We are honored to present the following interview with Dr. Craig Nichols, one of the leading Testis Cancer oncologists in the world. His candid and knowledgeable answers make this a "must read" document for anyone interested in testicular cancer...

Editor's Note: This interview is getting rather old. When it was first conducted, Dr Nichols was still at Indiana University and Lance Armstrong had not won the Tour de France even once. Nevertheless, the treatment of testicular cancer has not really changed all that much since the early 1990's, and the information presented here is basically accurate. I will endeavor to get the Q & A updated in 2013.

1) Indiana University has a world renowned reputation for treating testicular cancer. Why is IU so interested in this area? How long has IU been working in this area, and who are the key players, past and present?

2) What are the most current theories regarding the cause(s) of TC?

3) What are the main symptoms and tests that lead to a diagnosis of testicular cancer versus that of something else?

4) What is the best way to locate competent TC medical help in a given area?

5) What specific path(s) does TC use to spread throughout the body?

6) Why do an inguinal orchiectomy vs. a biopsy? Could you explain an inguinal orchiectomy?

7) Are there any situations in which the other testicle should be biopsied to identify pre-cancerous cells?

8) What kind of information do you need from the pathology report in order to determine the proper treatment?  Is TC something most pathologists are familiar with?

    CN: The primary information that is useful for treatment determinations is whether the tumor is of the non-seminomatous variety or pure seminoma. Even in patients who have a pathological appearance of pure seminoma, the elevation of alpha-fetoprotein in the serum mandates management as a non-seminoma.

    Secondary information that contributes to the management of the patient are the presence or absence of teratomatous elements, the presence of and percentage of embryonal cell carcinoma elements and the presence of vascular invasion (the venous or lymphatic channels within the testis). On occasion there are non-germ cell tumors of the testis for which very different management is required. These are quite rare tumors and any suspicion of a non-germ cell testicular tumor probably should suggest a pathology second opinion be obtained.

    Pathology in testis cancer can be complex. When coupled with tumor markers and clinical findings most experienced pathologists in larger centers are able to render correct diagnoses. Situations that suggest the need for pathology review are unusual clinical circumstances, unanticipated lack of response to therapy, or unusual sites of disease.

9) What are the overall percentages of various types of tumors diagnosed?

    CN: Seminoma is far and away the most common subtype of testicular cancer and accounts for about 40% of all cases. Non-seminoma subtypes in various percentages account for the rest. Most common subtypes are teratocarcinoma and embryonal cell carcinoma. Pure choriocarcinoma and pure yolk sac tumors of the testis are rare.

10) Are you seeing an increase in testicular cancer in immunocompromised patients (i.e. AIDS)? Is the treatment any different for these patients?

11) What is the overall time table for testicular cancer recurrence?

12)What is the percentage of left side/right side TC cases?

13) How common are false negative tests in testicular cancer?

14) What level of trust should the doctors have in testicular cancer markers? Are there any new tests on the horizon?

15) If the patient's blood markers are elevated, does that always mean they have active cancer?

16) If a man is not concerned about fertility and cannot live with the risk of developing a contralateral primary tumor, should he receive preventive radiation?

17) Considering that testicular cancer has such a high cure rate, what are researchers concentrating on now? What are the research plans for the future?

18) Why aren't MRIs used instead of abdominal CT scans?

19) Would an MRI or PET scan show more details about a residual mass in the abdomen than CT scan in patients with seminoma?

20) What exactly is a PET scan, and what is it's role in testis cancer?

21) What is the normal time for microscopic cancer in the abdomen to grow into something recognizable (such as via CT)?

22) If a man has passed through puberty and has an undescended testicle that has not been brought down, how should it be managed?

23) Do patients with undescended testis have a higher risk of recurrence and is the risk of recurrence affected by whether or not the testis is "brought down"?

24) How common are non-germ cell tumors of the testis, and do they require the attention of a specialist?

25) Extragonadal germ cell tumors and choriocarcinomas are considered rare and deadly-could you talk a little bit about these entities?

26) What is the difference between germ cell tumors in men and women?

27) What are your thoughts on universal screening for testicular cancer?

28) Should a man taking replacement testosterone be concerned about long term carcinogenic effects?

29) Are patients who have had testicular cancer are more likely to develop cancers elsewhere than someone who has never had any form of cancer?

30) Are there any ideas why teratoma is benign in children and malignant in adults?

31) When is surveillance appropriate in someone with early stage testicular cancer?

32) Can radiation cause permanent infertility? What are the prime negative effects concerning radiation therapy and testicular cancer?

33) If a patient has had stage I seminoma and received adjuvant radiation therapy and subsequently develops a second early stage seminoma on the other side, could he receive additional radiation therapy?

34) What are the chances of recurrence after surveillance vs. adjuvant radiation therapy in stage I seminoma? If they are close, why isn't surveillance used more commonly?

35) Are there any situations where chemotherapy is appropriate for primary management of early stage non-seminoma? (For example, a patient with 100% embryonal cell on the orchiectomy specimen, normal blood markers and a negative CT scan).

36) Do different approaches to early stage non-seminoma (surveillance, retroperitoneal lymphadenectomy, adjuvant chemotherapy) have similar long term cure rates?

37) What are the chemotherapy treatments for patients with disseminated germ cell tumors, why are they used in combination, and why do some doctors prefer to delete bleomycin?

38) Are there any chemotherapy combinations that are better than others? Are there any regimens that fallen out of favor over the years?

39) Could you talk a little bit about the discovery of cisplatin and its place in the history of treating TC?

40) What is the difference between cisplatin and carboplatin?

41) What determines whether a patient should receive 2, 3, or 4 cycles of chemotherapy?

42) If the testis is a sanctuary site for chemo, how come all the germ cells are killed and the patient becomes infertile?

43) Is there any difference between the chemo regimens used for seminoma and nonseminoma? Is there any difference based on Staging?

44) Do cancer cells become resistant to chemotherapy?

45) Is there any difference between outpatient and inpatient chemo for testicular cancer? Is this a hospital or insurance decision, or is it just the wave of the future?

46) Is high dose chemotherapy still a viable option for patients with advanced disease or recurrent disease?

47) When and why is surgery needed after chemotherapy?

    CN: At Indiana University, the decision to add surgery to the treatment plan is considered in those patients with non seminoma and with residual abnormalities on X-ray after completing chemotherapy. The rationale for surgery is two fold:

  1. It verifies the nature of the residual abnormality. There are in essence three possibilities to account for residual radiographic abnormalities: teratoma 40% of cases, necrosis/fibrosis (scar tissue) in 40-50% of the cases, or residual cancer in 10-15% of the cases. The identification of residual cancer is important for two reasons --
  2. a) It is removed at surgery and this serves as a therapeutic maneuver in many patients.
    b) It identifies the need for further chemotherapy in these patients.

  3. The second important function of surgery is to remove teratoma. As discussed previously, it is important to remove teratoma in the process of the management of testicular cancer. Teratoma left behind can grow locally and cause obstruction of vital organs and in rare cases degenerate to germ cell malignancy. It is quite important that complete resection of teratoma be accomplished by an experienced surgeon.
  4. The timing of surgery is somewhat variable but ordinarily this is felt to be a semi-elective procedure. We like the patient to recover nutritionally and from the rigors of chemotherapy and, accordingly, we generally schedule the surgery 4-6 weeks after the last chemotherapy.

48) How does chemotherapy effect fertility and is there an increased risk of birth defects in patients who have received chemotherapy?

49) What treatment should be recommended for a patient with otherwise stage I non-seminoma but elevated tumor markers?

50) What is the latest word on testicular implants?

51) Some people have claimed that RPLND surgery is "barbaric" surgery and overly invasive in the era of modern medicine. Why is this procedure still used?

52) Could you describe the RPLND in layman's terms, and how "templates" are used?

53) How difficult is it to perform the RPLND, and are many urologists experienced with such procedures? How realistic is it to expect a curative yet nerve sparing procedure?

54) What are the dangers and concerns regarding RPLND?

55) How soon after orchiectomy should RPLND be performed to be considered useful?

56) If a patient is unable to have normal ejaculation after the RPLND, does it ever come back or can the function be improved by treatments?

57) Is it ever possible for the lymph nodes to grow back being surgically removed?

58) Is it ever necessary to have abdominal CTs after an RPLND, and are chest or pelvic CTs ever useful in surveillance strategies?

59) Do you foresee laparoscopic retroperitoneal lymphadenectomy in the future?

60) What is/are the primary determining factors between doing an RPLND (with or without chemo) vs. just doing chemo?

On behalf of all our readers, thank you very much...

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