer, and patients who have T1b cancer without LVI have a clinical biology similar to that of patients with T1a cancer. If LNM before surgery can be diagnosed with high sensitivity by better endoscopic techniques and/or molecular biomarkers, then a new therapeutic paradigm for T1b cancers could emerge. Further research is needed on patients with T1b esophageal adenocarcinoma.

AB - BACKGROUND. Lymphovascular invasion (LVI) and/or lymph node metastases (LNM) adversely influence the overall survival (OS) of patients with T1 esophageal adenocarcinoma. Although endoscopic therapy may be adequate for patients with T1a cancer, patients with T1b cancer require esophagectomy/ lymphadenectomy. The authors hypothesized that LVI status would subclassify T1b cancers and facilitate new therapeutic strategies. METHODS. Ninety-nine consecutive patients with T1 adenocarcinoma were analyzed after they underwent esophagectomy/lymphadenectomy. LNM was assessed in all patients, and LVI was assessed in 89 patients. OS was correlated with pathologic cancer stage in association with LVI and LNM. RESULTS. The 5-year OS rate for patients with T1a tumors (88%) was superior to that for patients with T1b tumors (62%; P = .001). The 5-year OS rate for patients who had cancers without LVI (85%) was superior to the rate for patients who had cancers with LVI (36%; P = .0001). It is noteworthy that, for cancers without LVI, the 5-year OS rate for patients with T1b tumors (77%) was similar to the rate for patients with T1a tumors (90%; P = .08), but it was superior to the rate for patients with T1b tumors that had LVI (27%; P = .006). The presence of LVI and/or LNM resulted in worse 5-year OS (≤37%) compared with the lack of LVI and/or LNM (88%; P < .001). The rate of LNM for patients who had T1b tumors without LVI still was 19%, and the relapse rate was 16%. CONCLUSIONS. The current results demonstrated that LVI distinguishes the biologic behavior of early esophageal cancer, and patients who have T1b cancer without LVI have a clinical biology similar to that of patients with T1a cancer. If LNM before surgery can be diagnosed with high sensitivity by better endoscopic techniques and/or molecular biomarkers, then a new therapeutic paradigm for T1b cancers could emerge. Further research is needed on patients with T1b esophageal adenocarcinoma.

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