Rationale for surgery after chemotherapy

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The rationale for post-chemotherapy RPLND is based on (1) the established diagnostic role, (2) the therapeutic efficacy of the procedure, (3) the natural history of residual masses, and (4) the decreasing morbidity of these surgical procedures.

With regard to the diagnostic role of RPLND, surgical resection after chemotherapy yields one of the following histologic findings: (1) pure necrosis or fibrosis, (2) teratoma with or without necrosis/fibrosis, (3) viable germ cell carcinoma to any degree, or (4) non-germ cell carcinoma to any degree. The frequencies of these histologies vary in the literature and are summarized in Table 1 [3-17]. In general, necrosis/fibrosis is found in 50%, teratoma in 35%, and viable germ cell tumor in 15%. The rare finding of non-germ cell elements (ie, malignant transformation) is addressed in another article in this issue. There is no established instrument, parameter, or nomo-gram to accurately predict the histology of the residual mass preoperatively. Because precise determination of the histology is crucial in dictating further therapy and follow-up, surgical excision is usually necessary. For instance, in the setting of negative serum tumor markers (STM) after chemotherapy, one cannot discern if the residual mass is necrosis/fibrosis only (destined never to harm the patient in long term follow-up without surgery) or if the mass harbors viable germ cell tumor. Proposed predictive models are discussed in a later section of this article.

Another rationale for post-chemotherapy RPLND is the established therapeutic benefit to complete removal of the residual mass, lo o o

Table 1

Histologic findings for standard post-chemotherapy retroperitoneal lymph node dissection studies in relation to tumor size

Study

Year N

Tumor Residual

Clinical marker masses Necrosis stage Chemotherapy levels (cm) N (%)

Median

Donohue et al

Bracken et al

Gelderman et al [84] Williams et al

Mulders et al

1982

51 II-IV

Induction

1983 45 III

Induction

Freiha et al [5] 1984 40 IIc = 10, Induction

Pizzocaro et al 1985 36 II-III Induction

Fossa et al [7] 1989 101 II-IV Induction

1988 35 III-IV

1989 29 II

1990 55 IIc-IV

Induction

Normal

Normal

Normal Normal Normal

Normal

22 not palpable,

23 palpable NS

NS NS

Induction, 23 normal,

4; 2nd line, 6 elevated 3 RT

Induction Normal > 1

16 (31%)

16 (31%)

19 (37%)

14 (64%) 8 (35%)

3 (14%) 7 (30%)

5 (23%) 7 (30%)

21 (52%)

18 (45%)

1 (3%)

16 (44%)

10 (28%)

10 (28%)

52 (51%)

37 (37%)

12 (12%)

17 (49%)

14 (40%)

4 (11%)

13 (52%)

9 (36%)

3 (12%)

31 (56%)

12 (22%)

12 (22%)

Fibrosis: 15/16

NED;

Teratoma:

15/16 NED;

cancer:

10/19 NED

13/22 (59%)

NED18/23

I M

(78%) NED

et

37 NED, 3

al

relapse

11/18 (61%)

NED

Fibrosis/

teratoma:

83/89 (93%)

NED; cancer:

7/12(58%)

NED

25/35 (66%)

NED

29/29 (100%)

NED

Fibrosis 93% (3 y); teratoma 92% (3 y); cancer: 27% (3 y)

Harding et al 1989 42 Ilb-IV Induction Normal [10]

Aass et al [11] 1991 173 II-IV Induction Normal

Kulkarni et al [12]

Aprikian et al [67]

1991 67 Ilb-IV

1994 40 IIb—III

Induction

Induction, 5 2nd line

Normal, 63%; elevated, 37% Normal

Steyerberg et al [26] Brenner et al [13]

Coogan et al (nerve sparing) [74]

Rabbani et al [36]

1995 556 II-IV

1996 24 II-IV

1996

1998 50 II & III

Induction

Induction, 21 salvage,

5 BM transplant

Induction,

6 2nd line, 3 BM transplant

Induction, 9 2nd line

Normal

22 normal, 2 elevated

Normal

Normal

Stage II: <5. 2 (5%); >5. 17 (42%); Stage II: NS NS

2-20

Stenning et al 1998 153 II-III [14]

Induction

Normal

85 (49%) 50 (25%) 38 (29%) 75 (49-107) 160/173 (92%)

13 (54%) 8 (33%) 3 (13%) NS 79% 5-y overall g survival j>

23 (28%) 54 (66%) 4 (5%) 35.5 (12-87) 79 NED, 1 g relapse, 1 Ï?

death 2

27/76 38/76 11/76 Right-sided Right: 20/22 S

45 (29%) 85 (56%) 23 (15%) 84 (24-120) Fibrosis: 90%

(continued on next page)

Table 1 (continued)

Tumor

Residual

Median

Clinical

marker

masses

Necrosis

Teratoma

Carcinoma

follow-up

Study

Year

N

stage

Chemotherapy

levels

(cm)

N (%)

N (%)

N (%)

(months)

Survival (%)

Donohue

1998

414

II-IV

Induction

Normal

NS

25%

52%

23%

108

Relapse rate

et al [33]

11.8%, CSS 95%

Napier

2000

48

II-IV

Induction

Normal

NS

15 (31%)

24 (50%)

9 (19%)

66 (12-153)

37/48 (77%)

et al [15]

NED

Hendry

2002

330

II-IV

Induction

46%

R1

84 (25%)

218 (66%)

28 (8%)

77

83% 5-y NED,

et al [16]

elevated

89% 5-y overall survival

Oldenburg

2003

87

II

Induction

19 elevated,

1 (0-2)

58 (67)

23 (26%)

6(7)

80 (15-148)

94% 5-y NED,

et al [40]

68 normal

96% 5-y overall survival

Albers et al [45]

2004

193

II-III

Induction

Normal

NS

35%

34%

31%

NS

NS

Muramaki

2004

24

II-III

Induction,

Normal

<3, 62.5%; >3,

15 (63%)

6 (25%)

3 (12%)

NS

Complete

et al [17]

12 2nd line

37.5%

resection: 100% 3-y CSS; incomplete resection: 50% 3-y CSS

Abbreviations: BM, bone marrow; CSS, cancer-specific survival; NED, no evidence of disease; NS, not specified; RT, radiotherapy.

Abbreviations: BM, bone marrow; CSS, cancer-specific survival; NED, no evidence of disease; NS, not specified; RT, radiotherapy.

particularly in the setting of residual viable GCT and teratoma. Fox and associates [18] from Indiana University reported on the results of 580 men who underwent post-chemotherapy RPLND, 417 after primary chemotherapy and 163 after salvage chemotherapy. Forty-three (10%) patients after primary chemotherapy and 90 (55%) after salvage chemotherapy had viable germ cell tumor in the resection specimens. Overall, in patients who had viable tumor in the post-chemotherapy mass, incomplete resection was associated with a significantly higher rate of death from testis cancer (88% in incomplete resections versus 40% in complete resections). The survival advantage of complete resection of viable germ cell tumor was even significant in the group of patients who did not receive further chemotherapy after RPLND, further supporting the therapeutic role of post-chemotherapy RPLND. In addition to the therapeutic benefit, surgical resection for remnant viable germ cell also confers staging benefits because the surgery removes the residual cancer, and patients who received only primary chemotherapy can then benefit from additional chemotherapy [18].

Perhaps as important as the diagnostic and therapeutic roles of post-chemotherapy RPLND for the patient who harbors viable GCT is the role of surgery in influencing the well-recognized natural history of teratoma and its impact on patient survival and morbidity. The finding of teratoma in the resected specimen confers a therapeutic benefit to the patient because surgery is the definitive treatment modality for teratomas that are not chemosensitive. Left alone, masses containing teratoma can remain stable, locally grow and potentially compromise vital adjacent organ function by compression (eg, growing teratoma syndrome [19]), or undergo malignant transformation or degeneration into other types of cancer, which are generally resistant to chemotherapy [20-22].

A final rationale for post-chemotherapy surgery is its now acceptable morbidity. This advance came about in part by refinements in surgical approaches, brought by a better understanding of the primary landing zones for metastatic spread in testis cancer and the anatomic relations of the hypogastric nerves that control ejaculation. These refinements include obviating the need for supra-hilar dissection, using modified unilateral surgical templates, and applying nerve-sparing techniques in selected cases. Another reason for the decreased morbidity is enhanced perioperative medical care

[23,24]. This topic is discussed further later in this article.

In summary, surgical resection of retroperito-neal lymph nodes after chemotherapy has the advantage of accurate determination of the retro-peritoneal histology and staging of the disease, factors that dictate the need for additional therapy and allow for improved prognostication. More importantly, complete resection of residual retro-peritoneal masses results in therapeutic control over any masses that may cause late relapse of GCT. In particular, teratoma may undergo malignant transformation, a deadly result of an uncontrolled retroperitoneum. The natural history and biology of late relapses are covered in a separate article in this issue. Lastly, the morbidities of the procedure do not outweigh the benefits of the diagnostic and therapeutic gains.

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